Premium
Flow Cytometric Analysis of CD2 Modulation on Human Peripheral Blood T Lymphocytes by Dharmendra Preparation of Mycobacterium leprae
Author(s) -
SHEELA R.,
ILANGUMARAN S.,
MUTHUKKARUPPAN V. R.
Publication year - 1991
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.1991.tb03750.x
Subject(s) - mycobacterium leprae , peripheral blood mononuclear cell , monoclonal antibody , cd8 , antigen , cd3 , immunology , t lymphocyte , biology , t cell , epitope , microbiology and biotechnology , chemistry , immune system , antibody , in vitro , leprosy , biochemistry
It has been reported previously that Mycobacterium leprae modulated CD2 on human peripheral blood T lymphocytes and that this modulation was accompanied by a marked reduction in the proliferative response of these cells to mitogens and antigens. In this study, we report that treatment of peripheral blood mononuclear cells from healthy individuals with Dharmedra preparation of M. leprae inhibited their ability to form rosettes with sheep red blood ceils. Flow cytometric analysis of Dharmendra lepromin‐treated cells showed that, in addition to CD2. CD4 and CD8 were modulated while the surface expression of CD3 was not affected. The specificity of CD2 modulation was confirmed by similar effects of Dharmendra lepromin on thymocytes and lymph node cells from human CD2 transgenic mice. The modulatory effect of Dharmendra lepromin was not observed at lower temperatures. Dharmendra lepromin treatment of activated T cells resulted in reduced binding of monoclonal antibodies to IL‐2R and D66 epitope of CD2. The modulatory effects were not observed with Dharmendra preparation of BCG or other preparations of M. leprae. Our results indicate that certain M. leprae. factor(s) specifically modulate(s) CD2, CD4, CD8 and IL‐2R but not CD3 on T lymphocytes. The suppressive effect of Dharmendra lepromin on the T‐cell proliferative response reported earlier may be explained by its modulatory effect on a number of T‐cell surface molecules.