ALOPECIA-AREATA - IMMUNOHISTOCHEMISTRY AND ULTRASTRUCTURE OF INFILTRATE AND IDENTIFICATION OF ADHESION MOLECULE RECEPTORS

Background. Alopecia areata (AA) is a noncicatricial alopecia with sti ll unknown pathogenesis, but increasing evidence suggests that an immu nologic process might be responsible for the disease. Materials and Me thods. Nineteen patients with AA were studied with ten of them in the progressive phase of the disease and nine in the stabilized phase, Bio psies of both affected and unaffected skin were taken. For immunohisto chemistry, monoclonal antibodies directed against CD3, CD4, CD8, CD10a , CD36, and HLA-DR antigens, were used, as well as antibodies directed against adhesion molecules ICAM-1, ELAM-1 and LFA-1. For electron mic roscopy (EM), specimens were fixed in glutaraldehyde-sodium cacodylate buffer, postfixed in osmium tetroxide, and stained with uranyl acetat e. For statistical analysis, sections from involved and uninvolved ski n of each patient for each antibody, the sign test, Fisher's F-test, a nd the Tukey-Kramer test were used. Results. There was a rich infiltra te of CD4+ cells and CD1a+ cells, particularly in the perivascular zon e of both unaffected and affected skin (here in the perivascular and i n the peribulbar zone) in the progressive phase of AA. In the stabiliz ed phase the infiltrate was scant, both in unaffected and affected ski n and limited to the peribulbar area. Receptors of adhesion molecules (ICAM-2, ELAM-1, LFA-1) were strongly expressed, mainly at the microva scular level in both unaffected and affected skin in the progressive p hase, but were only weakly or not at all expressed in the stabilized p hase, again in unaffected and affected skin. Ultrastructural data conf irmed the immunohistochemical findings and showed close contacts betwe en infiltrating lymphocytes and Langerhans'-lineage cells mainly in th e progressive phase. Conclusions. Our results suggest that: 1) an immu nologic process, apparently carried out by CD4+ lymphocytes and by den dritic CD1a+ and CD36+ cells, may play a key role at least in the earl y phase of the disease involving primarily microvessels and later on t he bulbar area; 2) the expression of adhesion molecule receptors is in volved at the beginning of the disease by mediating the adherence of l eukocytes to endothelial cells and subsequent trafficking into the der mis.