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In Vivo Retinoic Acid Modulates Expression of the Class II Major Histocompatibility Complex and Function of Antigen-Presenting Macrophages and Keratinocytes in Ultraviolet-Exposed Human Skin

1996; Elsevier BV; Volume: 106; Issue: 5 Linguagem: Inglês

10.1111/1523-1747.ep12338626

1523-1747

Laurent Meunier, John J. Voorhees, Kevin D. Cooper,

Retinoids in leukemia and cellular processes

Because retinoic acid (RA) can alter photoaging of the skin and repeated ultraviolet (UV)-induced immunologic injury may play a role in chronic photoaging, we asked whether RA alters the acute photoimmunologic effects of UV radiation. Two sites from each volunteer were treated with 0.1% RA or vehicle continuously for 24 h before and 24 h after a 4-minimal erythema dose UVB exposure. RA did not function as a sunscreen, as determined by quantitating the increase in redness after 1 minimal erythema dose to vehicle- and RA-pretreated sites (n = 12). By flow cytometric analysis of epidermal cell suspensions harvested 3 d after the UV-EC, RA treatment did not protect CD1+ Langerhans cells from being depleted by UV light and did not modify the number of UV-induced infiltrating CD36+CD11b+CD1-DR+ macrophages. RA treatment did, however, result in a 40% downregulation of human leukocyte antigen (HLA)-DR expression on these infiltrating macrophages (p = 0.016) (n = 11), in conjunction with a decrease in alloantigen-presenting cell activity of RA-treated UV-EC as measured by T-cell proliferations. RA also induced a 72% inhibition of the autologous T suppressor-inducer cell proliferation induced by UV-EC (vehicle: 21,813 +/- 7,302 cpm; RA; 5,299 +/-635 cpm) (n = 3). The downregulation could be due to RA-modulated keratinocytes; RA-treated UV-EC keratinocytes depleted of CD1a+ and DR+ antigen-presenting cells displayed a greater ability, relative to similarly treated vehicle-EC keratinocytes, to inhibit alloantigen presentation.(i) in vivo RA treatment did not protect human Langerhans cells from being depleted by UV and did not block infiltration of macrophages into sunburned skin; and (ii) RA did decrease autologous and allogeneic T-cell reactivity induced by macrophage antigen-presenting cells in UV-exposed epidermis, at least in part by downregulating their HLA-DR expression and by upregulating inhibitory signals from UV-irradiated keratinocytes.