Reversal of T-cell unresponsiveness through serine-esterase inhibitors mediated enhanced lymphokine induced microbicidal activities in kala-azar.
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.
Bimal
S
S
Division of Immunology, Rajendra Memorial Research Institute of Medical Sciences, Patna, India.
Lal
S L
SL
Lal
C S
CS
Singha
U K
UK
Saran
R
R
Sen
A B
AB
Sahay
V K
VK
D002464:Cell Migration Inhibition; D003602:Cytotoxicity, Immunologic; D004305:Dose-Response Relationship, Drug; D007111:Immunity, Cellular; D066298:In Vitro Techniques; D007898:Leishmaniasis, Visceral / Q000276:immunology*; D008213:Lymphocyte Activation / Q000187:drug effects*; D008262:Macrophage Activation; D008264:Macrophages / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology*; D014361:Trypsin Inhibitors / Q000494:pharmacology*
D014361:Trypsin Inhibitors