Serum Granulysin as a Possible Key Marker to Detect the Severity of Psoriasis

The pathogenesis of psoriasis involves dynamic interactions between multiple cell types and numerous cytokines in response to triggers in genetically predisposed individuals leading to activation of T cells and their migration into skin, in addition to dysregulation of immunological cell function, keratinocyte proliferation takes place.

Psoriatic lesions are densely infiltrated by T cells and dendritic cells , the majority of T cells in the dermis are T-helper cells, while T cytotoxic cells predominate in the epidermis. T helper1 secrets cytokines, such as interferon gamma, tumor necrosis factor-alpha and interleukin 12. Recently discovered population of T helper cells called T helper17 cells which secrets interleukin 17 and interleukin 22 which stimulates epidermal proliferation, while interleukin 17 is responsible for the release of proinflammatory cytokines, antimicrobial peptides and chemokines.

A significant upregulation of perforin-expressing lymphocytes, especially cytotoxic T cells and natural killer cells, has been observed in psoriatic patients at the systemic and local levels. Perforin is a prototype granular cytotoxic mediator that ensures the quick access of pro-apoptotic molecules, such as granzymes and granulysin, into the target cells to induce apoptosis .

Granulysin is well associated with diverse activities of natural killer cells and cytotoxic T cells in physiological and pathological settings and could be a useful serum marker for monitoring host cell mediated immune cytotoxic responses.

Granulysin contributes toward the defense mechanisms against mycobacterial and viral infections as it can kill microbial pathogens through disruption of their membrane integrity, this can explain why infections is extremely rare in psoriatic lesions as psoriasis had high tissue granulysin expression, which increased with increased clinical severity of the disease.