Pathophysiology of sarcoidosis

Pathophysiology of sarcoidosis

The pathogenesis begins with the uptake of an antigen (infectious, organic, anorganic) by a macrophage. This antigen-presenting cells binds a CD4+ T-cell thereby presenting the antigen on its MHC class II complex to the T-cell receptor. This evokes activation of the T-cell, which starts to produce all kinds of cytokines including IL-2, IL-12, IL-18, IFNγ and TGFβ. Actually the T-cell elicits an early response resulting in differentiation into

a Th1 effector cell. By producing IFNγ, this cell type activates macrophages and induces inflammation. The late reaction involves the differentiation of Th2 effector cells. The cytokines produces in this response (mainly TGFβ and IL-10) contribute to tissue scaring in the lungs. Granulomatous inflammation is characterised primarily by accumulation of monocytes, macrophages and activated T-lymphocytes, and key inflammatory mediators.