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T‐cell regulation by CD46 and its relevance in multiple sclerosis
Author(s) -
Astier Anne L.
Publication year - 2008
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/j.1365-2567.2008.02821.x
Subject(s) - cd46 , inflammation , multiple sclerosis , biology , immunology , experimental autoimmune encephalomyelitis , microbiology and biotechnology , cytokine , regulator , t cell , immune system , complement system , gene , genetics
Summary CD46 is a complement regulatory molecule expressed on every cell type, except for erythrocytes. While initially described as a regulator of complement activity, it later became a ‘magnet for pathogens’, binding to several viruses and bacteria. More recently, an alternative role for such complement molecules has emerged: they do regulate T‐cell immunity, affecting T‐cell proliferation and differentiation. In particular, CD46 stimulation induces Tr1 cells, regulatory T cells characterized by massive production of interleukin‐10 (IL‐10), a potent anti‐inflammatory cytokine. Hence, CD46 is likely to control inflammation. Indeed, data from CD46 transgenic mice highlight a role for CD46 in inflammation, with antagonist roles depending on the cytoplasmic tail being expressed. Furthermore, recent data have shown that CD46 is defective in multiple sclerosis, IL‐10 production being severely impaired in these patients. This lack of IL‐10 production probably participates in the inflammation observed in patients with multiple sclerosis. This review will summarize the data on CD46 and T cells, and how CD46 is likely involved in multiple sclerosis.