@article{open2944,
           month = {November},
          author = {Aqdas Mohammad and Sudeep K Maurya and Susanta Pahari and Sanpreet Singh and Nargis Khan and Kanupriya Sethi and Gurpreet Kaur and J N Agrewala},
            note = {The Copyright of this article belongs to ACS},
           title = {Immunotherapeutic Role of NOD-2 and TLR-4 Signaling as an Adjunct to Antituberculosis Chemotherapy},
       publisher = {Washington, D.C. : American Chemical Society},
         journal = {ACS applied materials \& interfaces},
           pages = {2999--3008},
            year = {2021},
        keywords = {Mycobacterium tuberculosis; antibiotics; host-directed therapy.},
             url = {http://crdd.osdd.net/open/2944/},
        abstract = {Tuberculosis (TB) treatment is lengthy and inflicted with severe side-effects. Here, we attempted a novel strategy to reinforce host immunity through NOD-like receptor (NOD-2) and Toll-like receptor (TLR-4) signaling in the murine model of TB. Intriguingly, we noticed that it not only bolstered the immunity but also reduced the dose and duration of rifampicin and isoniazid therapy. Further, we observed expansion in the pool of effector (CD44hi, CD62Llo, CD127hi) and central (CD44hi, CD62Lhi, CD127hi) memory CD4 T cells and CD8 T cells and increased the intracellular killing of Mycobacterium tuberculosis (Mtb) by activated dendritic cells [CD86hi, CD40hi, IL-6hi, IL-12hi, TNF-{\ensuremath{\alpha}}hi, nitric oxide (NO)hi] with significant reduction in Mtb load in the lungs and spleen of infected animals. We infer that the signaling through NOD-2 and TLR-4 may be an important approach to reduce the dose and duration of the drugs to treat TB.}
}