The inhibitory receptor LAG3 affects NK cell IFN-γ production through glycolysis and the PSAT1/STAT1/IFNG pathway
We demonstrate that lymphocyte activation gene 3 (LAG3) expression is upregulated on natural killer (NK) cells during HIV infection. LAG3 inhibits glycolysis in NK cells and also upregulates PSAT1 expression to suppress activation of the STAT1/IFNG pathway, thus restricting interferon-gamma producti...
Saved in:
| Published in | mBio Vol. 16; no. 6; p. e0023025 |
|---|---|
| Main Authors | , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
American Society for Microbiology
11.06.2025
|
| Subjects | |
| Online Access | Get full text |
Cover
Loading…
| Abstract | We demonstrate that lymphocyte activation gene 3 (LAG3) expression is upregulated on natural killer (NK) cells during HIV infection. LAG3 inhibits glycolysis in NK cells and also upregulates PSAT1 expression to suppress activation of the STAT1/IFNG pathway, thus restricting interferon-gamma production by NK cells. These results provide new clues to study the effects of LAG3 on the metabolism and functional exhaustion of NK cells and offer a potential target for the treatment of HIV. |
|---|---|
| AbstractList | Natural killer (NK) cells are integral to the innate immune system and crucial for antiviral defense. NK cell activation and functional state are suppressed by inhibitory receptors. Lymphocyte activation gene 3 (LAG3) is an important inhibitory receptor, but the associated signaling pathways that regulate lymphocyte function remain to be elucidated. In addition, the effect of LAG3 on NK cell function during HIV infection and its specific mechanisms are unclear. In this study, we observed that LAG3 expression by NK cells is elevated in HIV-infected individuals and inversely correlated with CD4/CD8 ratio and CD4+ T cell count. LAG3+ NK cells produce lower levels of interferon-gamma (IFN-γ), but LAG3-Fc protein significantly enhances NK cell function. The activation of LAG3 significantly inhibits IFN-γ production and Ki67 expression by NK cells. Our transcriptome sequencing and in vitro data show for the first time that LAG3 not only regulates the transcription of MYC and several glycolysis-related enzyme genes via the PI3K/AKT/mTOR signaling pathway to inhibit glycolysis in NK cells but also suppresses the STAT1/IFNG pathway by upregulating PSAT1 expression, thus limiting IFN-γ production by NK cells via these two different pathways. Overall, these results provide new insights and identify potential targets for immunotherapy of HIV infection.Natural killer (NK) cells are integral to the innate immune system and crucial for antiviral defense. NK cell activation and functional state are suppressed by inhibitory receptors. Lymphocyte activation gene 3 (LAG3) is an important inhibitory receptor, but the associated signaling pathways that regulate lymphocyte function remain to be elucidated. In addition, the effect of LAG3 on NK cell function during HIV infection and its specific mechanisms are unclear. In this study, we observed that LAG3 expression by NK cells is elevated in HIV-infected individuals and inversely correlated with CD4/CD8 ratio and CD4+ T cell count. LAG3+ NK cells produce lower levels of interferon-gamma (IFN-γ), but LAG3-Fc protein significantly enhances NK cell function. The activation of LAG3 significantly inhibits IFN-γ production and Ki67 expression by NK cells. Our transcriptome sequencing and in vitro data show for the first time that LAG3 not only regulates the transcription of MYC and several glycolysis-related enzyme genes via the PI3K/AKT/mTOR signaling pathway to inhibit glycolysis in NK cells but also suppresses the STAT1/IFNG pathway by upregulating PSAT1 expression, thus limiting IFN-γ production by NK cells via these two different pathways. Overall, these results provide new insights and identify potential targets for immunotherapy of HIV infection.We demonstrate that lymphocyte activation gene 3 (LAG3) expression is upregulated on natural killer (NK) cells during HIV infection. LAG3 inhibits glycolysis in NK cells and also upregulates PSAT1 expression to suppress activation of the STAT1/IFNG pathway, thus restricting interferon-gamma production by NK cells. These results provide new clues to study the effects of LAG3 on the metabolism and functional exhaustion of NK cells and offer a potential target for the treatment of HIV.IMPORTANCEWe demonstrate that lymphocyte activation gene 3 (LAG3) expression is upregulated on natural killer (NK) cells during HIV infection. LAG3 inhibits glycolysis in NK cells and also upregulates PSAT1 expression to suppress activation of the STAT1/IFNG pathway, thus restricting interferon-gamma production by NK cells. These results provide new clues to study the effects of LAG3 on the metabolism and functional exhaustion of NK cells and offer a potential target for the treatment of HIV. We demonstrate that lymphocyte activation gene 3 (LAG3) expression is upregulated on natural killer (NK) cells during HIV infection. LAG3 inhibits glycolysis in NK cells and also upregulates PSAT1 expression to suppress activation of the STAT1/IFNG pathway, thus restricting interferon-gamma production by NK cells. These results provide new clues to study the effects of LAG3 on the metabolism and functional exhaustion of NK cells and offer a potential target for the treatment of HIV. ABSTRACT Natural killer (NK) cells are integral to the innate immune system and crucial for antiviral defense. NK cell activation and functional state are suppressed by inhibitory receptors. Lymphocyte activation gene 3 (LAG3) is an important inhibitory receptor, but the associated signaling pathways that regulate lymphocyte function remain to be elucidated. In addition, the effect of LAG3 on NK cell function during HIV infection and its specific mechanisms are unclear. In this study, we observed that LAG3 expression by NK cells is elevated in HIV-infected individuals and inversely correlated with CD4/CD8 ratio and CD4+ T cell count. LAG3+ NK cells produce lower levels of interferon-gamma (IFN-γ), but LAG3-Fc protein significantly enhances NK cell function. The activation of LAG3 significantly inhibits IFN-γ production and Ki67 expression by NK cells. Our transcriptome sequencing and in vitro data show for the first time that LAG3 not only regulates the transcription of MYC and several glycolysis-related enzyme genes via the PI3K/AKT/mTOR signaling pathway to inhibit glycolysis in NK cells but also suppresses the STAT1/IFNG pathway by upregulating PSAT1 expression, thus limiting IFN-γ production by NK cells via these two different pathways. Overall, these results provide new insights and identify potential targets for immunotherapy of HIV infection.IMPORTANCEWe demonstrate that lymphocyte activation gene 3 (LAG3) expression is upregulated on natural killer (NK) cells during HIV infection. LAG3 inhibits glycolysis in NK cells and also upregulates PSAT1 expression to suppress activation of the STAT1/IFNG pathway, thus restricting interferon-gamma production by NK cells. These results provide new clues to study the effects of LAG3 on the metabolism and functional exhaustion of NK cells and offer a potential target for the treatment of HIV. Natural killer (NK) cells are integral to the innate immune system and crucial for antiviral defense. NK cell activation and functional state are suppressed by inhibitory receptors. Lymphocyte activation gene 3 (LAG3) is an important inhibitory receptor, but the associated signaling pathways that regulate lymphocyte function remain to be elucidated. In addition, the effect of LAG3 on NK cell function during HIV infection and its specific mechanisms are unclear. In this study, we observed that LAG3 expression by NK cells is elevated in HIV-infected individuals and inversely correlated with CD4/CD8 ratio and CD4 + T cell count. LAG3+ NK cells produce lower levels of interferon-gamma (IFN-γ), but LAG3-Fc protein significantly enhances NK cell function. The activation of LAG3 significantly inhibits IFN-γ production and Ki67 expression by NK cells. Our transcriptome sequencing and in vitro data show for the first time that LAG3 not only regulates the transcription of MYC and several glycolysis-related enzyme genes via the PI3K/AKT/mTOR signaling pathway to inhibit glycolysis in NK cells but also suppresses the STAT1/IFNG pathway by upregulating PSAT1 expression, thus limiting IFN-γ production by NK cells via these two different pathways. Overall, these results provide new insights and identify potential targets for immunotherapy of HIV infection. Natural killer (NK) cells are integral to the innate immune system and crucial for antiviral defense. NK cell activation and functional state are suppressed by inhibitory receptors. Lymphocyte activation gene 3 (LAG3) is an important inhibitory receptor, but the associated signaling pathways that regulate lymphocyte function remain to be elucidated. In addition, the effect of LAG3 on NK cell function during HIV infection and its specific mechanisms are unclear. In this study, we observed that LAG3 expression by NK cells is elevated in HIV-infected individuals and inversely correlated with CD4/CD8 ratio and CD4+ T cell count. LAG3+ NK cells produce lower levels of interferon-gamma (IFN-γ), but LAG3-Fc protein significantly enhances NK cell function. The activation of LAG3 significantly inhibits IFN-γ production and Ki67 expression by NK cells. Our transcriptome sequencing and in vitro data show for the first time that LAG3 not only regulates the transcription of MYC and several glycolysis-related enzyme genes via the PI3K/AKT/mTOR signaling pathway to inhibit glycolysis in NK cells but also suppresses the STAT1/IFNG pathway by upregulating PSAT1 expression, thus limiting IFN-γ production by NK cells via these two different pathways. Overall, these results provide new insights and identify potential targets for immunotherapy of HIV infection.IMPORTANCEWe demonstrate that lymphocyte activation gene 3 (LAG3) expression is upregulated on natural killer (NK) cells during HIV infection. LAG3 inhibits glycolysis in NK cells and also upregulates PSAT1 expression to suppress activation of the STAT1/IFNG pathway, thus restricting interferon-gamma production by NK cells. These results provide new clues to study the effects of LAG3 on the metabolism and functional exhaustion of NK cells and offer a potential target for the treatment of HIV. Natural killer (NK) cells are integral to the innate immune system and crucial for antiviral defense. NK cell activation and functional state are suppressed by inhibitory receptors. Lymphocyte activation gene 3 (LAG3) is an important inhibitory receptor, but the associated signaling pathways that regulate lymphocyte function remain to be elucidated. In addition, the effect of LAG3 on NK cell function during HIV infection and its specific mechanisms are unclear. In this study, we observed that LAG3 expression by NK cells is elevated in HIV-infected individuals and inversely correlated with CD4/CD8 ratio and CD4 T cell count. LAG3+ NK cells produce lower levels of interferon-gamma (IFN-γ), but LAG3-Fc protein significantly enhances NK cell function. The activation of LAG3 significantly inhibits IFN-γ production and Ki67 expression by NK cells. Our transcriptome sequencing and data show for the first time that LAG3 not only regulates the transcription of MYC and several glycolysis-related enzyme genes via the PI3K/AKT/mTOR signaling pathway to inhibit glycolysis in NK cells but also suppresses the STAT1/IFNG pathway by upregulating PSAT1 expression, thus limiting IFN-γ production by NK cells via these two different pathways. Overall, these results provide new insights and identify potential targets for immunotherapy of HIV infection. We demonstrate that lymphocyte activation gene 3 (LAG3) expression is upregulated on natural killer (NK) cells during HIV infection. LAG3 inhibits glycolysis in NK cells and also upregulates PSAT1 expression to suppress activation of the STAT1/IFNG pathway, thus restricting interferon-gamma production by NK cells. These results provide new clues to study the effects of LAG3 on the metabolism and functional exhaustion of NK cells and offer a potential target for the treatment of HIV. |
| Author | Yu, Xiaowen Zhang, Zining Geng, Wenqing Ge, Hongchi Lang, Bin Han, Xiaoxu Liu, Yufei Yin, Xiaowan Hu, Qinghai Jiang, Yongjun Guo, Nan Ding, Haibo Fu, Yajing Shang, Hong |
| Author_xml | – sequence: 1 givenname: Hongchi orcidid: 0009-0005-4306-6071 surname: Ge fullname: Ge, Hongchi – sequence: 2 givenname: Nan orcidid: 0009-0005-0242-8769 surname: Guo fullname: Guo, Nan – sequence: 3 givenname: Yufei orcidid: 0009-0007-7759-2875 surname: Liu fullname: Liu, Yufei – sequence: 4 givenname: Bin surname: Lang fullname: Lang, Bin – sequence: 5 givenname: Xiaowan surname: Yin fullname: Yin, Xiaowan – sequence: 6 givenname: Xiaowen surname: Yu fullname: Yu, Xiaowen – sequence: 7 givenname: Zining surname: Zhang fullname: Zhang, Zining – sequence: 8 givenname: Yajing surname: Fu fullname: Fu, Yajing – sequence: 9 givenname: Haibo surname: Ding fullname: Ding, Haibo – sequence: 10 givenname: Qinghai surname: Hu fullname: Hu, Qinghai – sequence: 11 givenname: Xiaoxu surname: Han fullname: Han, Xiaoxu – sequence: 12 givenname: Wenqing surname: Geng fullname: Geng, Wenqing – sequence: 13 givenname: Hong orcidid: 0000-0001-5333-8943 surname: Shang fullname: Shang, Hong – sequence: 14 givenname: Yongjun orcidid: 0000-0002-8606-3971 surname: Jiang fullname: Jiang, Yongjun |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/40298450$$D View this record in MEDLINE/PubMed |
| BookMark | eNptkU1v1DAQhi1URMvSI1fkI0JK6898nNCqosuKVUHqcrYcZ7LxKomDnYDyu_o_-pvwdkvVSvgwHs28fjya9y066V0PCL2n5IJSll92pXUXhDBOEiZfoTNGJUkySenJs_wUnYewJ_FwTnNO3qBTQViRC0nOkN82gG3f2NKOzs_Yg4EhZnizXHGs6xrMGPDNN2ygbfH6-ia5v8ODd9VkRut6PDbeTbsG79rZuHYONmDdV7EM-Mftcksvb7eHGB-u8KDH5o-e36HXtW4DnD_eC_Tz-sv26muy-b5aXy03iRYiGxNKBBWCFpnMaWmyQmqmSV4VZap5LgrCGaUEqKiIMCBLJuqccDBZSoysZFXzBVofuZXTezV422k_K6eteig4v1Paj9a0oJhgKcjKiKwmgtfxh6xOOcl5BpCXAiLr85E1TGUHlYF-9Lp9AX3Z6W2jdu63otEGztI8Ej4-Erz7NUEYVWfDYam6BzcFxWmRplSK6NICfTpKdeiY2rvJ93FPihJ1MF0dTFcPpismo_jD88meRvpncRQkR4HxLgQP9ZPk_8C_nri21w |
| Cites_doi | 10.1172/JCI16603 10.1002/1521-4141(2001010)31:10<2885::AID-IMMU2885>3.0.CO;2-2 10.1371/journal.ppat.1007429 10.1101/405134 10.1172/JCI125916 10.1016/s1074-7613(03)00264-4 10.3389/conf.fimmu.2015.05.00164 10.1126/science.272.5260.405 10.1182/blood.V97.10.3146 10.1126/scisignal.2001617 10.1038/ng1097 10.1038/s41388-020-1160-4 10.1016/j.coi.2012.04.011 10.1002/eji.200425797 10.1097/ACI.0000000000000011 10.1158/2159-8290.CD-18-0367 10.4049/jimmunol.1402176 10.4049/jimmunol.1100714 10.1101/2020.01.31.928200 10.1136/jitc-2020-001014 10.4049/jimmunol.1501783 10.1016/j.celrep.2019.03.004 10.1016/j.coi.2017.11.003 10.1080/2162402X.2016.1186314 10.1158/0008-5472.CAN-11-1620 10.3389/fonc.2018.00160 10.1084/jem.171.5.1393 10.4049/jimmunol.169.10.5392 10.1172/jci.insight.95128 10.1016/j.immuni.2007.03.017 10.3389/fimmu.2020.00167 10.3389/fimmu.2019.00835 10.1038/ni1138 10.1016/j.smim.2019.101305 10.3389/fimmu.2018.02341 10.1016/j.cell.2017.07.029 10.1186/s12967-023-04667-6 10.1186/s13075-017-1309-x 10.3389/fimmu.2017.00330 10.4049/jimmunol.1401558 10.1038/nrm2882 10.1002/jcp.28215 10.1038/s41392-020-0147-5 |
| ContentType | Journal Article |
| Copyright | Copyright © 2025 Ge et al. Copyright © 2025 Ge et al. 2025 Ge et al. |
| Copyright_xml | – notice: Copyright © 2025 Ge et al. – notice: Copyright © 2025 Ge et al. 2025 Ge et al. |
| DBID | AAYXX CITATION CGR CUY CVF ECM EIF NPM 7X8 5PM DOA |
| DOI | 10.1128/mbio.00230-25 |
| DatabaseName | CrossRef Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed MEDLINE - Academic PubMed Central (Full Participant titles) DOAJ Directory of Open Access Journals |
| DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) MEDLINE - Academic |
| DatabaseTitleList | MEDLINE - Academic CrossRef MEDLINE |
| Database_xml | – sequence: 1 dbid: DOA name: DOAJ Directory of Open Access Journals url: https://www.doaj.org/ sourceTypes: Open Website – sequence: 2 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 3 dbid: EIF name: MEDLINE url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search sourceTypes: Index Database |
| DeliveryMethod | fulltext_linktorsrc |
| Discipline | Biology |
| EISSN | 2150-7511 |
| Editor | Dandekar, Satya |
| Editor_xml | – sequence: 1 givenname: Satya surname: Dandekar fullname: Dandekar, Satya |
| ExternalDocumentID | oai_doaj_org_article_2426e5dc47f043f6a37f630837ee8b4e PMC12153268 mbio00230-25 40298450 10_1128_mbio_00230_25 |
| Genre | Journal Article |
| GroupedDBID | --- 0R~ 53G 5VS AAFWJ AAGFI AAUOK AAYXX ADBBV AENEX AFPKN ALMA_UNASSIGNED_HOLDINGS AOIJS BAWUL BCNDV BTFSW CITATION DIK E3Z EBS FRP GROUPED_DOAJ GX1 H13 HYE HZ~ KQ8 O5R O5S O9- OK1 P2P PGMZT RHI RNS RPM RSF CGR CUY CVF ECM EIF NPM 7X8 5PM M48 |
| ID | FETCH-LOGICAL-a447t-104144197581bc795a2a08d9b6a3849032110e14d04ce5b24f803ec760c5d5df3 |
| IEDL.DBID | M48 |
| ISSN | 2150-7511 |
| IngestDate | Wed Aug 27 01:20:45 EDT 2025 Thu Aug 21 18:24:34 EDT 2025 Wed Jul 02 04:44:41 EDT 2025 Thu Jun 12 01:38:34 EDT 2025 Sat Jun 14 01:31:04 EDT 2025 Thu Jul 03 08:35:55 EDT 2025 |
| IsDoiOpenAccess | true |
| IsOpenAccess | true |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 6 |
| Keywords | IFN-γ LAG3 HIV STAT1 NK glycolysis |
| Language | English |
| License | This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license. https://creativecommons.org/licenses/by/4.0 This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license. |
| LinkModel | DirectLink |
| MergedId | FETCHMERGED-LOGICAL-a447t-104144197581bc795a2a08d9b6a3849032110e14d04ce5b24f803ec760c5d5df3 |
| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 The authors declare no conflict of interest. Hongchi Ge, Nan Guo, Yufei Liu, and Bin Lang contributed equally to this article. The author order was determined by drawing straws. |
| ORCID | 0009-0005-0242-8769 0009-0007-7759-2875 0009-0005-4306-6071 0000-0001-5333-8943 0000-0002-8606-3971 |
| OpenAccessLink | https://doaj.org/article/2426e5dc47f043f6a37f630837ee8b4e |
| PMID | 40298450 |
| PQID | 3196615400 |
| PQPubID | 23479 |
| PageCount | 16 |
| ParticipantIDs | doaj_primary_oai_doaj_org_article_2426e5dc47f043f6a37f630837ee8b4e pubmedcentral_primary_oai_pubmedcentral_nih_gov_12153268 proquest_miscellaneous_3196615400 asm2_journals_10_1128_mbio_00230_25 pubmed_primary_40298450 crossref_primary_10_1128_mbio_00230_25 |
| PublicationCentury | 2000 |
| PublicationDate | 2025-06-11 |
| PublicationDateYYYYMMDD | 2025-06-11 |
| PublicationDate_xml | – month: 06 year: 2025 text: 2025-06-11 day: 11 |
| PublicationDecade | 2020 |
| PublicationPlace | United States |
| PublicationPlace_xml | – name: United States – name: 1752 N St., N.W., Washington, DC |
| PublicationTitle | mBio |
| PublicationTitleAbbrev | mBio |
| PublicationTitleAlternate | mBio |
| PublicationYear | 2025 |
| Publisher | American Society for Microbiology |
| Publisher_xml | – name: American Society for Microbiology |
| References | e_1_3_4_3_2 e_1_3_4_2_2 e_1_3_4_9_2 e_1_3_4_8_2 e_1_3_4_7_2 e_1_3_4_41_2 e_1_3_4_6_2 e_1_3_4_40_2 e_1_3_4_5_2 e_1_3_4_4_2 e_1_3_4_22_2 e_1_3_4_45_2 e_1_3_4_23_2 e_1_3_4_44_2 e_1_3_4_20_2 e_1_3_4_43_2 e_1_3_4_21_2 e_1_3_4_42_2 e_1_3_4_26_2 e_1_3_4_27_2 e_1_3_4_24_2 e_1_3_4_25_2 e_1_3_4_28_2 e_1_3_4_29_2 e_1_3_4_30_2 Monica VG (e_1_3_4_34_2) 2010; 344 e_1_3_4_11_2 e_1_3_4_12_2 e_1_3_4_33_2 e_1_3_4_32_2 e_1_3_4_10_2 e_1_3_4_31_2 e_1_3_4_15_2 e_1_3_4_38_2 e_1_3_4_16_2 e_1_3_4_37_2 e_1_3_4_13_2 e_1_3_4_36_2 e_1_3_4_14_2 e_1_3_4_35_2 e_1_3_4_19_2 e_1_3_4_17_2 e_1_3_4_18_2 e_1_3_4_39_2 Dupuis, S, Jouanguy, E, Al-Hajjar, S, Fieschi, C, Al-Mohsen, IZ, Al-Jumaah, S, Yang, K, Chapgier, A, Eidenschenk, C, Eid, P, Ghonaium, AA, Tufenkeji, H, Frayha, H, Al-Gazlan, S, Al-Rayes, H, Schreiber, RD, Gresser, I, Casanova, J-L (B41) 2003; 33 Tian, X, Zhang, A, Qiu, C, Wang, W, Yang, Y, Qiu, C, Liu, A, Zhu, L, Yuan, S, Hu, H, Wang, W, Wei, Q, Zhang, X, Xu, J (B8) 2015; 194 Putz, EM, Majoros, A, Gotthardt, D, Prchal-Murphy, M, Zebedin-Brandl, EM, Fux, DA, Schlattl, A, Schreiber, RD, Carotta, S, Müller, M, Gerner, C, Decker, T, Sexl, V (B39) 2016; 5 Miyazaki, T, Dierich, A, Benoist, C, Mathis, D (B16) 1996; 272 Monica, VG, Charles, GD (B33) 2010; 344 Natalia, T, Juan, H, Julie, L, Jennifer, J, Joshua, K, Maria, R, Keith, F (B20) 2015; 6 Ruffo, E, Wu, RC, Bruno, TC, Workman, CJ, Vignali, DAA (B6) 2019; 42 Narayanan, S, Ahl, PJ, Au, VB, Kaliaperumal, N, Connolly, JE (B18) 2020 Patsoukis, N, Weaver, JD, Strauss, L, Herbel, C, Seth, P, Boussiotis, VA (B25) 2017; 8 Mocikat, R, Braumüller, H, Gumy, A, Egeter, O, Ziegler, H, Reusch, U, Bubeck, A, Louis, J, Mailhammer, R, Riethmüller, G, Koszinowski, U, Röcken, M (B3) 2003; 19 Donnelly, RP, Loftus, RM, Keating, SE, Liou, KT, Biron, CA, Gardiner, CM, Finlay, DK (B26) 2014; 193 Lesinski, GB, Anghelina, M, Zimmerer, J, Bakalakos, T, Badgwell, B, Parihar, R, Hu, Y, Becknell, B, Abood, G, Chaudhury, AR, Magro, C, Durbin, J, Carson, WE (B37) 2003; 112 Keating, SE, Zaiatz-Bittencourt, V, Loftus, RM, Keane, C, Brennan, K, Finlay, DK, Gardiner, CM (B22) 2016; 196 Iouzalen, N, Andreae, S, Hannier, S, Triebel, F (B34) 2001; 31 Bettini, M, Szymczak-Workman, AL, Forbes, K, Castellaw, AH, Selby, M, Pan, X, Drake, CG, Korman, AJ, Vignali, DAA (B12) 2011; 187 Mah, AY, Rashidi, A, Keppel, MP, Saucier, N, Moore, EK, Alinger, JB, Tripathy, SK, Agarwal, SK, Jeng, EK, Wong, HC, Miller, JS, Fehniger, TA, Mace, EM, French, AR, Cooper, MA (B23) 2017; 2 Triebel, F, Jitsukawa, S, Baixeras, E, Roman-Roman, S, Genevee, C, Viegas-Pequignot, E, Hercend, T (B5) 1990; 171 Merino, A, Zhang, B, Dougherty, P, Luo, X, Wang, J, Blazar, BR, Miller, JS, Cichocki, F (B17) 2019; 129 Lu, L, Ikizawa, K, Hu, D, Werneck, MBF, Wucherpfennig, KW, Cantor, H (B1) 2007; 26 Kulkarni, S, Sitaru, C, Jakus, Z, Anderson, KE, Damoulakis, G, Davidson, K, Hirose, M, Juss, J, Oxley, D, Chessa, TAM, Ramadani, F, Guillou, H, Segonds-Pichon, A, Fritsch, A, Jarvis, GE, Okkenhaug, K, Ludwig, R, Zillikens, D, Mocsai, A, Vanhaesebroeck, B, Stephens, LR, Hawkins, PT (B30) 2011; 4 Robbins, SH, Tessmer, MS, Van Kaer, L, Brossay, L (B38) 2005; 35 Cooper, MA, Fehniger, TA, Turner, SC, Chen, KS, Ghaheri, BA, Ghayur, T, Carson, WE, Caligiuri, MA (B21) 2001; 97 Previte, DM, Martins, CP, O’Connor, EC, Marre, ML, Coudriet, GM, Beck, NW, Menk, AV, Wright, RH, Tse, HM, Delgoffe, GM, Piganelli, JD (B27) 2019; 27 Vanhaesebroeck, B, Guillermet-Guibert, J, Graupera, M, Bilanges, B (B31) 2010; 11 Martín-Fontecha, A, Thomsen, LL, Brett, S, Gerard, C, Lipp, M, Lanzavecchia, A, Sallusto, F (B2) 2004; 5 Lavon, I, Heli, C, Brill, L, Charbit, H, Vaknin-Dembinsky, A (B13) 2019; 10 Wei, SC, Duffy, CR, Allison, JP (B9) 2018; 8 Boudreau, JE, Hsu, KC (B4) 2018; 50 Wang, H, Cui, L, Li, D, Fan, M, Liu, Z, Liu, C, Pan, S, Zhang, L, Zhang, H, Zhao, Y (B36) 2020; 5 Graydon, CG, Balasko, AL, Fowke, KR (B7) 2019; 15 B19 Jouanguy, E, Gineau, L, Cottineau, J, Béziat, V, Vivier, E, Casanova, J-L (B40) 2013; 13 Chan, Y-C, Chang, Y-C, Chuang, H-H, Yang, Y-C, Lin, Y-F, Huang, M-S, Hsiao, M, Yang, C-J, Hua, K-T (B15) 2020; 39 Boisson-Dupuis, S, Kong, X-F, Okada, S, Cypowyj, S, Puel, A, Abel, L, Casanova, J-L (B42) 2012; 24 Fruman, DA, Chiu, H, Hopkins, BD, Bagrodia, S, Cantley, LC, Abraham, RT (B28) 2017; 170 Maruhashi, T, Sugiura, D, Okazaki, I-M, Okazaki, T (B35) 2020; 8 Workman, CJ, Dugger, KJ, Vignali, DAA (B32) 2002; 169 Koundouros, N, Poulogiannis, G (B24) 2018; 8 Wang, D, Zhou, W, Chen, J, Wei, W (B29) 2019; 234 Nakachi, S, Sumitomo, S, Tsuchida, Y, Tsuchiya, H, Kono, M, Kato, R, Sakurai, K, Hanata, N, Nagafuchi, Y, Tateishi, S, Kanda, H, Okamura, T, Yamamoto, K, Fujio, K (B14) 2017; 19 Lang, B, Wang, M, Zhang, Z, Fu, Y, Han, X, Hu, Q, Ding, H, Shang, H, Jiang, Y (B44) 2023; 21 Khan, M, Arooj, S, Wang, H (B10) 2020; 11 Woo, S-R, Turnis, ME, Goldberg, MV, Bankoti, J, Selby, M, Nirschl, CJ, Bettini, ML, Gravano, DM, Vogel, P, Liu, CL, Tangsombatvisit, S, Grosso, JF, Netto, G, Smeltzer, MP, Chaux, A, Utz, PJ, Workman, CJ, Pardoll, DM, Korman, AJ, Drake, CG, Vignali, DAA (B11) 2012; 72 Yin, X, Liu, T, Wang, Z, Ma, M, Lei, J, Zhang, Z, Fu, S, Fu, Y, Hu, Q, Ding, H, Han, X, Xu, J, Shang, H, Jiang, Y (B43) 2018; 9 |
| References_xml | – ident: e_1_3_4_38_2 doi: 10.1172/JCI16603 – ident: e_1_3_4_35_2 doi: 10.1002/1521-4141(2001010)31:10<2885::AID-IMMU2885>3.0.CO;2-2 – ident: e_1_3_4_8_2 doi: 10.1371/journal.ppat.1007429 – ident: e_1_3_4_20_2 doi: 10.1101/405134 – ident: e_1_3_4_18_2 doi: 10.1172/JCI125916 – ident: e_1_3_4_4_2 doi: 10.1016/s1074-7613(03)00264-4 – ident: e_1_3_4_21_2 doi: 10.3389/conf.fimmu.2015.05.00164 – ident: e_1_3_4_17_2 doi: 10.1126/science.272.5260.405 – ident: e_1_3_4_22_2 doi: 10.1182/blood.V97.10.3146 – ident: e_1_3_4_31_2 doi: 10.1126/scisignal.2001617 – ident: e_1_3_4_42_2 doi: 10.1038/ng1097 – ident: e_1_3_4_16_2 doi: 10.1038/s41388-020-1160-4 – ident: e_1_3_4_43_2 doi: 10.1016/j.coi.2012.04.011 – ident: e_1_3_4_39_2 doi: 10.1002/eji.200425797 – ident: e_1_3_4_41_2 doi: 10.1097/ACI.0000000000000011 – ident: e_1_3_4_10_2 doi: 10.1158/2159-8290.CD-18-0367 – ident: e_1_3_4_9_2 doi: 10.4049/jimmunol.1402176 – ident: e_1_3_4_13_2 doi: 10.4049/jimmunol.1100714 – ident: e_1_3_4_19_2 doi: 10.1101/2020.01.31.928200 – ident: e_1_3_4_36_2 doi: 10.1136/jitc-2020-001014 – ident: e_1_3_4_23_2 doi: 10.4049/jimmunol.1501783 – ident: e_1_3_4_28_2 doi: 10.1016/j.celrep.2019.03.004 – ident: e_1_3_4_5_2 doi: 10.1016/j.coi.2017.11.003 – ident: e_1_3_4_40_2 doi: 10.1080/2162402X.2016.1186314 – ident: e_1_3_4_12_2 doi: 10.1158/0008-5472.CAN-11-1620 – ident: e_1_3_4_25_2 doi: 10.3389/fonc.2018.00160 – ident: e_1_3_4_6_2 doi: 10.1084/jem.171.5.1393 – ident: e_1_3_4_33_2 doi: 10.4049/jimmunol.169.10.5392 – ident: e_1_3_4_24_2 doi: 10.1172/jci.insight.95128 – ident: e_1_3_4_2_2 doi: 10.1016/j.immuni.2007.03.017 – ident: e_1_3_4_11_2 doi: 10.3389/fimmu.2020.00167 – ident: e_1_3_4_14_2 doi: 10.3389/fimmu.2019.00835 – ident: e_1_3_4_3_2 doi: 10.1038/ni1138 – ident: e_1_3_4_7_2 doi: 10.1016/j.smim.2019.101305 – ident: e_1_3_4_44_2 doi: 10.3389/fimmu.2018.02341 – ident: e_1_3_4_29_2 doi: 10.1016/j.cell.2017.07.029 – ident: e_1_3_4_45_2 doi: 10.1186/s12967-023-04667-6 – ident: e_1_3_4_15_2 doi: 10.1186/s13075-017-1309-x – ident: e_1_3_4_26_2 doi: 10.3389/fimmu.2017.00330 – ident: e_1_3_4_27_2 doi: 10.4049/jimmunol.1401558 – volume: 344 year: 2010 ident: e_1_3_4_34_2 article-title: LAG-3 in cancer immunotherapy publication-title: Curr Top Microbiol Immunol – ident: e_1_3_4_32_2 doi: 10.1038/nrm2882 – ident: e_1_3_4_30_2 doi: 10.1002/jcp.28215 – ident: e_1_3_4_37_2 doi: 10.1038/s41392-020-0147-5 – volume: 129 start-page: 3770 year: 2019 end-page: 3785 ident: B17 article-title: Chronic stimulation drives human NK cell dysfunction and epigenetic reprograming publication-title: J Clin Invest doi: 10.1172/JCI125916 – volume: 8 year: 2018 ident: B24 article-title: Phosphoinositide 3-kinase/Akt signaling and redox metabolism in cancer publication-title: Front Oncol doi: 10.3389/fonc.2018.00160 – volume: 9 year: 2018 ident: B43 article-title: Expression of the inhibitory receptor TIGIT is up-regulated specifically on NK cells with CD226 activating receptor from HIV-infected individuals publication-title: Front Immunol doi: 10.3389/fimmu.2018.02341 – volume: 39 start-page: 2509 year: 2020 end-page: 2522 ident: B15 article-title: Overexpression of PSAT1 promotes metastasis of lung adenocarcinoma by suppressing the IRF1-IFNγ axis publication-title: Oncogene doi: 10.1038/s41388-020-1160-4 – volume: 8 year: 2020 ident: B35 article-title: LAG-3: from molecular functions to clinical applications publication-title: J Immunother Cancer doi: 10.1136/jitc-2020-001014 – ident: B19 article-title: Jin J , Ahn Y-O , Kim TM , Keam B , Kim D-W , Heo DS . n.d. The CD56bright CD62L+ NKG2A+ immature cell subset is dominantly expanded in human cytokine-induced memory-like NK cells . Immunology . doi: 10.1101/405134 – volume: 170 start-page: 605 year: 2017 end-page: 635 ident: B28 article-title: The PI3K pathway in human disease publication-title: Cell doi: 10.1016/j.cell.2017.07.029 – volume: 6 year: 2015 ident: B20 article-title: Low expression of activation and inhibitory molecules on NK cells and CD4+ T-cells is associated with viral control publication-title: Front Immunol doi: 10.3389/conf.fimmu.2015.05.00164 – volume: 171 start-page: 1393 year: 1990 end-page: 1405 ident: B5 article-title: LAG-3, a novel lymphocyte activation gene closely related to CD4 publication-title: J Exp Med doi: 10.1084/jem.171.5.1393 – volume: 33 start-page: 388 year: 2003 end-page: 391 ident: B41 article-title: Impaired response to interferon-α/β and lethal viral disease in human STAT1 deficiency publication-title: Nat Genet doi: 10.1038/ng1097 – volume: 344 year: 2010 ident: B33 article-title: LAG-3 in cancer immunotherapy publication-title: Curr Top Microbiol Immunol – volume: 72 start-page: 917 year: 2012 end-page: 927 ident: B11 article-title: Immune inhibitory molecules LAG-3 and PD-1 synergistically regulate T-cell function to promote tumoral immune escape publication-title: Cancer Res doi: 10.1158/0008-5472.CAN-11-1620 – volume: 5 start-page: 1260 year: 2004 end-page: 1265 ident: B2 article-title: Induced recruitment of NK cells to lymph nodes provides IFN-γ for TH1 priming publication-title: Nat Immunol doi: 10.1038/ni1138 – volume: 4 year: 2011 ident: B30 article-title: PI3Kβ plays a critical role in neutrophil activation by immune complexes publication-title: Sci Signal doi: 10.1126/scisignal.2001617 – volume: 187 start-page: 3493 year: 2011 end-page: 3498 ident: B12 article-title: Cutting edge: accelerated autoimmune diabetes in the absence of LAG-3 publication-title: J Immunol doi: 10.4049/jimmunol.1100714 – volume: 11 start-page: 329 year: 2010 end-page: 341 ident: B31 article-title: The emerging mechanisms of isoform-specific PI3K signalling publication-title: Nat Rev Mol Cell Biol doi: 10.1038/nrm2882 – volume: 26 start-page: 593 year: 2007 end-page: 604 ident: B1 article-title: Regulation of activated CD4+ T cells by NK cells via the Qa-1-NKG2A inhibitory pathway publication-title: Immunity doi: 10.1016/j.immuni.2007.03.017 – volume: 27 start-page: 129 year: 2019 end-page: 141 ident: B27 article-title: Lymphocyte activation gene-3 maintains mitochondrial and metabolic quiescence innaive CD4+ T cells publication-title: Cell Rep doi: 10.1016/j.celrep.2019.03.004 – volume: 194 start-page: 3873 year: 2015 end-page: 3882 ident: B8 article-title: The upregulation of LAG-3 on T cells defines a subpopulation with functional exhaustion and correlates with disease progression in HIV-infected subjects publication-title: J Immunol doi: 10.4049/jimmunol.1402176 – volume: 15 year: 2019 ident: B7 article-title: Roles, function and relevance of LAG3 in HIV infection publication-title: PLoS Pathog doi: 10.1371/journal.ppat.1007429 – volume: 8 start-page: 1069 year: 2018 end-page: 1086 ident: B9 article-title: Fundamental mechanisms of immune checkpoint blockade therapy publication-title: Cancer Discov doi: 10.1158/2159-8290.CD-18-0367 – volume: 19 year: 2017 ident: B14 article-title: Interleukin-10-producing LAG3+ regulatory T cells are associated with disease activity and abatacept treatment in rheumatoid arthritis publication-title: Arthritis Res Ther doi: 10.1186/s13075-017-1309-x – volume: 193 start-page: 4477 year: 2014 end-page: 4484 ident: B26 article-title: mTORC1-dependent metabolic reprogramming is a prerequisite for NK cell effector function publication-title: J Immunol doi: 10.4049/jimmunol.1401558 – volume: 112 start-page: 170 year: 2003 end-page: 180 ident: B37 article-title: The antitumor effects of IFN-alpha are abrogated in a STAT1-deficient mouse publication-title: J Clin Invest doi: 10.1172/JCI16603 – volume: 13 start-page: 589 year: 2013 end-page: 595 ident: B40 article-title: Inborn errors of the development of human natural killer cells publication-title: Curr Opin Allergy Clin Immunol doi: 10.1097/ACI.0000000000000011 – volume: 234 start-page: 14460 year: 2019 end-page: 14472 ident: B29 article-title: Upstream regulators of phosphoinositide 3-kinase and their role in diseases publication-title: J Cell Physiol doi: 10.1002/jcp.28215 – volume: 11 year: 2020 ident: B10 article-title: NK cell-based immune checkpoint inhibition publication-title: Front Immunol doi: 10.3389/fimmu.2020.00167 – volume: 272 start-page: 405 year: 1996 end-page: 408 ident: B16 article-title: Independent modes of natural killing distinguished in mice lacking Lag3 publication-title: Science doi: 10.1126/science.272.5260.405 – volume: 19 start-page: 561 year: 2003 end-page: 569 ident: B3 article-title: Natural killer cells activated by MHC class I(low) targets prime dendritic cells to induce protective CD8 T cell responses publication-title: Immunity doi: 10.1016/s1074-7613(03)00264-4 – volume: 97 start-page: 3146 year: 2001 end-page: 3151 ident: B21 article-title: Human natural killer cells: a unique innate immunoregulatory role for the CD56bright subset publication-title: Blood doi: 10.1182/blood.V97.10.3146 – volume: 24 start-page: 364 year: 2012 end-page: 378 ident: B42 article-title: Inborn errors of human STAT1: allelic heterogeneity governs the diversity of immunological and infectious phenotypes publication-title: Curr Opin Immunol doi: 10.1016/j.coi.2012.04.011 – volume: 21 year: 2023 ident: B44 article-title: Inhibitory receptor CD47 binding to plasma TSP1 suppresses NK-cell IFN-γ production via activating the JAK/STAT3 pathway during HIV infection publication-title: J Transl Med doi: 10.1186/s12967-023-04667-6 – volume: 5 year: 2016 ident: B39 article-title: Novel non-canonical role of STAT1 in natural killer cell cytotoxicity publication-title: Oncoimmunology doi: 10.1080/2162402X.2016.1186314 – year: 2020 ident: B18 publication-title: LAG3 is a central regulator of NK cell cytokine production ;Cold Spring Harbor Laboratory – volume: 196 start-page: 2552 year: 2016 end-page: 2560 ident: B22 article-title: Metabolic reprogramming supports IFN-γ production by CD56bright NK cells publication-title: J Immunol doi: 10.4049/jimmunol.1501783 – volume: 2 year: 2017 ident: B23 article-title: Glycolytic requirement for NK cell cytotoxicity and cytomegalovirus control publication-title: JCI Insight doi: 10.1172/jci.insight.95128 – volume: 10 year: 2019 ident: B13 article-title: Blood levels of co-inhibitory-receptors: a biomarker of disease prognosis in multiple sclerosis publication-title: Front Immunol doi: 10.3389/fimmu.2019.00835 – volume: 8 year: 2017 ident: B25 article-title: Immunometabolic regulations mediated by coinhibitory receptors and their impact on T cell immune responses publication-title: Front Immunol doi: 10.3389/fimmu.2017.00330 – volume: 169 start-page: 5392 year: 2002 end-page: 5395 ident: B32 article-title: Cutting edge: molecular analysis of the negative regulatory function of lymphocyte activation gene-3 publication-title: J Immunol doi: 10.4049/jimmunol.169.10.5392 – volume: 31 start-page: 2885 year: 2001 end-page: 2891 ident: B34 article-title: LAP, a lymphocyte activation gene-3 (LAG-3)-associated protein that binds to a repeated EP motif in the intracellular region of LAG-3, may participate in the down-regulation of the CD3/TCR activation pathway publication-title: Eur J Immunol doi: 10.1002/1521-4141(2001010)31:10<2885::AID-IMMU2885>3.0.CO;2-2 – volume: 50 start-page: 102 year: 2018 end-page: 111 ident: B4 article-title: Natural killer cell education in human health and disease publication-title: Curr Opin Immunol doi: 10.1016/j.coi.2017.11.003 – volume: 42 start-page: 101305 year: 2019 ident: B6 article-title: Lymphocyte-activation gene 3 (LAG3): the next immune checkpoint receptor publication-title: Semin Immunol doi: 10.1016/j.smim.2019.101305 – volume: 5 year: 2020 ident: B36 article-title: Overexpression of PSAT1 regulated by G9A sustains cell proliferation in colorectal cancer publication-title: Signal Transduct Target Ther doi: 10.1038/s41392-020-0147-5 – volume: 35 start-page: 757 year: 2005 end-page: 765 ident: B38 article-title: Direct effects of T‐bet and MHC class I expression, but not STAT1, on peripheral NK cell maturation publication-title: Eur J Immunol doi: 10.1002/eji.200425797 |
| SSID | ssj0000331830 |
| Score | 2.416301 |
| Snippet | We demonstrate that lymphocyte activation gene 3 (LAG3) expression is upregulated on natural killer (NK) cells during HIV infection. LAG3 inhibits glycolysis... Natural killer (NK) cells are integral to the innate immune system and crucial for antiviral defense. NK cell activation and functional state are suppressed by... ABSTRACT Natural killer (NK) cells are integral to the innate immune system and crucial for antiviral defense. NK cell activation and functional state are... |
| SourceID | doaj pubmedcentral proquest asm2 pubmed crossref |
| SourceType | Open Website Open Access Repository Aggregation Database Index Database |
| StartPage | e0023025 |
| SubjectTerms | Antigens, CD - genetics Antigens, CD - immunology Antigens, CD - metabolism Female Glycolysis HIV HIV Infections - immunology Humans IFN-γ Immunology Interferon-gamma - metabolism Killer Cells, Natural - immunology Killer Cells, Natural - metabolism LAG3 Lymphocyte Activation Gene 3 Protein Male Research Article Signal Transduction STAT1 STAT1 Transcription Factor - genetics STAT1 Transcription Factor - metabolism |
| SummonAdditionalLinks | – databaseName: American Society for Microbiology Open Access dbid: AAUOK link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwjV3bbtQwELXKVki8IO4sNxmBeEvrOHbsPAbEtlBYkLor9c2ykwmNRLOr7lZov4v_4JuYyWXFViDxEkVxnMuc8fhMLmcYe61MEBCDiFRWYIKSgYlCpnEBhS5CVaYB6G_kz9P0eK4-numzPSaHf2F6C64O_OqifZG_HdnSHl6EenHQsuZI6htsX8tMiRHbz_P5l5PtkxWRkJ-KQVDzej-MvXhsuTMPtXL9f-OY1z-V_GPumdxht3vSyPMO5btsD5p77GZXRnJzn10i1rxuzutQ0ytzjkEMlrjGP-VHCffdFxt8esLpKT3_MJlGv37yZSf1irDwvlYP__Z9g25BEiXcNyVuBv71NJ_Fh6czWmLHI04VjH_4zQM2n7yfvTuO-loKkVfKrDHaKkqdMkwP4lCYTHvphS2zkPrEqkwklAhCrEqhCtBBqsqKBAqTikKXuqySh2zULBp4zLiKQ1CQIk80QpWxxe7BFGA9Tv0F-GTMXpGB3QCla_MMaR3B4FoYnNRj9mawv1t2whr_2vEtobPdifSw2w3oHa4fXo6IBuiyUKYSKqnwpkyVJkgvDYDFqx2zlwO2DscPmds3sLhaOQpByOowlI3Zow7r7akU6dMrjS12xwt2rmW3panPW41uEu1AZmyf_JcxnrJbkuoKU02k-BkbrS-v4DmSnXV40Xv3bzO8-o8 priority: 102 providerName: American Society for Microbiology – databaseName: DOAJ Directory of Open Access Journals dbid: DOA link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV1ba9swFBYjMNjLWHdN2w2Njb15kS3Jkh_TsbS7hUFT6JuQ5OPVsDqhSRn5Xfsf-009x3ZKMjb2shdjdMHinKNzseXvY-y1MkFACiJRRcQCpQCThELjBaKOoSrzAPQ38pdpfnKmPp7r8y2qLzoT1sEDd4IbUQgBXUZlKqFklXtpqlxi4mAAbFBA3hdj3lYx1fpgSbYqNqCamR1dhnr-ts24E6LFHvjlZbYTi1rI_j_lmb8fl9yKP5MH7H6fOPJxt-A9dgeah-xuRyW5fsSuUN-8bi7qUNNnc46ODBZ4xz-PjyX33akNPv3E6U09_zCZJr9-8kUH94qq4T1fD__2fY2mQTAl3DclNgP_ejqepaPTGV1x4jEnFuMffv2YnU3ez96dJD2fQuKVMiv0uIrKpwJLhDREU2ifeWHLIqBQrSqEpGIQUlUKFUGHTFVWSIgmF1GXuqzkEzZo5g08Y1ylAWWfY65ohCpTi9ODiWA9hv8IXg7ZKxKw6zfE0rW1RmYdqcG1anCZHrI3G_m7RQeu8beBR6Sd20GEid02oKW43lLcvyxlyF5udOtwD5G4fQPz66UjN4SZHbqzIXva6fr2UYow6pXGHrtjBTtr2e1p6osWp5uAOzA7tvv_Y_UH7F5G1MNEm5QessHq6hqeYz60Ci9a078BlTIGmg priority: 102 providerName: Directory of Open Access Journals |
| Title | The inhibitory receptor LAG3 affects NK cell IFN-γ production through glycolysis and the PSAT1/STAT1/IFNG pathway |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/40298450 https://journals.asm.org/doi/10.1128/mbio.00230-25 https://www.proquest.com/docview/3196615400 https://pubmed.ncbi.nlm.nih.gov/PMC12153268 https://doaj.org/article/2426e5dc47f043f6a37f630837ee8b4e |
| Volume | 16 |
| hasFullText | 1 |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwjV1fb9MwELdgExIviP8rsMoIxFu2_LFj5wGhgGgHYwVprdQ3y3YuW6UtLW0n6Ofie_CZdpekg05D4sWKHDuJfefz7xz7d4y9FsqFEEEYiMyjg5KBClwmMQEvvSuL1AGdRj4apAcj8Xksx38ohdoOXNzo2lE8qdH8bO_n99U7HPBvmwMwev_cTaZ7NZgOYnmbbeOkpGiMHrVIvzbKCSkvrbjgHBcGCnHGmnHz-hPQONvFebwxUdV8_jeB0Ot7Kf-anHr32b0WVfK8UYMH7BZUD9mdJs7k6hGbozLwSXU6cRP6p87RysEMr_iXvJ9w22zp4INDTsv4_FNvEPz-xWcNFyzKjbfBfPjJ2Qr1hjhMuK0KzAb-7TgfRvvHQ0qxYp9TiOMfdvWYjXofhx8OgjbYQmCFUEs0x4J8qwz9h8h5lUkb21AXmUttokUWJuQpQiSKUHiQLhalDhPwKg29LGRRJk_YVjWtYIdxETknIEUgqUJRRBqrO-VBW8QGHmzSYa-og81a2KZ2RGJtSAymFoOJZYe9Wfe_mTXMG_8q-J6kc1WICLPrjOn8xLTjzxASAVl4ocpQJCU2SpVpgvhTAWj82g57uZatwQFG3W0rmF4sDNkohH1o6zrsaSPrq1cJIrAXEu_oDS3Y-JbNO9XktCbxJlYPhM762f828zm7G1PsYYqbFL1gW8v5BewiIFq6LtvO89HXw269oIBpfxx1a_W_BPzoCXg |
| linkProvider | Scholars Portal |
| linkToHtml | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwjV1bb9MwFLbGJgQviOsoVyMQb9mcxI6dx4DoOtoVpLXS3iw7OWFBW1qtnVB_F_-D38Q5SVrRCSRerMix5cTn-Pg7vnyHsXdSewEhiECmOTooKejApwoTyFXuyyLxQLeRT8bJYCo_n6mzHZas78J8p7i8F4sDt7hs9vFpYNNCdBeP0Bxe-mp20CDnIFK32B7tG6Jm72XZ9Mtws7oiYtJVsSbVvFkP7S82EG3NRQ1l_99w5s3jkn_MP_377F4HHHnWSvoB24H6IbvdhpJcPWJXKG9e1eeVr2jbnKMhgzk-8VF2FHPXntrg4yGnlXp-3B8Hv37yeUv3iqLhXbwe_u1ihapBNCXc1QVmA_96mk3Cw9MJpVjxiFMU4x9u9ZhN-58mHwdBF08hcFLqJVpcSe5Tii5C6HOdKhc5YYrUJy42MhUxOYMQykLIHJSPZGlEDLlORK4KVZTxE7Zbz2p4yrgMvZeQIFbUQhahwepe52AcTv85uLjH3lIH225ALGzja0TGkhhsIwYbqR57v-5_O2_JNf5V8ANJZ1OIOLGbDFQR2w0xS2ADVJFLXQoZl_hTukxihJgawODX9tibtWwtjiHqblfD7HphyQwhskNz1mP7raw3TUniqJcK35gtLdj6lu03dXXe8HQTcQeiY_PsvzrjNbszmJyM7Oh4PHzO7kYUZ5hiJIUv2O7y6hpeIvhZ-ledpv8G9nz-8g |
| linkToPdf | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwjV3bbtQwELVKKxAviDtbbkYg3tI6iR0nj-GybdmyVOqu1DfLdiY0UptddbdC-138B9_ETC4rtgKJlyhK4lzmjMdn4uQMY--kdgJCEIHMPCYoGejAZQoX4JV3ZZE4oL-Rv46Tw6n8cqbOtljS_wvTWXCxZxeXzUQ-9ex5UXb1CNP9S1fN9hrmHETqFtuhiSr07508n34brd-uiJh8VfSimjfbYfzF80cbY1Ej2f83nnnzc8k_xp_hfXavI448b5F-wLagfshut6UkV4_YFeLNq_q8chVNm3MMZDDHNX6cH8Tctl9t8PGI05t6fjQcB79-8nkr94rQ8K5eD_9-sULXIJkSbusCNwM_Oc0n4f7phJbY8IBTFeMfdvWYTYefJx8Pg66eQmCl1EuMuJLSpwxThNB5nSkbWZEWmUtsnMpMxJQMQigLIT0oF8kyFTF4nQivClWU8RO2Xc9qeMa4DJ2TkCBX1EIWYYrNnfaQWhz-Pdh4wN6SgU0Pp2lyjSg1BINpYDCRGrD3vf3NvBXX-NeBHwid9UGkid1sQA8xXRczRDZAFV7qUsi4xIfSZRIjxdQAKd7tgL3psTXYh8jctobZ9cJQGEJmh-FswJ62WK8vJUmjXirck254wca9bO6pq_NGp5uEO5Adp7v_ZYzX7M7Jp6E5PhqPnrO7EZUZphJJ4Qu2vby6hpfIfZbuVefovwHbjf6O |
| openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=The+inhibitory+receptor+LAG3+affects+NK+cell+IFN-%CE%B3+production+through+glycolysis+and+the+PSAT1%2FSTAT1%2FIFNG+pathway&rft.jtitle=mBio&rft.au=Ge%2C+Hongchi&rft.au=Guo%2C+Nan&rft.au=Liu%2C+Yufei&rft.au=Lang%2C+Bin&rft.date=2025-06-11&rft.issn=2150-7511&rft.eissn=2150-7511&rft.volume=16&rft.issue=6&rft_id=info:doi/10.1128%2Fmbio.00230-25&rft.externalDBID=n%2Fa&rft.externalDocID=10_1128_mbio_00230_25 |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=2150-7511&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=2150-7511&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=2150-7511&client=summon |