Adhesion molecules in lesions of American cutaneous leishmaniasis.

Accessory signals, which include adhesion molecules, MHC-II molecules and cytokines, are necessary to foster the interaction between memory T cells and epidermal cells, that is required to promote cutaneous inflammatory responses. American cutaneous leishmaniasis (ACL) is characterized by a spectrum of immunological manifestations, and is a prototype disease for the study of regulatory mechanisms involved in immune protection against protozoal infection. In the present study, we show that diffuse cutaneous leishmaniasis (DCL) epidermis contains keratinocytes that do not express ICAM-1 and HLA-DR molecules. Langerhans cells (LC) are within normal values or somewhat lower, and a very few cells expressing the HB15 molecule--a new described member of the Ig superfamily--are found in such lesions. Mucocutaneous leishmaniasis (MCL) epithelium shows an increased expression of ICAM-1 and HLA-DR molecules, few HB15+ cells, and an absence of epithelial LC. Localized cutaneous leishmaniasis (LCL) epidermis displays ICAM-1+ keratinocytes organized in patches, a uniform expression of HLA-DR, hyperplasia of LC, and numerous HB15+ cells. In all forms of the disease, infiltrating T cells express more LFA-1 beta than LFA-1 alpha, but LFA-1 beta+ T cells are more abundant in LCL granulomas. In contrast, there are more LFA-1 alpha+ T cells in DCL and MCL than in LCL granulomas. LCL lesions also show the highest numbers of HB15+ cells within the granuloma. These results indicate the importance of adhesion molecules in ACL lesions, and open new possibilities for therapeutic schemes oriented towards the control of cell migration.

Serum levels of tumor necrosis factor in patients with American cutaneous leishmaniasis.

The purpose of this study was to evaluate serum levels of TNF-alpha in patients with either of the three clinical forms of American cutaneous leishmaniasis. The 86 patients examined were classified as having either the localized (LCL: 22 patients), mucocutaneous (MCL: 45 patients), or the rare diffuse (DCL: 19 patients) form of the disease. Our results show a significant increase in the mean level of TNF-alpha in the three groups of patients when compared to controls. MCL patients produce significantly higher levels of TNF-alpha than DCL patients. The proportion of individuals positive for serum TNF-alpha was significantly higher in both MCL and DCL patients than in the controls. No significant differences were found in the level of TNF-alpha when compared between before and after cure of 12 patients with MCL. There were no significant correlations between the level of TNF-alpha and the skin test diameter. The results will be discussed in terms of the pathogenesis of the disease in its different clinical forms.