Immunopathologic demonstration of T lymphocyte subpopulations and interleukin 2 in granuloma annulare.
Immunopathologic aspects of granuloma annulare were studied in frozen sections of nine skin biopsy specimens with monoclonal antibodies directed against T lymphocytes, Langerhans' cells, interleukin 2, and interleukin 2 receptors in conjunction with immunoperoxidase techniques. The predominant lymphocyte was an activated T lymphocyte (Leu 1+, HLA-DR+) with an excess of helper/inducer phenotype (Leu 3a+) as compared with suppressor/cytotoxic phenotype (Leu 2a+). Langerhans' cells were increased in the epidermis and numerous OKT6+ cells were observed in the perivascular and granulomatous infiltrate. Both interleukin 2-positive cells and interleukin 2 receptor-positive cells were identified in the dermal lesions according to observed reactivity with the corresponding monoclonal antibodies. These findings suggest that a cell-mediated immune response producing cytokines may be important in the pathogenesis of granuloma annulare. Comparison of these results with skin specimens from patients with sarcoidosis and from a patient with granuloma annulare having some of the histologic features of sarcoidosis, suggests that the cutaneous infiltrate in granuloma annulare represents a response distinct from that of sarcoidosis.
D000911:Antibodies, Monoclonal / Q000276:immunology; D006099:Granuloma / Q000276:immunology*; D006684:HLA-DR Antigens; D000949:Histocompatibility Antigens Class II / Q000276:immunology; D006801:Humans; D007124:Immunoenzyme Techniques; D007376:Interleukin-2 / Q000276:immunology*; D007801:Langerhans Cells / Q000276:immunology; D011971:Receptors, Immunologic / Q000276:immunology; D015375:Receptors, Interleukin-2; D012507:Sarcoidosis / Q000276:immunology; D012871:Skin Diseases / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology*
D000911:Antibodies, Monoclonal; D006684:HLA-DR Antigens; D000949:Histocompatibility Antigens Class II; D007376:Interleukin-2; D011971:Receptors, Immunologic; D015375:Receptors, Interleukin-2