Reversal of T-cell unresponsiveness through serine-esterase inhibitors mediated enhanced lymphokine induced microbicidal activities in kala-azar

Indian J Exp Biol. 1992 Jan;30(1):54-6.

Abstract

After presenting processed glycoprotein of Leishmania donovani to T-cell, macrophage seeks the help of a panel of T-cells lymphokines to transform from a state that sustains intra cellular replication of parasite to an effector state for destructing parasites. But esterase and trypsin of macrophage membrane prevent T-cells to release MIF. Role of soya-bean trypsin inhibitor (STI) has been exposed in the present study with a view to alter esterase functional behaviour of macrophage for control of T-cell activation and also, if T-cells once made responsive to antigen by STI do alter macrophage response to T-cells or not. Results establish STI as potent effector molecule, which can serve as an adjuvant to candidate T-cell epitope and synthetic peptide for development of anti-Kala-azar vaccine protocol in future.

MeSH terms

  • Cell Migration Inhibition
  • Cytotoxicity, Immunologic
  • Dose-Response Relationship, Drug
  • Immunity, Cellular*
  • In Vitro Techniques
  • Leishmaniasis, Visceral / immunology*
  • Lymphocyte Activation / drug effects*
  • Macrophage Activation
  • Macrophages / immunology
  • T-Lymphocytes / immunology*
  • Trypsin Inhibitors / pharmacology*

Substances

  • Trypsin Inhibitors