Figure 1.

The impaired immune system in patients with systemic lupus erythematosus (SLE). Defective apoptotic clearance allows deposition of immune complexes which can stimulate B and T cells. Hyperactive B cells then produce auto-antibodies which activate complement, causing tissue damage. Plasmacytoid dendritic cells (pDCs) activated by immune complexes then release excessive interferon α/β (IFNα/β), again causing tissue damage. At each pathway, the known associated loci are indicated. All of the loci produce loss of both self-tolerance and autoimmunity, as seen in SLE. APC, antigen-presenting cell; BANK1, B-cell scaffold protein with ankyrin repeats 1; BLK, B lymphoid tyrosine kinase; HLA-DRB1, human leukocyte antigen-DRB1; IFIH1, interferon-induced helicase 1; IL10, interleukin-10; IRF, interferon regulatory factor; ITGAM, integrin, alpha M; LYN, V-yes-1 Yamaguchi sarcoma viral-related oncogene homolog; MHC, major histocompatibility complex; Mφ, microphage; NCF2, neutrophil cytosolic factor 2; PRDM1-ATG5, PR domain containing 1, with ZNF domain-autophagy-related 5 homolog; PTPN22, protein tyrosine phosphatase, non-receptor type 22; RasGRP3, RAS guanyl releasing protein 3; STAT4, signal transducer and activator of transcription 4; TCR, T-cell receptor; TNFAIP3, tumor necrosis factor, alpha-induced protein 3; TNFSF4, tumor necrosis factor superfamily, member 4; TNIP1, TNFAIP3- interacting protein 1; UBE2L3, ubiquitin-conjugating enzyme E2L 3.

Guerra et al. Arthritis Research & Therapy 2012 14:211   doi:10.1186/ar3844
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