Eczema pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Edzel Lorraine Co, D.M.D., M.D.
Overview
The mechanism of disease of eczema involves a complex interplay of abnormalities of skin microbiomes, a dysfunction in the epidermal barrier, and an immune dysregulation. [1] There are two main theories on the existence of atopic dermatitis, also known as atopic eczema - the inside-out hypothesis, and the outside-in hypothesis.
Pathophysiology
- Affected skin involves the uptake of antigens and allergensby the epidermal dendritic cells, dermal dendritic cells, and Langerhan cells.
- Sensory nerves are activated by the released cytokines interleukins 4,13 and 31 (IL-4, IL-13, and IL-31), which are responsible for the pruritic sensation.
- As the event becomes chronic, an increased expression of keratinocyte and Th-cell-derived cytokines is achieved, with more pruritogens contributing to itch sensation. [1]
Hypotheses on development of Eczema
- There are two main theories on the existence of atopic dermatitis, also known as atopic eczema - the inside-out hypothesis, and the outside-in hypothesis.[2]
- Inside-out hypothesis
- This hypothesis denotes that some allergic triggers weaken the skin barrier that leads to more introduction of allergens to the area, causing more inflammatory reaction.[2]
- Outside-in hypothesis
- This hypothesis suggests that an impairment of the skin barrier should occur first before the onset of atopic dermatitis.
- This involves the down-regulation of filaggrin genes (FLG) responsible for maintenance of the proper function of skin barrier.[2] [3]
Genetic Inheritance
- There are 34 genetic loci which are thought to be associated with eczema.
- These regions contain several genes which have important [immunological]] functions, such as T-cell activation, type-2 helper cell differentiation, and innate immunity. [4] [5][6]
References
- ↑ 1.0 1.1 Feld M, Garcia R, Buddenkotte J, Katayama S, Lewis K, Muirhead G; et al. (2016). "The pruritus- and TH2-associated cytokine IL-31 promotes growth of sensory nerves". J Allergy Clin Immunol. 138 (2): 500–508.e24. doi:10.1016/j.jaci.2016.02.020. PMID 27212086.
- ↑ 2.0 2.1 2.2 Silverberg NB, Silverberg JI (2015). "Inside out or outside in: does atopic dermatitis disrupt barrier function or does disruption of barrier function trigger atopic dermatitis?". Cutis. 96 (6): 359–61. PMID 26761930.
- ↑ Leung DY, Guttman-Yassky E (2014). "Deciphering the complexities of atopic dermatitis: shifting paradigms in treatment approaches". J Allergy Clin Immunol. 134 (4): 769–79. doi:10.1016/j.jaci.2014.08.008. PMC 4186710. PMID 25282559.
- ↑ Paternoster L, Standl M, Waage J, Baurecht H, Hotze M, Strachan DP; et al. (2015). "Multi-ancestry genome-wide association study of 21,000 cases and 95,000 controls identifies new risk loci for atopic dermatitis". Nat Genet. 47 (12): 1449–1456. doi:10.1038/ng.3424. PMC 4753676. PMID 26482879.
- ↑ Weidinger S, Willis-Owen SA, Kamatani Y, Baurecht H, Morar N, Liang L; et al. (2013). "A genome-wide association study of atopic dermatitis identifies loci with overlapping effects on asthma and psoriasis". Hum Mol Genet. 22 (23): 4841–56. doi:10.1093/hmg/ddt317. PMC 3820131. PMID 23886662.
- ↑ Martin MJ, Estravís M, García-Sánchez A, Dávila I, Isidoro-García M, Sanz C (2020). "Genetics and Epigenetics of Atopic Dermatitis: An Updated Systematic Review". Genes (Basel). 11 (4). doi:10.3390/genes11040442. PMC 7231115 Check
|pmc=value (help). PMID 32325630 Check|pmid=value (help).