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Rajatava Basu

Researcher at University of Alabama at Birmingham

Publications -  24
Citations -  1470

Rajatava Basu is an academic researcher from University of Alabama at Birmingham. The author has contributed to research in topics: Leishmania donovani & T cell. The author has an hindex of 12, co-authored 23 publications receiving 1254 citations. Previous affiliations of Rajatava Basu include Indian Institute of Chemical Biology & Charité.

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HLA Class I—Restricted T Cell Epitopes of the Kinetoplastid Membrane Protein—11 Presented by Leishmania donovani—Infected Human Macrophages

TL;DR: In this article, the authors scan the entire sequence of the leishmanial protein kinetoplastid membrane protein (kmp)-11 with overlapping nonapeptides and identify peptides that specifically trigger interferon- gamma secretion by human CD8+ T cells.
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Mapping the Antigenicity of the Parasites in Leishmania donovani Infection by Proteome Serology

TL;DR: Proteomics-based dissection of the serospecificities of leishmaniasis patients provides a comprehensive inventory of the complexity and interindividual heterogeneity of the host-responses to and variations in the antigenicity of the Leishmania parasites.
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KMP-11 DNA immunization significantly protects against L. donovani infection but requires exogenous IL-12 as an adjuvant for comparable protection against L. major

TL;DR: A comparative evaluation of effector mechanisms in the assessment of cross-specific protection by K MP-11 and KMP-11/IL-12 immunization against these two prevalent forms of leishmaniasis is provided.
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Hybrid Cell Vaccination Resolves Leishmania donovani Infection by Eliciting a Strong CD8+ Cytotoxic T-Lymphocyte Response with Concomitant Suppression of Interleukin-10 (IL-10) but Not IL-4 or IL-13

TL;DR: The present study reports the first implementation of HCV immunotherapy in an infectious disease model, establishing strong antigen-specific CTL generation as a correlate ofHCV-mediated antileishmanial immunity that is reversed by in vivo CD8+ T-cell depletion of HCv-treated mice.
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Leishmania donovani isolates with antimony-resistant but not -sensitive phenotype inhibit sodium antimony gluconate-induced dendritic cell activation.

TL;DR: It is demonstrated that SbRLD but not SbSLD prevents SAG-induced DC activation by suppressing a PI3K-dependent NF-κB pathway and provides the evidence for differential host-pathogen interaction mediated by S bRLD and Sb SLD.