title: The Inflammatory Response in Psoriasis: a Comprehensive Review.
abstract: Psoriasis is a chronic inflammatory autoimmune disease characterized by an excessively aberrant hyperproliferation of keratinocytes. The pathogenesis of psoriasis is complex and the exact mechanism remains elusive. However, psoriasis is thought to result from a combination of genetic, epigenetic, and environmental influences. Recent studies have identified that epigenetic factors including dysregulated DNA methylation levels, abnormal histone modification and microRNAs expressions are involved in the development of psoriasis. The interplay of immune cells and cytokines is another critical factor in the pathogenesis of psoriasis. These factors or pathways include Th1/Th2 homeostasis, the Th17/Treg balance and the IL-23/Th17 axis. Th17 is believed particularly important in psoriasis due to its pro-inflammatory effects and its involvement in an integrated inflammatory loop with dendritic cells and keratinocytes, contributing to an overproduction of antimicrobial peptides, inflammatory cytokines, and chemokines that leads to amplification of the immune response. In addition, other pathways and signaling molecules have been found to be involved, including Th9, Th22, regulatory T cells, γδ T cells, CD8(+) T cells, and their related cytokines. Understanding the pathogenesis of psoriasis will allow us to develop increasingly efficient targeted treatment by blocking relevant inflammatory signaling pathways and molecules. There is no cure for psoriasis at the present time, and much of the treatment involves managing the symptoms. The biologics, while lacking the adverse effects associated with some of the traditional medications such as corticosteroids and methotrexate, have their own set of side effects, which may include reactivation of latent infections. Significant challenges remain in developing safe and efficacious novel targeted therapies that depend on a better understanding of the immunological dysfunction in psoriasis.
authors.affiliation: Department of Dermatology, Second Xiangya Hospital, Hunan Key Laboratory of Medical Epigenomics, Central South University, Changsha, Hunan, China.
authors.forename: Yaxiong
authors.initials: Y
authors.lastname: Deng
authors.affiliation: Division of Rheumatology, Allergy and Clinical Immunology, University of California at Davis, 451 Health Sciences Drive, Suite 6510, Davis, CA, 95616, USA.
authors.forename: Christopher
authors.initials: C
authors.lastname: Chang
authors.affiliation: Department of Dermatology, Second Xiangya Hospital, Hunan Key Laboratory of Medical Epigenomics, Central South University, Changsha, Hunan, China. epigenetics2010@126.com.|Second Xiangya Hospital, Central South University, #139 Renmin Middle Rd, Changsha, Hunan, 410011, China. epigenetics2010@126.com.
authors.forename: Qianjin
authors.initials: Q
authors.lastname: Lu
mesh_terms: D000818:Animals; D015551:Autoimmunity; D003131:Combined Modality Therapy; D016207:Cytokines / Q000378:metabolism; D019468:Disease Management; D044127:Epigenesis, Genetic; D005786:Gene Expression Regulation; D020022:Genetic Predisposition to Disease; D014644:Genetic Variation; D006801:Humans; D007107:Immune System / Q000166:cytology / Q000276:immunology / Q000378:metabolism; D018836:Inflammation Mediators / Q000378:metabolism; D011565:Psoriasis / Q000209:etiology* / Q000378:metabolism* / Q000473:pathology / Q000628:therapy; D015398:Signal Transduction; D016896:Treatment Outcome
chemical_list: D016207:Cytokines; D018836:Inflammation Mediators
keywords: Adverse effect; Biologics; Cytokines; Dendritic cells; Inflammatory response; Psoriasis; T cells