Induce Effector Functions

The effector functions can be divided into 2 chapters

  • complement activation. Phylogenetically seen, complement is an old defense system of our body against foreign. It is part of the innate immune system expressed in worms and primitive sea animals. Some complement components might thus evolve since the middle miocene epoch or the tertiary period
  • Target cells carrying complement and Fc-receptors exert their specific cell functions, begin to proliferate and infiltrate inflammatory tissue

The common denominator of each effector function is the induction of inflammatory processes for which cytokines, small molecular weight polypeptides, oxygen radicals and further, in part unidentified mediators, allow infiltration of tissues with polymorphonuclear leukocytes and upregulation of acute phase reactants to combat the inflammation inducing agents. Immune complexes potentiate the effector functions of certain cells, such as lymphocytes and monocytes/macrophages.

Effector function can also be operative at the cellular level As an example, intestinal double-positive CD4(+)CD8(+) T cells kindle highly activated memory cells with an increased capacity to produce cytokines, of which IL-17 is currently on the forefront. IL-17 is classified as a highlight at the autoimmunity congress in Ljubljana (Slovenia), may 2010. Deficiency of complement factor H-related plasma proteins can favour haemolytic uremic syndrome (HUS). Factor H plays a role in senile macular degeneration and mutations in complement factor genes are a new laboratory trail to shed light on clinically relevant complement malfunction.

 

 

 

 

The complement system is like an enzyme cascade with three different major inflows: activation of the crucial C3 component may be achieved be the phylogenetically older alternate and lectin pathways and by the younger classical pathway. Abbreviations: Man:mannose, MBL: mannose binding lectin, MASP: mannose activating surface protein. The regulatory proteins H and I are not shown; they regulate excessive complement activation.

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Prof. U. E. Nydegger M.D.
Alumnus University of Bern, Switzerlland
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last modification
march 2010