T‐bet‐expressing B cells contribute to the autoreactive plasma cell pool in Lyn‐/‐ mice
Systemic Lupus Erythematosus (SLE) is characterized by pathogenic autoantibodies against nucleic acid‐containing antigens. Understanding which B‐cell subsets give rise to these autoantibodies may reveal therapeutic approaches for SLE that spare protective responses. Mice lacking the tyrosine kinase...
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| Published in | European journal of immunology Vol. 53; no. 8; pp. e2250300 - n/a |
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| Main Authors | , , |
| Format | Journal Article |
| Language | English |
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01.08.2023
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| Abstract | Systemic Lupus Erythematosus (SLE) is characterized by pathogenic autoantibodies against nucleic acid‐containing antigens. Understanding which B‐cell subsets give rise to these autoantibodies may reveal therapeutic approaches for SLE that spare protective responses. Mice lacking the tyrosine kinase Lyn, which limits B and myeloid cell activation, develop lupus‐like autoimmune diseases characterized by increased autoreactive plasma cells (PCs). We used a fate‐mapping strategy to determine the contribution of T‐bet+ B cells, a subset thought to be pathogenic in lupus, to the accumulation of PCs and autoantibodies in Lyn‐/‐ mice. Approximately, 50% of splenic PCs in Lyn‐/‐ mice originated from T‐bet+ cells, a significant increase compared to WT mice. In vitro, splenic PCs derived from T‐bet+ B cells secreted both IgM and IgG anti‐dsDNA antibodies. To determine the role of these cells in autoantibody production in vivo, we prevented T‐bet+ B cells from differentiating into PCs or class switching in Lyn‐/‐ mice. This resulted in a partial reduction in splenic PCs and anti‐dsDNA IgM and complete abrogation of anti‐dsDNA IgG. Thus, T‐bet+ B cells make an important contribution to the autoreactive PC pool in Lyn‐/‐ mice.
Lyn‐/‐ mice, a model of lupus, have increased T‐bet+ follicular B cells and age‐associated B cells. Plasma cells derived from T‐bet‐expressing B cells (marked by a Tbx21‐cre.tomato reporter) accumulate in the spleens of Lyn‐/‐ mice and give rise to some IgM, and the majority of IgG, anti‐dsDNA autoantibodies. |
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| AbstractList | Systemic Lupus Erythematosus (SLE) is characterized by pathogenic autoantibodies against nucleic acid‐containing antigens. Understanding which B‐cell subsets give rise to these autoantibodies may reveal therapeutic approaches for SLE that spare protective responses. Mice lacking the tyrosine kinase Lyn, which limits B and myeloid cell activation, develop lupus‐like autoimmune diseases characterized by increased autoreactive plasma cells (PCs). We used a fate‐mapping strategy to determine the contribution of T‐bet+ B cells, a subset thought to be pathogenic in lupus, to the accumulation of PCs and autoantibodies in Lyn‐/‐ mice. Approximately, 50% of splenic PCs in Lyn‐/‐ mice originated from T‐bet+ cells, a significant increase compared to WT mice. In vitro, splenic PCs derived from T‐bet+ B cells secreted both IgM and IgG anti‐dsDNA antibodies. To determine the role of these cells in autoantibody production in vivo, we prevented T‐bet+ B cells from differentiating into PCs or class switching in Lyn‐/‐ mice. This resulted in a partial reduction in splenic PCs and anti‐dsDNA IgM and complete abrogation of anti‐dsDNA IgG. Thus, T‐bet+ B cells make an important contribution to the autoreactive PC pool in Lyn‐/‐ mice.
Lyn‐/‐ mice, a model of lupus, have increased T‐bet+ follicular B cells and age‐associated B cells. Plasma cells derived from T‐bet‐expressing B cells (marked by a Tbx21‐cre.tomato reporter) accumulate in the spleens of Lyn‐/‐ mice and give rise to some IgM, and the majority of IgG, anti‐dsDNA autoantibodies. Systemic Lupus Erythematosus (SLE) is characterized by pathogenic autoantibodies against nucleic acid-containing antigens. Understanding which B cell subsets give rise to these autoantibodies may reveal therapeutic approaches for SLE that spare protective responses. Mice lacking the tyrosine kinase Lyn, which limits B and myeloid cell activation, develop lupus-like autoimmune disease characterized by increased autoreactive plasma cells (PCs). We used a fate-mapping strategy to determine the contribution of T-bet+ B cells, a subset thought to be pathogenic in lupus, to the accumulation of PCs and autoantibodies in Lyn−/− mice. Approximately 50% of splenic PCs in Lyn−/− mice originated from T-bet+ cells, a significant increase compared to wild type mice. In vitro , splenic PCs derived from T-bet+ B cells secreted both IgM and IgG anti-dsDNA antibodies. To determine the role of these cells in autoantibody production in vivo , we prevented T-bet+ B cells from differentiating into PCs or class switching in Lyn−/− mice. This resulted in a partial reduction in splenic PCs and anti-dsDNA IgM and complete abrogation of anti-dsDNA IgG. Thus, T-bet+ B cells make an important contribution to the autoreactive PC pool in Lyn−/− mice. Lyn−/− mice, a model of lupus, have increased T-bet+ follicular B cells and age associated B cells. Plasma cells derived from T-bet expressing B cells (marked by a Tbx21-cre.tomato reporter) accumulate in the spleens of Lyn−/− mice and give rise to some IgM, and the majority of IgG, anti-dsDNA autoantibodies. Abstract Systemic Lupus Erythematosus (SLE) is characterized by pathogenic autoantibodies against nucleic acid‐containing antigens. Understanding which B‐cell subsets give rise to these autoantibodies may reveal therapeutic approaches for SLE that spare protective responses. Mice lacking the tyrosine kinase Lyn, which limits B and myeloid cell activation, develop lupus‐like autoimmune diseases characterized by increased autoreactive plasma cells (PCs). We used a fate‐mapping strategy to determine the contribution of T‐bet + B cells, a subset thought to be pathogenic in lupus, to the accumulation of PCs and autoantibodies in Lyn ‐/‐ mice. Approximately, 50% of splenic PCs in Lyn ‐/‐ mice originated from T‐bet + cells, a significant increase compared to WT mice. In vitro, splenic PCs derived from T‐bet + B cells secreted both IgM and IgG anti‐dsDNA antibodies. To determine the role of these cells in autoantibody production in vivo , we prevented T‐bet + B cells from differentiating into PCs or class switching in Lyn ‐/‐ mice. This resulted in a partial reduction in splenic PCs and anti‐dsDNA IgM and complete abrogation of anti‐dsDNA IgG. Thus, T‐bet + B cells make an important contribution to the autoreactive PC pool in Lyn ‐/‐ mice. Systemic Lupus Erythematosus (SLE) is characterized by pathogenic autoantibodies against nucleic acid‐containing antigens. Understanding which B‐cell subsets give rise to these autoantibodies may reveal therapeutic approaches for SLE that spare protective responses. Mice lacking the tyrosine kinase Lyn, which limits B and myeloid cell activation, develop lupus‐like autoimmune diseases characterized by increased autoreactive plasma cells (PCs). We used a fate‐mapping strategy to determine the contribution of T‐bet+ B cells, a subset thought to be pathogenic in lupus, to the accumulation of PCs and autoantibodies in Lyn‐/‐ mice. Approximately, 50% of splenic PCs in Lyn‐/‐ mice originated from T‐bet+ cells, a significant increase compared to WT mice. In vitro, splenic PCs derived from T‐bet+ B cells secreted both IgM and IgG anti‐dsDNA antibodies. To determine the role of these cells in autoantibody production in vivo, we prevented T‐bet+ B cells from differentiating into PCs or class switching in Lyn‐/‐ mice. This resulted in a partial reduction in splenic PCs and anti‐dsDNA IgM and complete abrogation of anti‐dsDNA IgG. Thus, T‐bet+ B cells make an important contribution to the autoreactive PC pool in Lyn‐/‐ mice. Systemic Lupus Erythematosus (SLE) is characterized by pathogenic autoantibodies against nucleic acid-containing antigens. Understanding which B-cell subsets give rise to these autoantibodies may reveal therapeutic approaches for SLE that spare protective responses. Mice lacking the tyrosine kinase Lyn, which limits B and myeloid cell activation, develop lupus-like autoimmune diseases characterized by increased autoreactive plasma cells (PCs). We used a fate-mapping strategy to determine the contribution of T-bet+ B cells, a subset thought to be pathogenic in lupus, to the accumulation of PCs and autoantibodies in Lyn-/- mice. Approximately, 50% of splenic PCs in Lyn-/- mice originated from T-bet+ cells, a significant increase compared to WT mice. In vitro, splenic PCs derived from T-bet+ B cells secreted both IgM and IgG anti-dsDNA antibodies. To determine the role of these cells in autoantibody production in vivo, we prevented T-bet+ B cells from differentiating into PCs or class switching in Lyn-/- mice. This resulted in a partial reduction in splenic PCs and anti-dsDNA IgM and complete abrogation of anti-dsDNA IgG. Thus, T-bet+ B cells make an important contribution to the autoreactive PC pool in Lyn-/- mice.Systemic Lupus Erythematosus (SLE) is characterized by pathogenic autoantibodies against nucleic acid-containing antigens. Understanding which B-cell subsets give rise to these autoantibodies may reveal therapeutic approaches for SLE that spare protective responses. Mice lacking the tyrosine kinase Lyn, which limits B and myeloid cell activation, develop lupus-like autoimmune diseases characterized by increased autoreactive plasma cells (PCs). We used a fate-mapping strategy to determine the contribution of T-bet+ B cells, a subset thought to be pathogenic in lupus, to the accumulation of PCs and autoantibodies in Lyn-/- mice. Approximately, 50% of splenic PCs in Lyn-/- mice originated from T-bet+ cells, a significant increase compared to WT mice. In vitro, splenic PCs derived from T-bet+ B cells secreted both IgM and IgG anti-dsDNA antibodies. To determine the role of these cells in autoantibody production in vivo, we prevented T-bet+ B cells from differentiating into PCs or class switching in Lyn-/- mice. This resulted in a partial reduction in splenic PCs and anti-dsDNA IgM and complete abrogation of anti-dsDNA IgG. Thus, T-bet+ B cells make an important contribution to the autoreactive PC pool in Lyn-/- mice. Systemic Lupus Erythematosus (SLE) is characterized by pathogenic autoantibodies against nucleic acid-containing antigens. Understanding which B-cell subsets give rise to these autoantibodies may reveal therapeutic approaches for SLE that spare protective responses. Mice lacking the tyrosine kinase Lyn, which limits B and myeloid cell activation, develop lupus-like autoimmune diseases characterized by increased autoreactive plasma cells (PCs). We used a fate-mapping strategy to determine the contribution of T-bet B cells, a subset thought to be pathogenic in lupus, to the accumulation of PCs and autoantibodies in Lyn mice. Approximately, 50% of splenic PCs in Lyn mice originated from T-bet cells, a significant increase compared to WT mice. In vitro, splenic PCs derived from T-bet B cells secreted both IgM and IgG anti-dsDNA antibodies. To determine the role of these cells in autoantibody production in vivo, we prevented T-bet B cells from differentiating into PCs or class switching in Lyn mice. This resulted in a partial reduction in splenic PCs and anti-dsDNA IgM and complete abrogation of anti-dsDNA IgG. Thus, T-bet B cells make an important contribution to the autoreactive PC pool in Lyn mice. |
| Author | Schneider, Jalyn Ottens, Kristina Satterthwaite, Anne B. |
| AuthorAffiliation | 1 Department of Internal Medicine, UT Southwestern Medical Center, Dallas, TX, 75390 2 Department of Immunology, UT Southwestern Medical Center, Dallas, TX, 75390 |
| AuthorAffiliation_xml | – name: 2 Department of Immunology, UT Southwestern Medical Center, Dallas, TX, 75390 – name: 1 Department of Internal Medicine, UT Southwestern Medical Center, Dallas, TX, 75390 |
| Author_xml | – sequence: 1 givenname: Kristina surname: Ottens fullname: Ottens, Kristina organization: UT Southwestern Medical Center – sequence: 2 givenname: Jalyn surname: Schneider fullname: Schneider, Jalyn organization: UT Southwestern Medical Center – sequence: 3 givenname: Anne B. surname: Satterthwaite fullname: Satterthwaite, Anne B. email: anne.satterthwaite@utsouthwestern.edu organization: UT Southwestern Medical Center |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/37134326$$D View this record in MEDLINE/PubMed |
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| Keywords | Lyn autoantibody T-bet lupus plasma cell |
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| Snippet | Systemic Lupus Erythematosus (SLE) is characterized by pathogenic autoantibodies against nucleic acid‐containing antigens. Understanding which B‐cell subsets... Systemic Lupus Erythematosus (SLE) is characterized by pathogenic autoantibodies against nucleic acid-containing antigens. Understanding which B-cell subsets... Abstract Systemic Lupus Erythematosus (SLE) is characterized by pathogenic autoantibodies against nucleic acid‐containing antigens. Understanding which B‐cell... Systemic Lupus Erythematosus (SLE) is characterized by pathogenic autoantibodies against nucleic acid-containing antigens. Understanding which B cell subsets... |
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| SubjectTerms | Animals Antigens Autoantibodies autoantibody Autoimmune diseases Cell activation Cell differentiation Cell fate Class switching Immunoglobulin G Immunoglobulin M Lupus Lupus Erythematosus, Systemic Lymphocytes B Lyn Mice plasma cell Plasma Cells Protein-tyrosine kinase Spleen src-Family Kinases - genetics Systemic lupus erythematosus T-Box Domain Proteins - genetics T-Box Domain Proteins - metabolism T‐bet |
| Title | T‐bet‐expressing B cells contribute to the autoreactive plasma cell pool in Lyn‐/‐ mice |
| URI | https://onlinelibrary.wiley.com/doi/abs/10.1002%2Feji.202250300 https://www.ncbi.nlm.nih.gov/pubmed/37134326 https://www.proquest.com/docview/2848716485/abstract/ https://www.proquest.com/docview/2809547031/abstract/ https://pubmed.ncbi.nlm.nih.gov/PMC10524956 |
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