Until The Early 1980S, Psoriasis Was Believed To Be A Disease

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Until the early 1980s, psoriasis was believed to be a disease primarily of epidermal keratinocyte proliferation and the cutaneous inflammatory infiltrate to be a secondary event. However, subsequent studies presented evidences that innate as well as adaptive immunity are crucial in the initiation and maintenance of psoriatic plaques. Type 1 and type 17 T lymphocytes secrete respectively (IFN-γ), (IL-2), IL-17, IL-22, in addition to TNF-α and IL6 (Gisondi and Girolomoni 2009).
The pathophysiology of psoriasis is characterized by epidermal hyperproliferation, enhanced antigen presentation, T helper 1 cytokine production, T cell expansion, and angiogenesis. (El-Darouti and Abdel Hay, 2010 ).
The current understanding of the molecular
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a. T lymphocyte activation this occurs in a series of steps, the first of which is incorporation of unidentified antigens by APCs in the epidermis and dermis. This process involves binding of the antigens to the MHC on the APC surface and the APC migrates to the lymph nodes. There, the APC binds reversibly and briefly with naïve or resting T cells through interactions between surface molecules located on both cells. Next, the MHC presents the antigen to a T lymphocyte receptor to begin activation of the T lymphocyte. The second signal for T lymphocyte activation is a non-antigen/ cell-cell interaction known as costimulation. If costimulation does not occur, the T lymphocyte will either undergo apoptosis or become unresponsive. Costimulation involves pairing of receptor with ligand on the T cell; these pairs include (LFA)-3 interacting with CD2, B7 interacting with CD28, and ICAM-1 interacting with LFA-1 (Lebwohl, 2003).

Figure(4): Activation of naive CD4+ T cells by APCs (Sabat et al., 2007)

a. Migration(trafficking) into the skin
The activated T lymphocytes expand, which results in proliferation of antigen-recognizing T lymphocytes, memory effector cells. The T lymphocytes enter the circulatory system and, via cell-cell interactions with endothelial cells of the blood vessel, migrate to the inflamed skin. (Lebwohl, 2003) During maturation, T-cells express new cell surface

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