T-bet Knockout Prevents Helicobacter felis-Induced Gastric Cancer
Helicobacter infection is the primary risk factor for gastric cancer, with the cytokine environment within the gastric mucosa the strongest predictor of disease risk. Elevated TNF-alpha, IL-1beta, and low IL-10 are associated with the highest risk. In this study, we used C57BL/6 mice to identify T-b...
Saved in:
Published in | The Journal of immunology (1950) Vol. 183; no. 1; pp. 642 - 649 |
---|---|
Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Am Assoc Immnol
01.07.2009
|
Subjects | |
Online Access | Get full text |
Cover
Loading…
Abstract | Helicobacter infection is the primary risk factor for gastric cancer, with the cytokine environment within the gastric mucosa the strongest predictor of disease risk. Elevated TNF-alpha, IL-1beta, and low IL-10 are associated with the highest risk. In this study, we used C57BL/6 mice to identify T-bet as a central regulator of the cytokine environment during Helicobacter felis infection. We infected male and female C57BL/6 and C57BL/6-T-bet knockout (KO) litter mates with H. felis and examined the bacterial colonization, immune response, and mucosal damage at varying time points. T-bet KO mice maintained infection for 15 mo at similar levels to wild-type mice. Infection and immune response did not differ between male and female mice. Despite sustained infection, T-bet KO mice respond with a blunted Th1 response associated with preservation of parietal and chief cells and protection from the development of gastric cancer. Unexpectedly, T-bet KO mice develop a gastric environment that would not be expected based on the phenotype of T-bet KO CD4 cells alone. T-bet KO mice respond to H. felis infection with a markedly blunted IL-1beta and TNF-alpha and elevated IL-10 levels. Activity of this one master regulator modulates the expression of the key gastric mucosal cytokines associated with gastric cancer and may be a target for therapy to restore immune balance clinically in patients at risk for gastric cancer. |
---|---|
AbstractList | Abstract
Helicobacter infection is the primary risk factor for gastric cancer, with the cytokine environment within the gastric mucosa the strongest predictor of disease risk. Elevated TNF-α, IL-1β, and low IL-10 are associated with the highest risk. In this study, we used C57BL/6 mice to identify T-bet as a central regulator of the cytokine environment during Helicobacter felis infection. We infected male and female C57BL/6 and C57BL/6-T-bet knockout (KO) liter mates with H. felis and examined the bacterial colonization, immune response, and mucosal damage at varying time points. T-bet KO mice maintained infection for 15 mo at similar levels to wild-type mice. Infection and immune response did not differ between male and female mice. Despite sustained infection, T-bet KO mice respond with a blunted Th1 response associated with preservation of parietal and chief cells and protection from the development of gastric cancer. Unexpectedly, T-bet KO mice develop a gastric environment that would not be expected based on the phenotype of T-bet KO CD4 cells alone. T-bet KO mice respond to H. felis infection with a markedly blunted IL-1β and TNF-α and elevated IL-10 levels. Activity of this one master regulator modulates the expression of the key gastric mucosal cytokines associated with gastric cancer and may be a target for therapy to restore immune balance clinically in patients at risk for gastric cancer. Helicobacter infection is the primary risk factor for gastric cancer, with the cytokine environment within the gastric mucosa the strongest predictor of disease risk. Elevated TNF-alpha, IL-1beta, and low IL-10 are associated with the highest risk. In this study, we used C57BL/6 mice to identify T-bet as a central regulator of the cytokine environment during Helicobacter felis infection. We infected male and female C57BL/6 and C57BL/6-T-bet knockout (KO) litter mates with H. felis and examined the bacterial colonization, immune response, and mucosal damage at varying time points. T-bet KO mice maintained infection for 15 mo at similar levels to wild-type mice. Infection and immune response did not differ between male and female mice. Despite sustained infection, T-bet KO mice respond with a blunted Th1 response associated with preservation of parietal and chief cells and protection from the development of gastric cancer. Unexpectedly, T-bet KO mice develop a gastric environment that would not be expected based on the phenotype of T-bet KO CD4 cells alone. T-bet KO mice respond to H. felis infection with a markedly blunted IL-1beta and TNF-alpha and elevated IL-10 levels. Activity of this one master regulator modulates the expression of the key gastric mucosal cytokines associated with gastric cancer and may be a target for therapy to restore immune balance clinically in patients at risk for gastric cancer. |
Author | Kurt-Jones, Evelyn Liu, Jian Hua Stoicov, Calin Houghton, JeanMarie Bowen, Glennice Whary, Mark Fan, Xueli |
Author_xml | – sequence: 1 fullname: Stoicov, Calin – sequence: 2 fullname: Fan, Xueli – sequence: 3 fullname: Liu, Jian Hua – sequence: 4 fullname: Bowen, Glennice – sequence: 5 fullname: Whary, Mark – sequence: 6 fullname: Kurt-Jones, Evelyn – sequence: 7 fullname: Houghton, JeanMarie |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/19535625$$D View this record in MEDLINE/PubMed |
BookMark | eNpFkL1PwzAUxC1URD9gZ0KZ2FKe49iJx6qCtqISDGW2HOeFpiRxsRMi_nuCKOr0dNLdvdNvSkaNbZCQWwrzGGL5cCjrumtsNQcJwCm9IBPKOYRCgBiRCUAUhTQRyZhMvT8AgIAoviJjKjnjIuITstiFGbbBc2PNh-3a4NXhFzatD9ZYlcZm2rTogmIQPtw0eWcwD1bat640wVI3Bt01uSx05fHmdGfk7elxt1yH25fVZrnYhoYl0IY5NVpoHg0DkkQCR8mxoJhGiaGMFbkEanJZAMtBZEwXEjBNCwTOMhyWRmxG7v96j85-duhbVZfeYFXpBm3nlUhiYCxlgxH-jMZZ7x0W6ujKWrtvRUH9YlP_2NQJ2xC5O3V3WY35OXDidH6-L9_3felQ-VpX1WCnqu97mjJFlYgj9gPuXHjV |
CitedBy_id | crossref_primary_10_1186_s12876_020_01331_x crossref_primary_10_1007_s00262_012_1358_6 crossref_primary_10_1038_mi_2010_53 crossref_primary_10_1111_j_1523_5378_2011_00877_x crossref_primary_10_4049_jimmunol_1101772 crossref_primary_10_1002_path_2933 crossref_primary_10_1080_17474124_2021_1845140 crossref_primary_10_1371_journal_pone_0087505 crossref_primary_10_3390_toxins8060187 crossref_primary_10_4049_jimmunol_1000749 crossref_primary_10_1111_j_1523_5378_2010_00780_x crossref_primary_10_26508_lsa_202000967 crossref_primary_10_1016_j_micpath_2018_06_033 crossref_primary_10_3389_fimmu_2014_00116 crossref_primary_10_31146_1682_8658_ecg_221_1_21_30 crossref_primary_10_1111_j_1523_5378_2010_00777_x crossref_primary_10_1016_j_mrrev_2010_03_001 crossref_primary_10_18632_aging_101848 crossref_primary_10_1111_j_1523_5378_2011_00861_x crossref_primary_10_1053_j_gastro_2017_09_002 crossref_primary_10_1007_s00204_016_1747_2 crossref_primary_10_1172_jci_insight_94035 crossref_primary_10_1038_nrmicro3016 crossref_primary_10_1038_s41388_020_1241_4 |
Cites_doi | 10.1002/ijc.2910410205 10.1007/s10120-001-8010-z 10.1016/S0016-5085(03)00157-4 10.3322/canjclin.49.1.8 10.1128/IAI.01887-05 10.1016/S0016-5085(00)70412-4 10.1086/315788 10.3892/or.10.1.57 10.1128/IAI.68.3.1189-1195.2000 10.1006/meth.2001.1262 10.1038/35006081 10.4049/jimmunol.162.7.4053 10.4049/jimmunol.166.12.7456 10.4049/jimmunol.173.5.3329 10.1177/1756283X08093567 10.1038/labinvest.3700260 10.1007/s10120-007-0420-0 10.1155/2001/850308 10.1073/pnas.96.19.10800 10.1128/IAI.73.10.6311-6321.2005 10.1034/j.1600-0463.2003.1110203.x 10.1016/j.ccr.2008.10.011 10.1158/1055-9965.EPI-06-0189 10.1016/S0016-5085(03)80094-X 10.1053/j.gastro.2005.02.066 10.1152/ajpgi.00267.2007 10.1016/S0016-5085(98)70581-5 10.1053/j.gastro.2007.06.026 10.1084/jem.20011956 10.1016/j.micinf.2005.05.017 10.1038/75015 10.1073/pnas.0700021104 10.1053/gast.2002.30298 10.1016/S0092-8674(00)80702-3 10.1128/AEM.01675-06 10.1002/1096-9896(2000)9999:9999<::AID-PATH759>3.0.CO;2-A 10.1128/IAI.68.8.4802-4804.2000 |
ContentType | Journal Article |
DBID | CGR CUY CVF ECM EIF NPM AAYXX CITATION 7X8 |
DOI | 10.4049/jimmunol.0900511 |
DatabaseName | Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed CrossRef MEDLINE - Academic |
DatabaseTitle | MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) CrossRef MEDLINE - Academic |
DatabaseTitleList | CrossRef MEDLINE |
Database_xml | – sequence: 1 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: 2 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 | Medicine Biology |
EISSN | 1550-6606 |
EndPage | 649 |
ExternalDocumentID | 10_4049_jimmunol_0900511 19535625 www183_1_642 |
Genre | Journal Article Research Support, N.I.H., Extramural |
GrantInformation_xml | – fundername: NCI NIH HHS grantid: R01 CA113564 |
GroupedDBID | - 2WC 34G 39C 3O- 53G 55 5GY 5RE 5VS 79B 85S 8RP AALRV AARDX ABEFU ABFLS ABOCM ABPPZ ABPTK ACGFS ACIWK ACNCT ACPRK ADACO ADBBV ADKFC AENEX AETEA AFFNX AFRAH AJYGW ALMA_UNASSIGNED_HOLDINGS BAWUL D0L DIK DU5 E3Z EBS EJD F5P FH7 FRP GX1 H13 IH2 K-O K78 KQ8 L7B MVM O0- OK1 P0W P2P PQEST PQQKQ R.V RHF RHI RZQ SJN TWZ WH7 WOQ X X7M XJT ZA5 ZE2 ZGI --- -~X .55 18M ABCQX ABJNI ACGFO ADNWM AFHIN AFOSN AHWXS AIZAD BTFSW CGR CUY CVF ECM EIF NPM TR2 W8F XSW XTH YHG AAYXX CITATION 7X8 |
ID | FETCH-LOGICAL-c370t-d1ca6a5202477905e95ef1e827c133fd901cd9f03d06b3af90e88fe053be62523 |
ISSN | 0022-1767 |
IngestDate | Sat Aug 17 01:15:39 EDT 2024 Thu Sep 26 17:18:50 EDT 2024 Sat Sep 28 07:54:53 EDT 2024 Tue Nov 10 19:20:43 EST 2020 |
IsDoiOpenAccess | false |
IsOpenAccess | true |
IsPeerReviewed | true |
IsScholarly | true |
Issue | 1 |
Language | English |
LinkModel | OpenURL |
MergedId | FETCHMERGED-LOGICAL-c370t-d1ca6a5202477905e95ef1e827c133fd901cd9f03d06b3af90e88fe053be62523 |
Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
OpenAccessLink | https://journals.aai.org/jimmunol/article-pdf/183/1/642/1318363/zim01309000642.pdf |
PMID | 19535625 |
PQID | 67403383 |
PQPubID | 23479 |
PageCount | 8 |
ParticipantIDs | proquest_miscellaneous_67403383 crossref_primary_10_4049_jimmunol_0900511 pubmed_primary_19535625 highwire_smallpub1_www183_1_642 |
ProviderPackageCode | RHF RHI |
PublicationCentury | 2000 |
PublicationDate | 20090701 2009-Jul-01 2009-07-01 |
PublicationDateYYYYMMDD | 2009-07-01 |
PublicationDate_xml | – month: 07 year: 2009 text: 20090701 day: 01 |
PublicationDecade | 2000 |
PublicationPlace | United States |
PublicationPlace_xml | – name: United States |
PublicationTitle | The Journal of immunology (1950) |
PublicationTitleAlternate | J Immunol |
PublicationYear | 2009 |
Publisher | Am Assoc Immnol |
Publisher_xml | – name: Am Assoc Immnol |
References | 11781287 - Gastroenterology. 2002 Jan;122(1):119-33 10611152 - Gastroenterology. 2000 Jan;118(1):36-47 8658212 - Semin Oncol. 1996 Jun;23(3):281-91 3338870 - Int J Cancer. 1988 Feb 15;41(2):184-97 11390498 - J Immunol. 2001 Jun 15;166(12):7456-61 16177302 - Infect Immun. 2005 Oct;73(10):6311-21 10080136 - Dig Dis Sci. 1999 Mar;44(3):465-78 15940628 - Gastroenterology. 2005 Jun;128(7):1937-52 11180161 - J Pathol. 2001 Feb;193(2):162-8 17681184 - Gastroenterology. 2007 Aug;133(2):659-72 10678925 - Infect Immun. 2000 Mar;68(3):1189-95 15765119 - Lab Invest. 2005 May;85(5):702-15 16861655 - Infect Immun. 2006 Aug;74(8):4673-84 11846609 - Methods. 2001 Dec;25(4):402-8 9516388 - Gastroenterology. 1998 Apr;114(4):675-89 12469145 - Oncol Rep. 2003 Jan-Feb;10(1):57-63 12716387 - APMIS. 2003 Feb;111(2):309-14 10746728 - Nature. 2000 Mar 23;404(6776):398-402 10950781 - J Infect Dis. 2000 Sep;182(3):856-64 16985030 - Cancer Epidemiol Biomarkers Prev. 2006 Sep;15(9):1674-87 10761931 - Cell. 2000 Mar 17;100(6):655-69 10200775 - CA Cancer J Clin. 1999 Jan-Feb;49(1):8-31, 1 15322196 - J Immunol. 2004 Sep 1;173(5):3329-36 17991709 - Am J Physiol Gastrointest Liver Physiol. 2008 Jan;294(1):G263-75 10201928 - J Immunol. 1999 Apr 1;162(7):4053-61 20953278 - Therap Adv Gastroenterol. 2008 Jul;1(1):19-31 10485906 - Proc Natl Acad Sci U S A. 1999 Sep 14;96(19):10800-5 16260169 - Microbes Infect. 2006 Jan;8(1):52-60 11846063 - Gastric Cancer. 2001;4(4):198-205 10899893 - Infect Immun. 2000 Aug;68(8):4802-4 18977329 - Cancer Cell. 2008 Nov 4;14(5):408-19 11493951 - Can J Gastroenterol. 2001 Jul;15(7):469-74 17142378 - Appl Environ Microbiol. 2007 Feb;73(3):1010-3 12730860 - Gastroenterology. 2003 May;124(5):1193-201 10802709 - Nat Med. 2000 May;6(5):536-42 17577615 - Gastric Cancer. 2007;10(2):75-83 17307869 - Proc Natl Acad Sci U S A. 2007 Feb 20;104(8):2827-30 11994418 - J Exp Med. 2002 May 6;195(9):1129-43 2023010203584845500_R11 2023010203584845500_R33 2023010203584845500_R10 2023010203584845500_R32 2023010203584845500_R31 2023010203584845500_R30 2023010203584845500_R15 2023010203584845500_R37 2023010203584845500_R14 2023010203584845500_R36 2023010203584845500_R13 2023010203584845500_R35 2023010203584845500_R12 2023010203584845500_R34 2023010203584845500_R29 2023010203584845500_R28 2023010203584845500_R27 2023010203584845500_R22 2023010203584845500_R21 2023010203584845500_R20 2023010203584845500_R26 2023010203584845500_R25 2023010203584845500_R24 2023010203584845500_R23 2023010203584845500_R19 2023010203584845500_R18 2023010203584845500_R17 2023010203584845500_R39 2023010203584845500_R16 2023010203584845500_R38 2023010203584845500_R2 2023010203584845500_R1 2023010203584845500_R4 2023010203584845500_R3 2023010203584845500_R6 2023010203584845500_R5 2023010203584845500_R8 2023010203584845500_R7 2023010203584845500_R9 |
References_xml | – ident: 2023010203584845500_R1 doi: 10.1002/ijc.2910410205 – ident: 2023010203584845500_R31 doi: 10.1007/s10120-001-8010-z – ident: 2023010203584845500_R6 doi: 10.1016/S0016-5085(03)00157-4 – ident: 2023010203584845500_R2 doi: 10.3322/canjclin.49.1.8 – ident: 2023010203584845500_R33 doi: 10.1128/IAI.01887-05 – ident: 2023010203584845500_R17 doi: 10.1016/S0016-5085(00)70412-4 – ident: 2023010203584845500_R19 doi: 10.1086/315788 – ident: 2023010203584845500_R3 – ident: 2023010203584845500_R30 doi: 10.3892/or.10.1.57 – ident: 2023010203584845500_R11 doi: 10.1128/IAI.68.3.1189-1195.2000 – ident: 2023010203584845500_R18 doi: 10.1006/meth.2001.1262 – ident: 2023010203584845500_R5 doi: 10.1038/35006081 – ident: 2023010203584845500_R22 doi: 10.4049/jimmunol.162.7.4053 – ident: 2023010203584845500_R8 doi: 10.4049/jimmunol.166.12.7456 – ident: 2023010203584845500_R13 doi: 10.4049/jimmunol.173.5.3329 – ident: 2023010203584845500_R35 doi: 10.1177/1756283X08093567 – ident: 2023010203584845500_R21 doi: 10.1038/labinvest.3700260 – ident: 2023010203584845500_R36 doi: 10.1007/s10120-007-0420-0 – ident: 2023010203584845500_R4 doi: 10.1155/2001/850308 – ident: 2023010203584845500_R20 – ident: 2023010203584845500_R23 doi: 10.1073/pnas.96.19.10800 – ident: 2023010203584845500_R27 doi: 10.1128/IAI.73.10.6311-6321.2005 – ident: 2023010203584845500_R29 doi: 10.1034/j.1600-0463.2003.1110203.x – ident: 2023010203584845500_R37 doi: 10.1016/j.ccr.2008.10.011 – ident: 2023010203584845500_R39 doi: 10.1158/1055-9965.EPI-06-0189 – ident: 2023010203584845500_R14 doi: 10.1016/S0016-5085(03)80094-X – ident: 2023010203584845500_R10 doi: 10.1053/j.gastro.2005.02.066 – ident: 2023010203584845500_R28 doi: 10.1152/ajpgi.00267.2007 – ident: 2023010203584845500_R9 doi: 10.1016/S0016-5085(98)70581-5 – ident: 2023010203584845500_R12 doi: 10.1053/j.gastro.2007.06.026 – ident: 2023010203584845500_R34 doi: 10.1084/jem.20011956 – ident: 2023010203584845500_R38 doi: 10.1016/j.micinf.2005.05.017 – ident: 2023010203584845500_R15 doi: 10.1038/75015 – ident: 2023010203584845500_R24 doi: 10.1073/pnas.0700021104 – ident: 2023010203584845500_R25 doi: 10.1053/gast.2002.30298 – ident: 2023010203584845500_R16 doi: 10.1016/S0092-8674(00)80702-3 – ident: 2023010203584845500_R26 doi: 10.1128/AEM.01675-06 – ident: 2023010203584845500_R32 doi: 10.1002/1096-9896(2000)9999:9999<::AID-PATH759>3.0.CO;2-A – ident: 2023010203584845500_R7 doi: 10.1128/IAI.68.8.4802-4804.2000 |
SSID | ssj0006024 |
Score | 2.1689582 |
Snippet | Helicobacter infection is the primary risk factor for gastric cancer, with the cytokine environment within the gastric mucosa the strongest predictor of... Abstract Helicobacter infection is the primary risk factor for gastric cancer, with the cytokine environment within the gastric mucosa the strongest predictor... |
SourceID | proquest crossref pubmed highwire |
SourceType | Aggregation Database Index Database Publisher |
StartPage | 642 |
SubjectTerms | Adenocarcinoma - immunology Adenocarcinoma - microbiology Adenocarcinoma - prevention & control Animals Female Gastric Mucosa - immunology Gastric Mucosa - microbiology Gastric Mucosa - pathology Genetic Predisposition to Disease Helicobacter felis - immunology Helicobacter Infections - immunology Helicobacter Infections - pathology Helicobacter Infections - prevention & control Interleukin-1beta - physiology Male Mice Mice, Inbred C57BL Mice, Knockout Stomach Neoplasms - immunology Stomach Neoplasms - microbiology Stomach Neoplasms - prevention & control T-Box Domain Proteins - deficiency T-Box Domain Proteins - genetics T-Box Domain Proteins - physiology Tumor Necrosis Factor-alpha - physiology |
Title | T-bet Knockout Prevents Helicobacter felis-Induced Gastric Cancer |
URI | http://www.jimmunol.org/cgi/content/abstract/183/1/642 https://www.ncbi.nlm.nih.gov/pubmed/19535625 https://search.proquest.com/docview/67403383 |
Volume | 183 |
hasFullText | 1 |
inHoldings | 1 |
isFullTextHit | |
isPrint | |
link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV3Nb9MwFLfKEGgXBOOrfOYAB1Slc2LHiY8wsVagcWGTeovi1JYmlRStySoQfzzvxXaSFSYxLlESRXbs99P78vsg5I0WidRa85ApXoRcIR8UYhkqpYzOUlNmGv2QJ1_E_Ix_WiSL0ejXMLukVtPy51_zSv6HqvAO6IpZsjegbDcovIB7oC9cgcJw_Tcah0rXk88V8DQML3blmDYoS4DAqi3EPDHwsJmE2KMDz_pnBXbqKCdHSO6LoW7aZ4nZQhKYOWIrNL1tz8HowGvwtV7DDJc2ZGR13iHs2PpTFw1M2sX6nDctVpCVzJveAbDeWpY3W2GEjUOYd0DILlh1mBAQpbarxlQ7PpqAVSqouMpo2R-IsmxT2ApbTgILW8R0l7lzMGaQubvlT6lEjhL1gswf3u_Ity7qEOwdHCP3I-RuhFvkdpzKBANCZ4s-QEjQmPta87g8e8iNIxzu_sNVpcYXmr7eaGmVl9P75J6javDeQugBGenqgNyxfUh_HJC7Jy7C4iH50GIq8JgKPKaCIaaCFlOBx1TgMBVYTD0iZ8cfT4_moeuzEZYspXW4jMpCFEkM68Xqk4mWiTaRzuK0jBgzS1AZy6U0lC2pUKwwkuosM9hTRGkwn2P2mOxV60o_JUHBMhNxJQ2jJS95JjOjBAhck4EcBcVoTN75jcq_23Iq-XVkGZPXfifzzbditYIdjPLtdgs4yqMcMANf-A3OgSviUVdR6XWzyUXKKTpfxuSJ3fd-NpkwNPqf3eBPnpP9HvgvyF590eiXoIvW6lULmd_yQIh- |
link.rule.ids | 315,786,790,27955,27956 |
linkProvider | Geneva Foundation for Medical Education and Research |
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=T-bet+Knockout+Prevents+Helicobacter+felis+-Induced+Gastric+Cancer&rft.jtitle=The+Journal+of+immunology+%281950%29&rft.au=Stoicov%2C+Calin&rft.au=Fan%2C+Xueli&rft.au=Liu%2C+Jian+Hua&rft.au=Bowen%2C+Glennice&rft.date=2009-07-01&rft.issn=0022-1767&rft.eissn=1550-6606&rft.volume=183&rft.issue=1&rft.spage=642&rft.epage=649&rft_id=info:doi/10.4049%2Fjimmunol.0900511&rft.externalDBID=n%2Fa&rft.externalDocID=10_4049_jimmunol_0900511 |
thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0022-1767&client=summon |
thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0022-1767&client=summon |
thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0022-1767&client=summon |