The roles of cells and cytokines in the pathogenesis of psoriasis

Abstract

Psoriasis is considered an immune chronic disease in which T cells are accepted as important. Nowadays, it is believed that psoriasis is most likely a T helper (Th)1/Th17 induced inflammatory disease. However, some other cells, such as endothelial cells, dendritic cells, monocytic cells, neutrophils, keratinocytes, and several cytokines, appear to have, at different stages of the disease, an important role in its pathogenesis. For instance, the response to psoriasis therapy is dependent not only on the inactivation of Th1 and Th17 immune responses but also on the inactivation of dendritic cell products. Moreover, interleukin (IL)-23 deregulation appears to be an independent factor in the pathogenesis of psoriasis. Indeed, currently, the IL-23/Th17 axis is believed to be crucial in psoriasis pathogenesis, and its inhibition appears to be important for therapeutic achievement. This review presents the roles and interactions of cells and cytokines that are related to psoriasis pathogenesis.

Circulating tumour necrosis factor is highly correlated with brainstem serotonin transporter availability in humans

“…Firstly, this is a condition where inflammation is fundamental in its pathophysiology and depression is highly prevalent (Coimbra et al, 2012;Gladman et al, 2005;Hayes and Koo, 2010;Kurd et al, 2010;Nestle et al, 2009;Schmitt and Ford, 2007). Secondly, this population gave us the ideal opportunity to explore the effect of TNF antagonism on 5-HTT.…”

CD1b-autoreactive T cells contribute to hyperlipidemia-induced skin inflammation in mice

“…Mice show skin-predominant but systemic inflammation as well as the prominent neutrophilia and T cell-derived IL-17 and reversal of disease with anti-IL-17, all of which have been observed in human psoriasis (7). A hallmark of human psoriatic skin is a Th1-and Th17-biased cytokine milieu (8,9). Recently the importance of IL-17A as a key driver of psoriasis has become clear, based on IL-17-directed therapies.…”

“…Psoriasis, a primarily T cell-driven autoimmune disease, affects approximately 1% to 3% of humans (3,7). Activation and subsequent cytokine secretion by self-peptide-reactive T cells contribute to disease maintenance (8,9). Further, T cell responses in psoriasis patients are largely Th17 and Th1 biased (8,9).…”

“…Activation and subsequent cytokine secretion by self-peptide-reactive T cells contribute to disease maintenance (8,9). Further, T cell responses in psoriasis patients are largely Th17 and Th1 biased (8,9). In fact, anti-TNF is a mainstay of therapy for psoriasis, and anti-IL-17A therapy was recently approved as a first-line systemic treatment (10,11).…”

Skin, Inflammation and Sulfurous Waters: What is Known, What is Believed

“…Relevant cytokines produced by the keratinocytes of psoriatic lesions, such as IL-6 and IL-8, have been shown to induce keratinocyte proliferation (11). The more recently described IL-15, IL-17, IL-19, IL-20, IL-22 and IL-23, that also are found in psoriatic lesions and which also influence keratinocyte proliferation, are mainly produced by cells of hematopoietic origin such as dendritic (DC), macrophages, lymphocytes and granulocytes (12). Studies on the role of interleukins secreted by Thl7 cells (IL-17 and IL-22) revealed a complex interaction between T cells and keratinocytes (11, 12) in several inflammatory skin pathologies including acanthosis, atopic dermatitis, cutaneous lupus erythematosus (13).…”