IL-10- and TGF-beta-mediated susceptibility in kala-azar and post-kala-azar dermal leishmaniasis: The significance of amphotericin B in the control of Leishmania donovani infection in India
Metadata of CSIR Papers
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| Title |
IL-10- and TGF-beta-mediated susceptibility in kala-azar and post-kala-azar dermal leishmaniasis: The significance of amphotericin B in the control of Leishmania donovani infection in India
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| Creator |
Saha, S
Mondal, S Ravindran, R Bhowmick, S Modak, D Mallick, S Rahman, M Kar, S Goswami, R Guha, SK Pramanik, N Saha, B Ali, N |
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| Subject |
Immunology
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| Description |
Visceral leishmaniasis (VL) or kala-azar is known to be associated with a mixed Th1-Th2 response, and effective host defense requires the induction of IFN-gamma and IL-12. We address the role of the differential decline of IL-10 and TGF-beta in response to sodium antimony gluconate (SAG) and amphotericin B (AmB), the therapeutic success of SAG and AmB in Indian VL, and the significance of IL-10 and TGF-beta in the development and progression of post-kazla-azar dermal leishmaniasis (PKDL). In the active disease, PBNIC from VL patients showed suppressed Ag-specific lymphoproliferation, IFN-gamma and IL-12 productions and elevation of IL-10 and TGF-beta. Cure corresponded with an elevation in IFN-gamma and IL-12 production and down-regulation of IL-10 and TGF-beta. Both CD4(+) and CD8(+) T cells were involved in IFN-gamma and IL-10 production. Interestingly, the retention and maintenance of residual IL-10 and TGF-beta in some SAG-treated individuals and the elevation of IL-10 and TGF-beta in PKDL, a sequel to kala-azar, probably reflects the role of these cytokines in reactivation of the disease in the form of PKDL. Contrastingly, AmB treatment of VL resulted in negligible TGF-beta levels and absolute elimination of IL-10, reflecting the better therapeutic activity of AmB and its probable role in the recent decline in PKDL occurrences in India. Moreover, elucidation of immune responses in Indian PKDL patients revealed a spectral pattern of disease progression where disease severity could be correlated inversely with lymphoproliferation and directly with TGF-beta, IL-10, and Ab production. In addition, the enhancement of CD4(+)CD25(+) T cells in active VL, their decline at cure, and reactivation in PKDL suggest their probable immunosuppressive role in these disease forms.
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| Publisher |
AMER ASSOC IMMUNOLOGISTSBETHESDA9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
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| Date |
2011-09-20T12:12:27Z
2011-09-20T12:12:27Z 2007 |
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| Type |
Article
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| Identifier |
JOURNAL OF IMMUNOLOGY
0022-1767 http://hdl.handle.net/123456789/14280 |
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| Language |
English
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