Background: Acne vulgaris is a disease of the pilosebaceous unit characterized by increased sebum production, hyperkeratinization, and immune responses to (PA). Here, we explore a possible mechanism by which a lipid receptor, G2A, regulates immune responses to a commensal bacterium.
Objective: To elucidate the inflammatory properties of G2A in monocytes in response to PA stimulation.
Pityriasis rubra pilaris (PRP) is a rare, difficult to treat papulosquamous disorder that responds variably to retinoids and immunosuppression. Successful use of biologics for treating PRP has been described in the literature by case reports and a limited number of case series. To provide additional data, we retrospectively analyzed cases of PRP treated with biologics at our institution.
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