Annoying Psoriasis and Atopic Dermatitis: A Narrative Review

Abstract

Skin is an important organ that mainly functions as a barrier. Skin diseases can damage a person's self-confidence and reduce their willingness to socialize, as well as their social behavior and willingness. When the skin appearance is abnormal, in addition to affecting the quality of life, it often leads to personal, social, and psychological dysfunction and even induces depression. Psoriasis and atopic dermatitis are common chronic skin diseases. Their prevalence in the world is 3-10%, and there is an increasing trend year by year. These congenital or acquired factors cause the dysfunction of the immune system and then destroy the barrier function of the skin. Because these patients are flooded with a variety of inflammatory mediators, this causes skin cells to be in chronic inflammation. Therefore, psoriasis and atopic dermatitis are also considered systemic chronic inflammatory diseases. In the healthcare systems of developed countries, it is unavoidable to spend high costs to relieve symptoms of psoriasis and atopic dermatitis patients, because psoriasis and atopic dermatitis have a great influence on individuals and society. Giving a lot of attention and developing effective treatment methods are the topics that the medical community must work on together. Therefore, we used a narrative review manuscript to discuss pathogenesis, clinical classification, incidence, and treatment options, including topical medication, systemic therapeutics, immunosuppressive medication for psoriasis, and atopic dermatitis, as well as also comparing the differences between these two diseases. We look forward to providing readers with comprehensive information on psoriasis and atopic dermatitis through this review article.

Keywords: atopic dermatitis; psoriasis.

Figure 1

When non-lesional skin is damaged by trauma, infection, and/or medications, KCs release antimicrobial peptides, LL-37, and nucleic acids (self-DNA and self-RNA). LL-37-self-DNA and LL-37-self-RNA complexes stimulate pDCs and mDCs, respectively. pDCs also stimulate mDCs via Type I IFN and TNFα. mDCs produce TNFα, IL12, and IL23 to recruit and activate Th1, Th22, and Th17 cells. They further produce cytokines that upregulate KC proliferation and downregulate KC differentiation, thereby causing inflammation. Regulated primarily by IL23, Th17 cells produce IL17A, which acts on KCs to increase the production of chemokines (CXCL-1 and CXCL-8), which in turn recruit neutrophils and induce transcription of multiple proinflammatory genes. Lesional skin will sustain the inflammatory condition through the cycle associated with the TNFα-IL23-IL17 axis. A variety of novel biologics targeting cytokines of this axis are effective in blocking the inflammatory cycle and improving the clinical condition. pDC, plasmacytoid dendritic cell; mDC, myeloid dendritic cell; IFN, interferon; TNFα, tumor necrosis factor-a; IL, interleukin; JAK, Janus kinase; TYK2, tyrosine kinase 2; STAT, signal transducer and activator of transcription; NF-κB, nuclear factor kappa-light-chain-enhancer of activated B cells.

Figure 2

Genetic predisposition and environmental factors can result in skin defects, such as abnormal desquamation and degradation of antimicrobial peptides. Allergens and pathogens can then penetrate through the defective skin barrier, upon which they are recognized by LCs and DCs. LCs and DCs induce the activation and accumulation of Th2 cells from lymph nodes. Th2 cells produce cytokines such as IL4, IL5, IL13, and IL31. These cytokines activate Ms and Es, which further produce IgE. IgE and IL31 then contribute to itching sensations. Scratching the skin causes lichenification and injury, which increases transepidermal water loss and allows more allergens and pathogens to penetrate the skin barrier.