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Chaudhary, R., Amit, A., Yadav, A., Singh, A., Kumar, V., Singh, S.K., Narayan, S., Das, V.N.R., Pandey, K., Kumar, A., Das, P. and Bimal, S. (2014) Immunomodulation in Human Dendritic Cells Leads to Induction of Interferon-Gamma Production by Leishmania donovani Derived KMP-11 Antigen via Activation of NF-κB in Indian kala-azar Patients. Biomed Research International, 2014, Article ID: 947606.

has been cited by the following article:

• TITLE: A New Vaccine Strategy of Dendritic Cell Presented Kinetoplastid Membrane (KMP-11) as Immunogen for Control against Experimental Visceral Leishmaniasis

  AUTHORS: Rajesh Chaudhary, Ajay Amit, Akhilesh Kumar, Manas R. Dikhit, Krishna Pandey, Pradeep Das, Sanjiva Bimal

  KEYWORDS: Visceral Leishmaniasis, Kinetoplastid Membrane Protein 11, Soluble Leishmania Antigen, Interferon-ϒ, Interleukin-12, Interleukin-10, Dendritic Cell Primed KMP-11

  JOURNAL NAME: Modern Research in Inflammation, Vol.6 No.3, August 22, 2017

  ABSTRACT: Available reports suggest that, Leishmania donovani antigen KMP-11 may be significant in the modulation of immune responses in visceral leishmaniasis (VL). This study evaluated vaccine prospect of presentation of KMP-11 antigen through murine dendritic cells against VL in infected BALB/c mice. We report here that immunization with KMP-11 delivered through bone marrow derived dendritic cells can lead to killing of L. donovani in infected BALB/c mice. Furthermore, the strategy to use KMP-11 as vaccine delivered through DCs can stimulate the production of IFN-g, IL-12, IL-2R and TNF-α with concomitant down-regulation of IL-10 and IL-4. Furthermore, anti-leishmanial defence function (ROS) of splenocytes was observed increased in the presence of DC-delivered KMP-11 vaccination accompanied with an increased p38-MAPK signalling in vaccinated splenocytes. We summarized from our data that KMP-11 delivered through DCs has potential for eliciting protective immunity through pro-inflammatory cytokines (IFN-γ, IL-12, IL-2, TNF-α) following an up-regulation in signalling event of p38-MAPK. Therefore the study suggests a new control strategy against VL in future.