Abstract
Psoriasis is a chronic inflammatory skin disease induced by multifactorial causes and is characterized by bothersome, scaly reddish plaques, especially on frequently chafed body parts, such as extensor sites of the extremities. The latest advances in molecular-targeted therapies using biologics or small-molecule inhibitors help to sufficiently treat even the most severe psoriatic symptoms and the extra cutaneous comorbidities of psoriatic arthritis. The excellent clinical effects of these therapies provide a deeper understanding of the impaired quality of life caused by this disease and the detailed molecular mechanism in which the interleukin (IL)-23/IL-17 axis plays an essential role. To establish standardized therapeutic strategies, biomarkers that define deep remission are indispensable. Several molecules, such as cytokines, chemokines, antimicrobial peptides, and proteinase inhibitors, have been recognized as potent biomarker candidates. In particular, blood protein markers that are repeatedly measurable can be extremely useful in daily clinical practice. Herein, we summarize the molecular mechanism of psoriasis, and we describe the functions and induction mechanisms of these biomarker candidates.
Highlights
While systemic treatment using biologics can reduce neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR) and improve psoriatic skin and arthropathic symptoms [85,86], it is not always correlated with the severity of psoriasis skin lesions as evaluated by the Psoriasis Area and Severity Index (PASI), suggesting that the NLR and PLR are better at reflecting systemic inflammation [87]
Serum IL-36γ levels are increased in cases of plaque-type psoriasis, and they are closely correlated with the respective severity; the elevated levels can be normalized when adequate treatment is provided [118]
In cases of plaque-type psoriasis, BD-2-protein levels significantly increase both in lesional epidermis and in serum, and serum levels are closely correlated with skin lesion severity as rated by the PASI score [156] and with serum IL-17A levels but not with the IL-17F levels [89]
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. This review describes the molecular p genesis of psoriasis and changes in biomarkers that occur along its disease activity, f other physiologicmarkers characteristics reliable indicator that reflects sufficient remission ing onorblood-protein that[16]. A toid dendritic (pDCs) to produce substantive interferon (IFN)-α, which activate complex ofcells antimicrobial peptides (AMP), such as LL-37, and self-nucleotides derived from damaged keratinocytes via toll-like receptors (TLRs), potentiate the function of eloid (conventional) DCs [18,19,20]. These activated DCs release tumor necrosis factor Kines and chemokines from the epidermal keratinocytes, resulting in a vicious circle of inflammatory reactions
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