A Review of the Involvement of Disturbed Treg/CTC Ratios in the Sustained Proliferation of Psoriasis with a Brief Gender Distribution Analysis

Abstract

Aurangzeb Pirzada

Aim: To provide evidence from current literature that psoriasis is an autoimmune disorder involving a highly proliferated effector response in relation to a suppressed, inactivated and outnumbered regulatory component.
Disease Background Pathophysiology: Discusses the octet phenotypes, histological analyses, epidemiological data, additional components followed by briefly reflecting on its psychoanalytical aspects.
Evidence Based Review: Provides a historical perspective of Treg research and spans Treg details across cellular, molecular and genetic details mentioning its subtypes, TCR signalling comparison and marker diversity moving onto bringing FOXP3 under spotlight to discuss its structure, pathways followed by establishing a link between Treg and psoriasis.
Materials and Methods: Discusses laboratory techniques namely, flow cytometry, Western Blot, quantitative-RT-PCR and culturing techniques (invitro assays) for T cells and cytokines.
Results: Focus on disease relationship with IFN/TNFs/CCRs/FOXP3 and Shh to some extent providing figures and tables for ease of quantification.
Discussion: Critically evaluates the listed research followed by an easy to follow explanation per figure/table listed in Results section.
Conclusion: Entailed with discussion is a brief overview of current treatments in light of which new theories will be summed up in this section in light of all of the contents of this article.

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