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Atopic dermatitis: triggering factors.

M A Morren·B Przybilla·M Bamelis·B Heykants·A Reynaers·H Degreef
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Abstract

Atopic dermatitis is a hereditary disorder, frequently associated with allergic rhinitis and bronchial asthma. The disease may be influenced by many triggering factors such as irritants, aeroallergens, food, microbial organisms, sex hormones, stress factors, sweating, and climatologic factors. Moreover, it is important to be aware of contact allergy as a complicating factor. This review deals with recent clinical, experimental, and some therapeutic data on these triggering factors.

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M A Morren, B Przybilla, M Bamelis, B Heykants, A Reynaers, H Degreef. 1994. Atopic dermatitis: triggering factors.. https://doi.org/10.1016/s0190-9622(94)70213-6

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Single-cell transcriptome revealed the aberrant keratinocytes activation in antigen presentation in atopic dermatitis.

BACKGROUND: Atopic dermatitis (AD), a common chronic inflammatory skin disease, has been extensively studied using single-cell genomics. However, keratinocytes, as key effector cells in AD, have underlying mechanisms remain incompletely understood and require further investigation. METHODS: We integrated single-cell transcriptomic data from skin tissues of healthy controls, chronic active AD patients, spontaneously healed AD (SHAD) patients, and an ovalbumin-induced AD mouse model. The study particularly emphasized the gene expression and cellular dynamics of keratinocytes across the different groups, as well as their interactions with immune cells. RESULTS: Compared to healthy controls, we observed significant changes in the keratinocyte transcriptome, cellular state, and keratinocyte-immune cell ligand-receptor interactions in AD skin, particularly the marked activation of genes involved in antigen processing and presentation. Interestingly, such gene activation was not observed in keratinocytes from the ovalbumin-induced AD mouse model, despite its phenotype closely resembling human AD. Furthermore, in SHAD, we identified a recovery of both the ligand-receptor interaction patterns and antigen processing and presentation genes, accompanied by a notable shift in the transcriptome. This involved a significant downregulation of genes related to cytoplasmic transcription and oxidative phosphorylation. Notably, this pattern was not observed in the self-healing mouse model following the removal of ovalbumin stimulation. CONCLUSION: Our results suggest that the persistent activation of antigen processing and presentation pathways in keratinocytes may be a key driver of chronic inflammation in AD. Therefore, redirecting anti-allergic therapeutic strategies from solely targeting immune cells to targeting of keratinocyte-mediated antigen presentation may offer a more effective approach. Furthermore, we raise concerns about the use of ovalbumin-induced mouse models to recapitulate human chronic AD, as the underlying mechanisms may differ significantly.

Dermatitis, Atopic↗
PubMed1997

Atopic dermatitis may be a genetically determined dysmaturation of ectodermal tissue, resulting in disturbed T-lymphocyte maturation. A hypothesis.

Although atopic dermatitis is a skin disorder, it includes immune deviations such as T-cell accumulation and activation in the skin, resulting in chronic, relapsing eczema. The T-lymphocyte activation in the skin is not accompanied by specific allergies in up to two thirds of the patients. It has been shown that T-cell lines and clones can be established from skin biopsies of patients with atopic dermatitis showing cytokine-dependent, but antigen-independent, continuous growth in vitro. This indicates the existence of skin-homing T-lymphocytes with growth requirements different from those of mature T-lymphocytes in the blood. We suggest that atopic dermatitis is a genetically determined change of ectodermal tissue. The thymic epithelium is derived from the ectoderm, and because of that we hypothesize that the maturation of the T-cell immune system of persons who develop atopic dermatitis is disturbed due to a faulty selection of T-lymphocytes in the thymus. "Dys"-matured T-cells leave the thymus as a consequence of faulty selection and continue their growth in the skin. The cells are eventually eradicated by the immune surveillance conducted by the normal part of the patients' immune system and as a consequence of diminished output of faulty selected T-lymphocytes during maturation. Because of the increased proliferation capacity of the aberrant T-cells, a cytokine imbalance occurs and in some patients this leads to the development of type I allergies due to a skewing of the humoral immune system towards IgE production.

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