01994nas a2200289   4500000000100000008004100001260001300042653001200055653001800067653001100085653002400096653002400120653001200144653002100156653002400177653001800201100001300219700001500232700001200247700001100259700001600270245007600286300001100362490000700373520131000380022001401690       1999                            d  c1999 Apr10aCalcium10aCell Division10aHumans10aInositol Phosphates10aIntracellular Fluid10aleprosy10aProtein Kinase C10aSignal Transduction10aT-Lymphocytes1 aSharma N1 aSharma V K1 aGupta A1 aKaur I1 aGanguly N K00aImmunological defect in leprosy patients: altered T-lymphocyte signals.  a355-620 v233 a<p>The early events of activation were studied in paucibacillary (TT/BT) and multibacillary (BL/LL) leprosy patients by stimulation of their lymphocytes with mitogenic agents (calcium ionophore A23187/PMA) and Micobacterium leprae antigen (PGL-1). Maximum proliferation in response to PMA/A23187 and PGL-1 was observed in the BT/TT patients and the control group, respectively. Inositol triphosphate (IP3) and calcium were constitutively elevated in BT/TT and LL/BL patients. PMA/A23187 caused an increase in both IP3 and [Ca2+]i in BT/TT patients and controls. PGL-1 marginally increased IP3 levels in BT/TT patients. In the LL/BL patients, although PMA/A23187 increased IP3 levels, but no change was seen in [Ca2+]i, PGL-1 had no effect. Protein kinase C levels were seen to be associated with particulate fractions in BT/TT patients and were found to increase further in response to PMA/A23187. PGL-1 did not increase translocation of protein kinase C in controls or LL/BL patients. A preactivated and sensitised state of T-lymphocytes was observed in BT/TT patients, responsive to antigen and mitogens, whereas the cells of LL/BL patients were unresponsive to PGL-1. The altered signal transduction events characterised in the MB patients thus correlate well with the anergic state of their cells.</p>  a0928-8244