@article{1370,
  keywords = {Calcium, Cell Division, Humans, Inositol Phosphates, Intracellular Fluid, leprosy, Protein Kinase C, Signal Transduction, T-Lymphocytes},
  author = {Sharma N and Sharma V K and Gupta A and Kaur I and Ganguly N K},
  title = {Immunological defect in leprosy patients: altered T-lymphocyte signals.},
  abstract = {<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>},
  year = {1999},
  journal = {FEMS immunology and medical microbiology},
  volume = {23},
  pages = {355-62},
  month = {1999 Apr},
  issn = {0928-8244},
  doi = {10.1111/j.1574-695X.1999.tb01257.x},
  language = {eng},
}