ArticleJournal of immunology (Baltimore, Md. : 1950)2012
The lupus-prone NZM2410/NZW strain-derived Sle1b sublocus alters the germinal center checkpoint in female mice in a B cell-intrinsic manner.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 39 citations in OpenAlex.
- Article
- Increased development of T-betClinical immunology (Orlando, Fla.) · 2023Article
- Context-Dependent miR-21 Regulation of TLR7-Mediated Autoimmune and Foreign Antigen-Driven Antibody-Forming Cell and Germinal Center Responses.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- STAT4 Is Largely Dispensable for Systemic Lupus Erythematosus-like Autoimmune- and Foreign Antigen-Driven Antibody-Forming Cell, Germinal Center, and Follicular Th Cell Responses.ImmunoHorizons · 2021Article
- miRNA-Mediated Control of B Cell Responses in Immunity and SLE.Frontiers in immunology · 2021Review
- Serine Phosphorylation of the STAT1 Transactivation Domain Promotes Autoreactive B Cell and Systemic Autoimmunity Development.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Article
- Type II but Not Type I IFN Signaling Is Indispensable for TLR7-Promoted Development of Autoreactive B Cells and Systemic Autoimmunity.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Impaired B cell anergy is not sufficient to breach tolerance to nuclear antigen in Vκ8/3H9 lupus-prone mice.PloS one · 2020Article
- Estrogen Receptor Alpha Signaling Is Responsible for the Female Sex Bias in the Loss of Tolerance and Immune Cell Activation Induced by the Lupus Susceptibility LocusFrontiers in immunology · 2020Article
- Selenium supplementation suppresses immunological and serological features of lupus in B6.Sle1b mice.Autoimmunity · 2019Article
- Self-DNA at the Epicenter of SLE: Immunogenic Forms, Regulation, and Effects.Frontiers in immunology · 2019Review
- B-Cell-Intrinsic Type 1 Interferon Signaling Is Crucial for Loss of Tolerance and the Development of Autoreactive B Cells.Cell reports · 2018Article
- Dysregulated Lymphoid Cell Populations in Mouse Models of Systemic Lupus Erythematosus.Clinical reviews in allergy & immunology · 2017Review
- CD74 Deficiency Mitigates Systemic Lupus Erythematosus-like Autoimmunity and Pathological Findings in Mice.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Spontaneous germinal centers and autoimmunity.Autoimmunity · 2017Review
- Multiple tolerance defects contribute to the breach of B cell tolerance in New Zealand Black chromosome 1 congenic mice.PloS one · 2017Article
- IFN-γ receptor and STAT1 signaling in B cells are central to spontaneous germinal center formation and autoimmunity.The Journal of experimental medicine · 2016Article
- Lupus-Prone Mice Resist Immune Regulation and Transplant Tolerance Induction.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2016Article
- Distinct and synergistic roles of FcγRIIB deficiency and 129 strain-derived SLAM family proteins in the development of spontaneous germinal centers and autoimmunity.Journal of autoimmunity · 2015Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
C57BL/6 (B6) mice carrying the Sle1b sublocus (named B6.Sle1b), which harbors the lupus-associated NZM2410/NZW SLAM family genes, produce antinuclear Abs (ANAs). However, the role and mechanism(s) involved in the alteration of the germinal center (GC) tolerance checkpoint in the development of ANAs in these mice is not defined. In this study, we show significantly higher spontaneously formed GCs (Spt-GCs) in B6.Sle1b female mice compared with B6 controls. We also found a significant increase in CD4(+)CXCR5(hi)PD-1(hi) spontaneously activated follicular Th cells in B6.Sle1b female mice. Compared with B6 controls, B6.Sle1b female mice had increased numbers of proliferating B cells predominantly located in Spt-GCs. The elevated Spt-GCs in B6.Sle1b female mice were strongly associated with increased ANA-specific Ab-forming cells and ANA titers. The increased numbers of Spt-GCs and spontaneously activated follicular Th cells in B6.Sle1b mice were not the result of a generalized defect in B cells expressing Sle1b. Consistent with the elevated spontaneous response in B6.Sle1b mice, the attenuated GC response characteristic of DNA and p-azophenylarsonate reactive B cells from Ig V(H) knock-in mice (termed HKIR) were relieved in adoptively transferred recipients in the presence of Sle1b. Finally, by generating mixed bone marrow chimeras, we showed that the effect of Sle1b on Spt-GC, follicular Th cell, and autoantibody responses in B6.Sle1b mice was B cell autonomous. These data indicate that the NZM2410/NZW-derived Sle1b sublocus in conjunction with the female sex primarily affects B cells, leading to the alteration of the GC tolerance checkpoint and the generation of ANA-specific Ab-forming cells.
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