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Immunomodulation through CD40 and TLR-4: an approach to control tuberculosis (P4516)
The immune system have nature's one of the most fascinating mechanisms which continuously protects us against billions of pathogens. It operates through a very well organized network of cells that constantly rove, communicate and coordinate to protect the host. The cells of the immune system regulate through sequence of events involving myriad of molecules expressed on their surface (costimulatory molecules, toll-like receptors, etc.) and also by soluble mediators (cytokines, chemokines, defensins, complement components, etc.). Moreover, the intricate interaction of these molecules among different immune cells like T cells, B cells, dendritic cells (DCs), macrophages, etc., elicit their activation or inhibition, thereby conferring resistance against various pathogens and maintain homeostasis of the immune system. Signaling of these molecules that are expressed on the surface of immune cells can further enhance their efficacy in elimination of pathogens. The study conducted by us showed that concomitant signaling through CD40 and Toll-Like Receptor-4 augmented the production of nitric oxide and proinflammatory cytokines like IL-6, TNFa and IL-12 in Mycobacterium tuberculosis (Mtb) infected DCs. Further, activated DCs showed enhanced microbicidal function and significantly reduced the intracellular survival of Mtb. This study indicates that concomitant signaling through CD40 and TLR-4 can be employed as a therapeutic strategy to curb the intracellular growth of pathogens.
American Association of Immunologists, Inc. 178.12
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