TY - JOUR KW - Animals KW - Antibodies, Bacterial KW - Antibody Formation KW - Antigen Presentation KW - B-Lymphocytes KW - Humans KW - Immunity, Cellular KW - leprosy KW - Leprosy, lepromatous KW - Macrophages KW - Mice KW - Models, Immunological KW - Mycobacterium leprae KW - polymerase chain reaction KW - T-Lymphocytes, Helper-Inducer AU - Rojas-Espinosa O AU - Jiménez-Zamudio L AU - Arce-Paredes P AB -

Lepromatous leprosy in the human being evolves showing a progressive loss of cell mediated immunity (CMI) to the antigens of Mycobacterium leprae (ML). This does not prevent the host to respond with antibodies to the same microorganism. On the other hand, the production of antibodies to the great majority of exogenous antigens results from cell-to-cell interactions that involve the participation of helper T cells. On this ground, a satisfactory explanation for the loss of CMI to M. leprae (which indicates either the loss or inactivation of specific helper T cells), with no effect on the humoral response to the same microorganism (this implying the participation of functional specific helper T cells), was difficult to found. It was not until Mosmann established, in the mouse, the existence of two subpopulations of helper T cells, that a feasible explanation for the apparent immunological paradox observed in leprosy was possible to offer. The work described here, based to a great extent in our experience on murine leprosy, refers to recent concepts concerning this issue.

BT - Revista latinoamericana de microbiologia C1 - http://www.ncbi.nlm.nih.gov/pubmed/7709098?dopt=Abstract DA - 1994 Jul-Sep IS - 3 J2 - Rev. Latinoam. Microbiol. LA - spa N2 -

Lepromatous leprosy in the human being evolves showing a progressive loss of cell mediated immunity (CMI) to the antigens of Mycobacterium leprae (ML). This does not prevent the host to respond with antibodies to the same microorganism. On the other hand, the production of antibodies to the great majority of exogenous antigens results from cell-to-cell interactions that involve the participation of helper T cells. On this ground, a satisfactory explanation for the loss of CMI to M. leprae (which indicates either the loss or inactivation of specific helper T cells), with no effect on the humoral response to the same microorganism (this implying the participation of functional specific helper T cells), was difficult to found. It was not until Mosmann established, in the mouse, the existence of two subpopulations of helper T cells, that a feasible explanation for the apparent immunological paradox observed in leprosy was possible to offer. The work described here, based to a great extent in our experience on murine leprosy, refers to recent concepts concerning this issue.

PY - 1994 SP - 213 EP - 9 T2 - Revista latinoamericana de microbiologia TI - [Sequential activation of cellular and humoral immunity in leprosy: considerations based on recent findings]. VL - 36 SN - 0187-4640 ER -