C1q-Mediated Repression of Human Monocytes Is Regulated by Leukocyte-Associated Ig-Like Receptor 1 (LAIR-1)
作者： Myoungsun Son , Betty Diamond
DOI: 10.2119/MOLMED.2014.00185
关键词:
摘要: Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by abnormal function of both the innate and adaptive immune system, leading to loss tolerance self-antigens. Monocytes are key component system efficient producers multiple cytokines. In SLE, inappropriate activation monocytes thought contribute self-tolerance. this study, we demonstrate that type 1 interferon (IFN) production CpG-challenged can be suppressed C1q through activating leukocyte-associated Ig-like receptor-1 (LAIR-1), which contains immunoreceptor tyrosine-based inhibition motifs (ITIMs). The phosphorylation LAIR-1 interaction with SH2 domain-containing protein tyrosine phosphatase-1 (SHP-1) were enhanced after engagement C1q. Moreover, inhibited nuclear translocation regulatory factor (IRF)-3 IRF5 in CpG-stimulated monocytes. These data suggest model helps maintain monocyte tolerance, specifically respect Toll-like receptor-9-mediated activation.
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