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Toll-like receptor signaling: a perspective to develop vaccine against leishmaniasis.

Abstract
The toll-like receptors (TLRs) are the sentinel factor of the innate immunity, which are essential for host defense. These receptors detect the presence of conserved molecular patterns of potentially pathogenic microorganisms and contribute in both, cellular as well as humoral immune responses. Leishmania is an intracellular pathogen that silently invades host immune system. After phagocytosis, it divides and proliferates in the harmful environment of host macrophages by down-regulating its vital effector functions. In leishmaniasis, the outcome of the infection basically relies on the skewed balance between Th1/Th2 immune responses. Lots of work have been done and on progress but still characterization of either preventive or prophylactic candidate antigen/s is far from satisfactory. How does Leishmania regulate host innate immune system? Still it is unanswered. TLRs play very important role during inflammatory process of various diseases such as cancer, bacterial and viral infections but TLR signaling is comparatively less explained in leishmanial infection. In the context to Th1/Th2 dichotomy, identification of leishmanial antigens that modulate toll-like receptor signaling will certainly help in the development of future vaccine. This review will initially describe global properties of TLRs, and later will discuss their role in the pathogenesis of leishmaniasis.
AuthorsRakesh K Singh, Ankita Srivastava, Nisha Singh
JournalMicrobiological research (Microbiol Res) Vol. 167 Issue 8 Pg. 445-51 (Sep 06 2012) ISSN: 1618-0623 [Electronic] Germany
PMID22326459 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
CopyrightCopyright © 2012 Elsevier GmbH. All rights reserved.
Chemical References
  • Leishmaniasis Vaccines
  • Toll-Like Receptors
Topics
  • Humans
  • Leishmania (immunology, pathogenicity)
  • Leishmaniasis (immunology, prevention & control)
  • Leishmaniasis Vaccines (immunology)
  • Signal Transduction
  • Toll-Like Receptors (immunology)

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