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Updated: Jun 27, 2026

In vivo Imaging of Transgenic Leishmania Parasites in a Live Host
Published on: July 27, 2010
Evidence for involvement of TNFR1 and TIMPs in pathogenesis of post-kala-azar dermal leishmaniasis
N A Ansari1, G K Katara, V Ramesh
1Institute of Pathology (ICMR), Safdarjung Hospital Campus, New Dehli, India.
Abstract:
Semi-quantitative RT-PCR was exploited to analyse the intralesional cytokine gene expression in 14 post-kala-azar dermal leishmaniasis (PKDL) and 10 kala-azar (KA) patients. The data provided evidence for both inflammatory and non-inflammatory responses, as reflected by elevated tumour necrosis factor (TNF)-alpha and interleukin (IL)-10 in PKDL lesions compared with normal skin tissue (n = 6). The ratio of TNF-alpha : IL-10 message was 2.66 in PKDL cases, substantially higher than in KA (1.18). Investigation of TNF-alpha receptors (TNFR1 and TNFR2) revealed a significant down-regulation of TNFR1 transcript in both PKDL and KA compared with control. In the presence of elevated levels of TNF-alpha transcript, interference with type 1 effector activity in PKDL may be due to minimal expression of the TNFR1 gene. Investigation of matrix metalloproteinases, known to be induced by TNF-alpha, and the tissue inhibitors of matrix metalloproteinases (TIMPs), provided evidence for the roles of TIMP-1 and TIMP-3 in the pathogenesis of PKDL.
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