Autoimmune diseases effector mechanisms

The generation of peripheral Treg cells may result in the establishment of homeostasis after its disruption. Examples include infection, autoimmune diseases, certain forms of cancers and immunodeficiency syndrome. The mechanisms by which peripheral Treg cells induce self-tolerance and homeostasis may involve cytokines or cell-cell interaction. The cytokines IL-10 and TGF-(3 and molecules such as CTLA-4 are involved in the effector mechanisms of Treg cells. The indirect effects of Treg cells may be mediated via APCs or NK cells. More specifically, the assembly of immunological synapse between APCs and effector cells is modulated by Treg cells, which may be mediated via direct or indirect mechanisms. 

Complement system. A group of serum proteins with the capacity to interact with each other when activated. The chain reaction of the activated complement components results in formation of a lytic complex and several biologically active peptides of low molecular weight (anaphylatoxins). The system can be activated by antigen-antibody complexes (classical pathway) and by other components, e.g. bacteria (alternative pathway). As an effector mechanism of the humoral immune response, the activated complement system facilitates opsonization, phagocytosis, and lysis of cellular antigens. Some defects in components of complement are associated with autoimmune diseases (see complement deficiency). 

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