![]() ![]() These engage their respective receptors-a G protein–coupled receptor (GPCR) C3a receptor (C3aR) and the complement regulator CD46 (which binds C3b)-and induce autocrine interferon-γ (IFN-γ) ( 5, 6). ![]() ![]() In particular, C3a and C3b are generated intracellularly via cathepsin L–mediated cleavage of C3 in T cells upon TCR activation ( 4). Unexpectedly, the engagement of complement receptors on T cells is independent of systemic complement but instead is mediated in an autocrine manner by complement activation fragments produced by the T cell itself. However, complement also profoundly regulates adaptive immunity: In addition to T cell receptor (TCR) activation, costimulation, and the presence of interleukin (IL)–12 ( 2), human CD4 + T cells also depend on the activation of T cell–expressed complement receptors binding C3 activation fragments for normal T helper 1 (T H1) induction ( 3). Processing in serum of liver-derived C3 into C3a and C3b and of C5 into C5a and C5b activation fragments leads to opsonization and removal of invading microbes, mobilization of innate immune cells, and induction of inflammatory reactions ( 1). The complement system is an ancient innate immune sensor system that is essential for elimination of pathogens by the host. ![]()
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