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Review
. 2022 Feb 20;10(2):498.
doi: 10.3390/biomedicines10020498.

Orchestrated Cytokines Mediated by Biologics in Psoriasis and Its Mechanisms of Action

Aina Akmal Mohd Noor  1 , Maryam Azlan  2 , Norhanani Mohd Redzwan  1
Affiliations
Review

Orchestrated Cytokines Mediated by Biologics in Psoriasis and Its Mechanisms of Action

Aina Akmal Mohd Noor et al. Biomedicines. .

Abstract

Psoriasis is an autoimmune disease mediated by disturbed T cells and other immune cells, and is defined by deep-red, well-demarcated skin lesions. Due to its varied etiologies and indefinite standard pathogenesis, it is challenging to consider the right treatment exclusively for each psoriasis patient; thus, researchers yearn to seek even more precise treatments other than topical treatment and systemic therapy. Using biologics to target specific immune components, such as upregulated cytokines secreted by activated immune cells, is the most advanced therapy for psoriasis to date. By inhibiting the appropriate pro-inflammatory cytokines, cellular signaling can be altered and, thus, can inhibit further downstream inflammatory pathways. Herein, the roles of cytokines with their mechanisms of action in progressing psoriasis and how the usage of biologics alleviates cellular inflammation are discussed. In addition, other potential pro-inflammatory cytokines, with their mechanism of action, are presented herein. The authors hope that this gathered information may benefit future research in expanding the discovery of targeted psoriasis therapy.

Keywords: autoimmune disease; biologics; cytokines; immune cells; inhibitors; psoriasis.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
The summarized pathogenesis of psoriasis. Upon triggers, pDCs receive the signal via TLR8 and present the antigens to mDCs. mDCs activate Th1 and Th22 cells to release cytokines to generate hyperproliferative keratinocytes in the epidermis region. mDCs also present cytokines to Th17 cells to initiate keratinocyte hyperproliferation and the assembling of neutrophils to create Munro’s microabscesses. It is thought that once neutrophils undergo degranulation, this produces granular compounds, such as LL-37 and proteinase 3, which create an information loop to be detected again by pDCs. The cycle repeats. (AMP: antimicrobial proteins; PSORS: psoriasis susceptibility loci).
Figure 2
Figure 2
TNF-α inhibitors. Infliximab and adalimumab depict almost similar molecular structures with different Fv regions. Etanercept has specialized extracellular portions of human TNFR2. Certolizumab pegol is the most unique, as its Fc region is replaced with PEG molecules to lengthen its half-life.
Figure 3
Figure 3
Cytokine inhibitors and their respective blocking interests based on the postulated psoriasis pathogenesis. The overexpressed cytokines released by respective cells can be blocked, and this can downregulate the further inflammatory pathway.
See this image and copyright information in PMC

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