ArticleProceedings of the National Academy of Sciences of the United States of America2004
Dissection of the role of MHC class II A and E genes in autoimmune susceptibility in murine lupus models with intragenic recombination.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- Susceptibility to systemic autoimmunity rather than the presence of the HLA-DR4 peptide binding domain alone leads to severe inflammatory arthritis following inhalation of crystalline silica.Particle and fibre toxicology · 2026Article
- Mouse models, antibodies, and neuroimaging: Current knowledge and future perspectives in neuropsychiatric systemic lupus erythematosus (NPSLE).Frontiers in psychiatry · 2023Review
- Monocyte subsets involved in the development of systemic lupus erythematosus and rheumatoid arthritis.International immunology · 2019Review
- Microarray expression and functional analysis of circular RNAs in the glomeruli of NZB/W F1 mice with lupus nephritis.Experimental and therapeutic medicine · 2019Article
- Glomerular Proteomic Profiles in the NZB/W F1 Hybrid Mouse Model of Lupus Nephritis.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- A Restricted Role for FcγR in the Regulation of Adaptive Immunity.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Dual signaling by innate and adaptive immune receptors is required for TLR7-induced B-cell-mediated autoimmunity.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Role of MHC-linked susceptibility genes in the pathogenesis of human and murine lupus.Clinical & developmental immunology · 2012Review
- Genetics of SLE: evidence from mouse models.Nature reviews. Rheumatology · 2010Review
- Splenic phagocytes promote responses to nucleosomes in (NZB x NZW) F1 mice.Journal of immunology (Baltimore, Md. : 1950) · 2008Article
- Sle3 and Sle5 can independently couple with Sle1 to mediate severe lupus nephritis.Genes and immunity · 2007Article
- Genetic control of the spontaneous activation of CD4+ Th cells in systemic lupus erythematosus-prone (NZB x NZW) F1 mice.Genes and immunity · 2006Article
- Significance of MHC class II haplotypes and IgG Fc receptors in SLE.Springer seminars in immunopathology · 2006Review
- A Tlr7 translocation accelerates systemic autoimmunity in murine lupus.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Systemic lupus erythematosus (SLE) is a multigenic autoimmune disease, and the major histocompatibility complex (MHC) class II polymorphism serves as a key genetic element. In SLE-prone (NZB x NZW)F(1) mice, the MHC H-2(d/z) heterozygosity (H-2(d) of NZB and H-2(z) of NZW) has a strong impact on disease; thus, congenic H-2(d/d) homozygous F(1) mice do not develop severe disease. In this study, we used Ea-deficient intra-H-2 recombination to establish A(d/d)-congenic (NZB x NZW)F(1) mice, with or without E molecule expression, and dissected the role of class II A and E molecules. Here we found that A(d/d) homozygous F(1) mice lacking E molecules developed severe SLE similar to that seen in wild-type F1 mice, including lupus nephritis, autoantibody production, and spontaneously occurring T cell activation. Additional evidence revealed that E molecules prevent the disease in a dose-dependent manner; however, the effect is greatly influenced by the haplotype of A molecules, because wild-type H-2(d/z) F(1) mice develop SLE, despite E molecule expression. Studies on the potential of dendritic cells to present a self-antigen chromatin indicated that dendritic cells from wild-type F(1) mice induced a greater response of chromatin-specific T cells than did those from A(d/d) F(1) mice, irrespective of the presence or absence of E molecules, suggesting that the self-antigen presentation is mediated by A, but not by E, molecules. Our mouse models are useful for analyzing the molecular mechanisms by which MHC class II regions regulate the process of autoimmune responses.
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