Abstract
Autoimmune inflammation including autoantibody-induced inflammation is responsible for the lethal organ damage. Autoantibody-induced inflammation can be separated in two components, autoantibody production, and local inflammatory responses. Accumulating evidence has suggested that regulatory T cells (Treg) control both antibody production and the numbers and functions of effector cells such as innate cells and T helper cells. Autoantibodies are produced by both the follicular and extrafollicular pathways. Recently, follicular regulatory T cells (TFR) and Qa-1 restricted CD8+ Treg were identified as populations that are capable of suppressing follicular T helper cell (TFH)-mediated antibody production. In local inflammation, CD4+CD25+Foxp3+ Treg have the capacity to control inflammation by suppressing cytokine production in T helper cells. Although complement proteins contribute to autoantibody-induced local inflammation by activating innate cells, Treg including CD4+CD25+Foxp3+ Treg are able to suppress innate cells, chiefly via IL-10 production. IL-10-secreting T cells such as T regulatory type I (Tr1) and Tr1-like cells might also play roles in the control of Th17 and innate cells. Therefore, several kinds of Tregs have the potential to control autoimmune inflammation by suppressing both autoantibody production and the local inflammatory responses induced by autoantibodies.
Highlights
Autoimmune inflammation is responsible for the lethal organ damage, and autoantibodies play a pivotal role in triggering inflammation
Among five bortezomib-treated mice that displayed proteinuria of >100 mg/dl before treatment, four showed proteinuria of
CD4+CD25−LAG3+ T cells, which characteristically express the anergy-linked transcription factor Egr2, might be associated with autoantibody suppression, because T cell-specific Egr2-deficient mice exhibit lupus-like disease (Zhu et al, 2008) and polymorphisms in the EGR2 gene are associated with human systemic lupus erythematosus (SLE) susceptibility (Myouzen et al, 2010)
Summary
Autoimmune inflammation is responsible for the lethal organ damage, and autoantibodies play a pivotal role in triggering inflammation. Immune complexes are readily detectable in the articular tissues of rheumatoid arthritis (RA) patients and the glomeruli of systemic lupus erythematosus (SLE) patients. These immune complexes are regarded as important players in the pathogeneses of these diseases as they initiate and maintain the inflammatory cascade and tissue destruction. Complement fragments bound to immune complexes induce tissue injury, and FcR stimulation cumulatively activates mononuclear cells in situ, causing the activated cells to release pro-inflammatory cytokines. These responses attract neutrophils and macrophages, which can damage synoviocytes and chondrocytes. In anti-collagen antibody-induced arthritis (CAIA), complement activation, and www.frontiersin.org
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