Dual efficacy of dupilumab in a patient with concomitant atopic dermatitis and alopecia areata (original) (raw)
Related papers
Dermatology, 2008
Correspondence and Opinions surrounding the hair follicle [2]. However, this hypothesis was ruled out by a clinical trial which showed no efficacy of etanercept in the treatment of AA [6]. On the other hand, TNF-␣ appears to protect from hair loss since the blockade of TNF-␣-mediated effects by monoclonal antibodies resulted in the worsening of AA with infliximab in 1 patient [1] , the recurrence of AA in a patient treated with infliximab and adalimumab [cited in 2 ] and in the induction of AA in Pelivani's [2] and our present observations. That TNF-␣ blockers promote autoimmunity is known from both experimental and clinical studies [6]. In this respect, adalimumab, like other anti-TNF-␣ monoclonal antibodies, has been associated with the induction or aggravation of autoimmune diseases such as systemic lupus erythematosus and lupus-like syndrome [7]. Positive antinuclear antibody titers have been detected in patients treated with adalimumab and other anti-TNF-␣ therapies. Recent fundamental studies have shown that TNF-␣ promotes both the expansion and suppressive functions of CD4+ regulatory T cells which play an essential role in maintaining immune tolerance and preventing autoimmunity [8]. Therefore it is possible that anti-TNF-␣-induced autoimmunity is mediated by the inhibition of the suppressive functions of regulatory T cells [9] .
Immunological Properties of Atopic Dermatitis-Associated Alopecia Areata
International Journal of Molecular Sciences, 2021
Alopecia areata (AA) is regarded as a tissue-specific and cell-mediated autoimmune disorder. Regarding the cytokine balance, AA has been considered a type 1 inflammatory disease. On the other hand, AA often complicates atopic dermatitis (AD) and AD is regarded as type 2 inflammatory disease. However, the immunological aspects of AA in relation to AD are still poorly understood. Therefore, we aim to clarify the immunological properties of AD-associated AA. In this study, we performed comparative analysis of the expression of intracytoplasmic cytokines (IFN-γ, IL-4, and IL-13), chemokine receptors (CXCR3 and CCR4) in peripheral blood which were taken from healthy controls, non-atopic AA patients, AA patients with extrinsic AD, and AA patients with intrinsic AD by flowcytometric analysis. We also compared the scalp skin samples taken from AA patients with extrinsic AD before and after treatment with dupilumab. In non-atopic AA patients, the ratios of CD4+IFN-γ+ cells to CD4+IL-4+ cells...
Alopecia areata: autoimmunity--the evidence is compelling
The journal of investigative dermatology. Symposium proceedings / the Society for Investigative Dermatology, Inc. [and] European Society for Dermatological Research, 2003
There is strong evidence indicating that alopecia areata is a tissue-specific, autoimmune disease. Hair loss is associated with a perifollicular lymphocytic infiltrate made up primarily of CD4+ cells, along with a CD8+ intrafollicular infiltrate. Evidence of immune activation includes expression of HLA-DR; HLA-A,B,C; and ICAM-1 on the follicular epithelium. It is likely that the follicular expression of HLA-DR and ICAM-1 is induced by interferon-gamma produced by T cells. Antibodies to follicular epithelium are often present, but their significance is not known. Lesional scalp from alopecia areata patients grafted onto nude mice regrows hair coincident with a loss of infiltrating lymphocytes from the graft. Hair loss can be transferred to human scalp explants on SCID mice by injection of lesional T cells. It is necessary to activate the T cells by culture with follicular autoantigens. Melanocyte-associated antigens are also capable of activating T cells to induce hair loss, suggesti...