Skin‐homing T‐cell responses associated with Demodex infestation and rosacea

Abstract

Aims Our aim was to investigate the skin‐homing T‐cell immune responses triggered in patients with Demodex infestation and/or rosacea. Methods Collected whole blood samples were divided into four groups: control subjects; nonrosacea patients with Demodex infestation (Demodex group); papulopustular rosacea (PPR) patients without Demodex infestation (Rosacea group); and PPR patients with Demodex infestation (Rosacea/Demodex group). Following ex vivo activation, skin‐homing CLA+CD4+ T‐cell subset levels were monitored by flow cytometry. Results When compared with control subjects, among skin‐homing CD4+ T‐cell subsets analysed, Demodex patients had higher TH9 and Treg cell levels; Rosacea subjects displayed elevated TH1 cell levels; and Rosacea/Demodex patients exhibited increased frequencies of TH9 and TH22 cells. In contrast to Rosacea subjects, Rosacea/Demodex group members displayed higher TH2 cell levels; and when compared with Demodex groups, they had higher TH1 and TH2 but lower Treg cell levels. Demodex group members also exhibited higher Treg but lower TH1 and TH22 levels than Rosacea/Demodex group subjects. Conclusions The skin‐homing T‐cell responses associated with Demodex infestation and rosacea formation seem to influence each other. The present as well as future studies could contribute to the development of effective treatment strategies for demodicosis and rosacea.

The Pathogenic Role of Demodex Mites in Rosacea: A Potential Therapeutic Target Already in Erythematotelangiectatic Rosacea?

“…In rosacea, VEGF and its receptors, VEGF-R1 and VEGF-R2, are expressed not only by the epidermis, as in normal skin, but also by dermal infiltrating leukocytes (including lymphocytes, macrophages, and plasma cells) [141]. Moreover, accumulation of regulatory T cells has been observed [36,38], as in demodicosis [142]. This suggests that, as in tumoral processes, VEGF may induce T cell exhaustion in rosacea and, through collaboration with tolerogenic dendritic cells, may favor the initial proliferation of the mite during the development of ETR (Fig.…”

Which factors influence Demodex proliferation? A retrospective pilot study highlighting a possible role of subtle immune variations and sebaceous gland status

“…[1][2][3][4][5][6][7] They are acquired progressively by direct contact with the skin of other humans, 3 mainly within families, 2 and then slowly proliferate over time, under probable control of the host immune system, which they can modulate for their own survival. [8][9][10][11][12] The Demodex density (Dd) thus increases with age. 3,[13][14][15][16][17] Many factors have been reported to favor proliferation of the Demodex mite, including immunosuppression, [18][19][20][21][22][23] hypervascularizationrelated factors 10,[24][25][26][27][28] (likely via vascular endothelial growth factor [VEGF], 12 which has immunosuppressive properties 29 ), lack of use of soap combined with cosmetic overuse, 30 male sex, 13,31 high concentration of sebaceous glands 7,16 (such as on the cheeks 4,14,32,33 ), sebaceous hyperplasia, 3,6 and poor blood glucose control.…”

Comparison of the efficacy of tea tree (Melaleuca alternifolia) oil with other current pharmacological management in human demodicosis: A Systematic Review

“…Digestive enzymes such as protease and lipase secreted by the Demodex mites may provoke host protease-activated receptors, and may promote the expression of the anti-microbial peptide and upregulate pro-inflammatory cytokines (Bevins and Liu, 2007). The chitin exoskeleton of the mites, crystalline biological waste products and contaminant bacterium inside the mites such as Streptococci , Staphylococci , Bacillus cereus and Bacillus oleronius may trigger the inflammatory cascade by the toll-like receptor (TLR2) innate immunity pathway (Liu et al ., 2010) and may help the induction of T H 9 cells via IL-4 secretion (Gazi et al ., 2019). Bacillus oleronius may increase the release of the 83 and 62 kDa proteins that activate the inflammatory responses in the host (Lacey et al ., 2009).…”