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.