Abstract

Modulation of Th1 response generated against pathogens like M tuberculosis (Mtb) by helminths is an important, area of investigation, because of the prevalence of coinfections in TB endemic regions. In this study we have designed an approach to investigate how the Th1 response generated by Mtb is modulated by helminthic infection. We have used the ovalbumin – specific TCR transgenic adoptive transfer system, wherein the ability of Mtb-pulsed dendritic cells to initiate a Th1 response was studied on the background of a helminth infection. BALB/c mice were infected with N. brasiliensis, and groups of uninfected and infected mice were injected with CFSE labeled OVA-specific TCR transgenic T cells followed by intratracheal instillation of Mtb and ovalbumin peptide-pulsed bone marrow-derived dendritic cells. Analysis of the labeled transgenic T cells harvested from the draining lymph nodes indicated proliferation of T cells from both groups of mice. However, we observed significantly reduced level of IFNγ and a reciprocal increase in IL-4 in T cells derived form the helminth-infected mice. These findings indicate that helminth infection does not abrogate the priming ability of Mtb-pulsed DCs, but interferes with their ability to promote a Th1 response. The significance of the findings lies in the potential of helminth infections to modulate resistance to tuberculosis, and also to interfere with the efficacy of tuberculosis vaccines.

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