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Twelve patients with keratoacanthoma were studied to assess the role and importance of immunological factors in tumor regression. Direct immuno-fluorescence was determined with immunoglobulins, complement (C3), and fibrin to estimate the deposition of these factors in the lesion area. Indirect immunofluorescence was also undertaken using pemphigus and bullous pemphigoid sera against the keratoacanthoma lesion to study the presence or absence of tissue-specific antigens (T.S.A.) in intercellular substance and basement membrane. Finally, the cell-mediated immunity was studied using two in vitro parameters: (a) The estimation of T-lymphocytes through the formation of E-rosettes and (b) the estimation of the leukocyte migration inhibition factor (LIF). Our findings show that specific humoral immune mechanisms are apparently not involved in the spontaneous regression of keratoacanthoma. Cell-mediated immune mechanisms are evidently not responsible for the resolution of the tumor.

In 54 cases of dermatophytosis, sweat gland disturbances and their possible mechanisms were studied. The basic perspiratory malfunction was intense hypohidrosis, with some hyperhidrotic phenomena being observed at particular points of the exanthem (margin and disc) in a few cases. It is worth noting that in 51.85% of the cases, hypohidrotic phenomena were also observed in areas of normal skin adjacent to the lesions. One of the most important forms of perspiratory disturbances was the closure of sweat ducts at the keratin level. The inflammatory process in the dermis may also affect gland function. Finally, there is a discussion of the significance of perspiratory disturbances in relation to special aspects of the disease.

Neutrophil cell function in psoriasis was studied through polymorphonuclear cell adherence to nylon wool, chemotaxis under agarose, and phagocytosis of Candida albicans. Differences in PMN adherence were not found between psoriatics and controls. The chemotactic response to zymosan activated serum (ZAS) did not differ between psoriatic and normal PMNs. The psoriatic serum exhibited chemoattracting properties equal to ZAS. Psoriatic serum was shown to be chemoattracting to psoriatic and normal PMNs whereas normal serum was only to psoriatic cells. Differences in recognition mechanisms between psoriatic and normal cells are proposed. Phagocytosis of Candidaby psoriatic PMNS was earlier and more prolonged and candidacidal activity was earlier and definetely increased at given times compared to normal PMNs. A protective role of psoriatic PMNs in Munro's microabcesses against bacterial invasion is postulated.

Chemotaxis under agarose of psoriatic mixed mononuclear cells (MNs) and pure monocytes against Zymosan treated sera (ZAS), fresh psoriatic serum, and fresh normal serum was studied and compared with that of normal cells. Purification of monocytes was achieved on microexudate coated BHK flasks. Psoriatic MNs were found to be more chemotactic against psoriatic serum (P.S.) than normal MNs against normal serum (N.S.). Psoriatic cells were chemotactically more active than normal ones against psoriatic and normal serum but not against ZAS. Mixed mononuclear cells showed definitely increased chemotaxis over that of pure monocytes. When culture supernatants with lymphocyte derived factor (LDCF) activity were mixed with normal pure monocytes, the chemotactic activity of the monocytes recovered. It is, therefore, proposed that the LDCF from in vivostimulated psoriatic lymphocytes by antigenic or mitogenic substances of psoriatic plaque might be an essential factor for the increased chemotaxis of mixed psoriatic MNs compared to pure monocytes. This hypothesis also explains the increased chemoattracting capacity of psoriatic serum for psoriatic and normal MNs as due to the in vivorelease of lymphokine.

Frozen sections from squamous cell carcinomas (SCCs), basal cell carcinomas (BCCs), precancerous lesions (P.C.) and normal skin adjacent to lesions (N.S.) were studied by indirect immunoperoxidase for the detection of epithelial membrane antigen (EMA) and by PAP (peroxidase‐antiperoxidase) for total keratin (T.K.) and laminin (LM) to determine the significance of the appearance of neoantigens and the behavior of normal epidermal antigens during the process of carcinogenesis of the skin. Significant antigenic differences in all three antigens were revealed between SCCs and BCCs in the epidermis (EP) and tumor islands (T.I.). There were also significant differences in total keratin and laminin between SCC's and N.S. epidermis. SCCs did not show any significant differences in EMA from P.C. lesions, but T.K. was lower in P.C. lesions than in normal skin.

An immunohistological study of skin biopsy specimens from patients with early syphilis was undertaken before and after treatment (one day after intramuscular administration of 2.4 MIU benzathine penicillin and eight days later, after a total administration of 3.6 MIU. In chancres from seronegative patients treatment with 3.6 MIU usually resulted in fewer immunocompetent cells in the infiltrate. In lesions of secondary syphilis treatment with 2.4 MIU benzathine penicillin produced a significant decrease in immunocompetent cells. After treatment with 3.6 MIU there was no further decrease. It was worth noticing that even eight to nine days after the initial pretreatment biopsy, when 3.6 MIU had been administered, the overall lymphohistiocytic infiltrate was not substantially diminished. Significantly more suppressor (T8+) cells were found in lesions of primary syphilis than of secondary syphilis, and they showed remarkable exocytosis. Activated local T8+ cells may release immunosuppressive lymphokines. [ABSTRACT FROM PUBLISHER]