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Psoriasis
Psoriasis is one of the most common chronic inflammatory human skin diseases. Current knowledge indicates distinct overlap to other inflammatory as well as autoimmune disorders. However, the one or more relevant autoantigens could not be characterized so-far. A matter of current debate is if psoriasis is a primary autoimmune disease or secondarily evolving into autoimmunity as seen in other chronic inflammatory diseases. Related to this aspect is the concept of autoinflammation versus autoimmunity where psoriasis shares mechanisms of both entities. Though T-cells remain among the most important cellular players in the pathogenesis of psoriasis and current therapeutic strategies successfully target these cells or their products irrespective of these concepts.
Immune System Imbalance in Psoriasis
Psoriasis is characterized by being a mixed disease of autoimmunity and autoinflammation, both chronic conditions, these conditions are the expression of the imbalance of the immune system, where cytotoxic lymphocytes or also known inflammatory lymphocytes are responsible, in large part for the clinical changes of the patients, this imbalance of the immune system encompasses the cellular part and the inflammatory cytokine part.
The inflammatory cells responsible for the disease are cytotoxic lymphocytes, and the cytokines involved with IL-17, IL-34, INF. These inflammatory cytokines stimulate more cytotoxic lymphocytes to activate, this activation cycle that forms results in chronic tissue damage.
Cellular Immunotherapy for Psoriasis
T regulatory lymphocytes are responsible for inactivating cytotoxic lymphocytes, once these are activated, they release anti-inflammatory cytokines, that is, they will inactivate or block inflammatory cytokines, thus breaking the cycle of hyperactivation of the immune system. Autologous cellular immunotherapy with regulatory T lymphocytes has already proven to be effective when administered correctly.
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