ANTIGEN-PRESENTING CELLS IN HUMAN CUTANEOUS LEISHMANIASIS DUE TO LEISHMANIA-MAJOR

Citation
Am. Elhassan et al., ANTIGEN-PRESENTING CELLS IN HUMAN CUTANEOUS LEISHMANIASIS DUE TO LEISHMANIA-MAJOR, Clinical and experimental immunology, 99(3), 1995, pp. 445-453
Citations number
30
Categorie Soggetti
Immunology
ISSN journal
00099104
Volume
99
Issue
3
Year of publication
1995
Pages
445 - 453
Database
ISI
SICI code
0009-9104(1995)99:3<445:ACIHCL>2.0.ZU;2-0
Abstract
In this study biopsies from skin lesions and draining lymph nodes of p atients suffering from cutaneous leishmaniasis caused by Leishmania ma jor were examined by immunohistochemistry, and by light and electron m icroscopy to identify the types of antigen-presenting cells (APC) and their location, APC, identified morphologically and by their expressio n of specific cell markers, included Langerhans cells, macrophages, fo llicular dendritic cells, and interdigitating reticulum cells of the p aracortex of lymph nodes. These cells expressed MHC class II antigens and contained Leishmania antigen. Since some keratinocytes and endothe lial cells also showed these characteristics, they may also act as APC . By examining tissue samples from skin lesions and draining lymph nod es it was possible to follow the probable route of trafficking of vari ous inflammatory cells between the skin lesion and lymph nodes. Leishm ania antigen containing Langerhans cells were found in the epidermis, dermis and the regional lymph nodes. We believe these cells translocat e from the epidermis to the dermis, where they take up antigen and mig rate to the paracortex of the regional lymph nodes. There they are int imately associated with cells of the paracortex, and could be involved in the generation of Leishmania-specific T memory cells. LFA-1-positi ve T cells of the CD45RO phenotype were found in the skin lesion. Venu lar endothelium in the skin lesions expressed intercellular adhesion m olecule-1 (ICAM-1), which is the ligand for LFA-1. The migration of ly mphocytes from the vascular lumen to the site of inflammation is possi bly a result of the interaction of these two adhesion molecules.