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Montreal researchers identify defects of immune cells

hocytes primarily determine the susceptibility to oral candidiasis in transgenic mice expressing HIV-1 and developing an AIDS-like disease. Findings from this research further indicated that a diminution and functional defects of both dendritic cells and CD4+ cells cause susceptibility to candidiasis in these transgenic mice by preventing T lymphocyte mediated acquired immunity to Candida albicans. The results also showed extensive perturbations in the production of cytokines required for protection against oral candidiasis in the transgenic mice.

"These findings regarding the specific immune defects which trigger candidiasis are very promising," explains Dr. de Repentigny. "This new knowledge will be instrumental in designing more powerful and effective treatments, which will directly improve the health status of HIV-infected patients who suffer from candidiasis. Defective CD4+ T lymphocytes have long been suspected to be the leading cause of candidiasis, however, it never had been directly demonstrated. Now, they become designated targets for the development of novel treatments not only for candidiasis but other mucosal infections."

"Secondary infections are the major cause of morbidity and mortality in people infected by HIV/AIDS. Fungal infection due to candidiasis is one of these debilitating conditions," said Dr. Bhagirath Singh, Scientific Director of the Canadian Institutes of Health Research (CIHR) Institute of Infection and Immunity. "This work provides a new understanding of why candidiasis is not controlled by the body's immune cells, particularly the CD4+ T lymphocytes. It will also help us to develop better treatments to prevent these opportunistic infections in HIV patients."


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Source:University of Montreal


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