Serum level of <scp>IL</scp>‐4 predicts response to topical immunotherapy with diphenylcyclopropenone in alopecia areata

Gong, Yi; Zhang, Ying; Zhang, Xiaoting; Qi, Shiling; Li, Shuifeng; Ye, Yanting; Yang, Jiong; Caulloo, Sillani; McElwee, Kevin J.; Zhang, Xingqi

doi:10.1111/exd.13758

Cited by 25 publications

(36 citation statements)

References 41 publications

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“…Through its long history, a link between AA and inflammation has been well recognized 262 . It presents with a wide array of clinical and aetiological variations, 263,264 but in all instances it is a non‐scarring alopecia 265,266 . Histopathological examination reveals anagen stage HFs affected by a peri‐ and intra‐follicular inflammatory cell infiltrates primarily comprised of CD8 + T cells and CD4 + T cells, 267 as well as antigen‐presenting cells (APCs), 259,268 mast cells, 179 NK cells 88 and sometimes eosinophils 269 .…”

Section: Alopecia Areatamentioning

confidence: 99%

“…Since failure of IP mechanisms enables AA development, it is logical to anticipate that restoring and/or supplementing IP signalling is a highly effective way to treat AA and prevent future relapse. Exogenous factors could modify the nature and intensity of IP and its breakdown in AA including the HF and gut microbiomes, 326 the bioavailability of energy for immune cell activity 327 and atopic responses to environmental allergens, 264,328 for example. As such, targeting these external factors with treatment may facilitate IP regeneration in AA‐affected HFs.…”

Section: Therapeutic Perspectivesmentioning

confidence: 99%

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Hair follicle immune privilege and its collapse in alopecia areata

Bertolini

McElwee

Gilhar

et al. 2020

Experimental Dermatology

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181

157

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Anagen stage hair follicles (HFs) exhibit “immune privilege (IP)” from the level of the bulge downwards to the bulb. Both passive and active IP mechanisms protect HFs from physiologically undesired immune responses and limit immune surveillance. IP is relative, not absolute, and is primarily based on absent, or greatly reduced, intra‐follicular antigen presentation via MHC class I and II molecules, along with prominent expression of “no danger” signals like CD200 and the creation of an immunoinhibitory signalling milieu generated by the secretory activities of HFs. Perifollicular mast cells, Tregs and other immunocytes may also contribute to HF IP maintenance in healthy human skin. Collapse of anagen hair bulb IP is an essential prerequisite for the development of alopecia areata (AA). In AA, lesional HFs are rapidly infiltrated by NKG2D + T cells and natural killer (NK) cells, while perifollicular mast cells acquire a profoundly pro‐inflammatory phenotype and interact with autoreactive CD8+ T cells. Using animal models, significant functional evidence has accumulated that demonstrates the dominance of the immune system in AA pathogenesis. Purified CD8+T‐cell and NK cell populations alone, which secrete fγ, suffice to induce the AA phenotype, while CD4+T‐cells aggravate it, and Tregs and iNKT cells may provide relative protection against AA development. While IP collapse may be induced by exogenous agents, inherent IP deficiencies might confer increased susceptibility to AA for some individuals. Thus, a key goal for effective AA management is the re‐establishment of a functional HF IP, which will also provide superior protection from disease relapse.

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Section: Alopecia Areatamentioning

confidence: 99%

Section: Therapeutic Perspectivesmentioning

confidence: 99%

Hair follicle immune privilege and its collapse in alopecia areata

Bertolini

McElwee

Gilhar

et al. 2020

Experimental Dermatology

Self Cite

181

157

View full text Add to dashboard Cite

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“…With humans, adjunctive treatments against allergies could be used to observe whether there is an improved effect on AA resolution. From our observations, HDM desensitization might modulate the balance of Th1/Th2 cytokine activity in AA. Allergen desensitization or antihistamine use in atopic AA patients may not directly treat AA, but may change immune activity so as to enable hair growth in response to standard treatments.…”

Section: How To Test the Hypothesismentioning

confidence: 57%

“…In contrast, AA is considered a T cell–driven, Th1‐dominant lesion, primarily represented by IFNγ . However, both Th1 and Th2 cytokines are significantly elevated in AA patients . In AA mice, both Th1 and Th2 cytokines are increased very early in the disease pathogenesis, even in advance of overt hair loss .…”

Section: Premisementioning

confidence: 99%

Allergy promotes alopecia areata in a subset of patients

Zhang

McElwee

2019

Experimental Dermatology

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In this commentary, we focus on allergy as a facilitating factor in the pathogenesis of alopecia areata (AA). From previous studies on AA, it is well known that subsets of patients can have one or more of; seasonal relapse, comorbid atopic rhinitis, asthma and dermatitis, lesion infiltrating eosinophils and plasma cells, high levels of total IgE, specific IgE for house dust mites (HDMs), and/or disrupted skin barrier function by the evaluation of filaggrin. Allergy and AA share a similar genetic background; both contributing to an immune reaction imbalance. Furthermore, adjunctive treatment with antihistamines, or desensitization for HDM, can reduce the severity of alopecia in atopic AA patients. Therefore, allergies may contribute to the onset and relapse of AA. Identification of an allergic or atopic immune component in AA patient subsets may indicate adjunctive treatment intervention measures against allergies should be taken which may improve the success of conventional AA treatment.

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“…Zhang and colleagues also examine cytokine expression in AA patients undergoing treatment with diphencyprone (DCP) and conclude that patients exhibiting high levels of IL‐4 in their blood are less likely to respond to treatment . The response to contact sensitizing agents is variable, while some patients produce an excellent response, DCP fails to promote hair growth in others.…”

Section: Alopecia Areatamentioning

confidence: 99%