The anergy of annularity

We explain the types and historical studies of annular and arciform lesions. In addition, we present a study of annular lesions on a patient with Erythema Annulare Centrifugum (EAC), proven to be caused by a delayed type hypersensitivity (DTH) to trichophyton antigen, using monoclonal antibodies to identify subsets of tissue monocytes outside the EAC lesion, in the inflamed border of the same EAC lesion and inside the circle (anergic area) of the same EAC lesion. Macrophages (M), Langerhans' cells (LC), pan-T cells, and the T cell subsets of helper/inducer T cells, suppressor/cytotoxic T cells, activated T cells and Ia (HLA-immuno associated) T cells were identified, localized, and compared in the respective areas of the annular lesion. An adequate number of antigen presentor cells were present in the dermis (and epidermis) in all areas. Langerhans cells (LC) were outside the inflamed border. Macrophages were in the border and inside the circle. Also, there were an adequate number of antigen receptor cells in all areas; pan-T cells were abundant outside, in the border and inside the circle. Although there were remarkably fewer helper and suppressor T cells inside the circle, the ratio of helper to suppressor T cells remained the same and unchanged in all the areas. None of the above could explain the anergy of EAC annularity. The Ia T cells were abundant in the epidermis and dermis outside the inflamed border and in the inflamed border. However, they were completely absent inside the circle. There were no Ia T cells inside of the EAC inflamed border even though the total number of T cells were abundant in that area. Apparently, the T cells had temporarily lost (4-6 weeks) their HLA histocompatibility inside of the annular and arciform EAC lesions. Having done so, these T cells could no longer receive antigen from M and Lc, could not become activated and thus, could not produce this DTH (Type IV) reaction. This defect may explain the anergy of DTH annularity.