الفهرس 
Historical backgroundOnly 14 pages are availabe for public view
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Abstract
T cell responses during TB help contain M.tuberculosis in vivo but also cause collateral damage to host tissues. Immune regulatory mechanisms may limit this immunopathology, and suppressed cellular immune responses in patients with TB suggest the presence of regulatory activity.
A role for CD4+CD25+Tregs in suppression of immune responses directed against microbes has been described. Both IL-10 dependent and IL-10 independent pathways were involved in this suppression of T cell function by CD4+CD25+Treg cells.
The role played by CD4+CD25+Tregs has recently been investigated in the context of TB, and increased nTregs was observed in case patients with active TB.
This study was done to determine CD4+CD25+Tregs% and the levels of IL-10 mRNA expression in peripheral blood of patients with active pulmonary TB, in an attempt to assess a possible role of these cells in the immunopathogenesis of TB.
Venous blood samples were collected from 30 patients diagnosed as having pulmonary TB based on their clinical, radiological, and laboratory investigations. CD4+ CD25+ Treg cells’ % was detected by flowcytometry and the level of IL-10 mRNA expression in PBMCs by RT-PCR. Fifteen age and sex matched apparently healthy individuals were included in this study as a control group.
Patients with pulmonary TB showed significant elevation of their mean percentage of CD4+CD25+Treg cells while IL-10 mRNA expression in the PBMCs was significantly lowered compared to healthy controls.
The mean percentage of CD4+CD25+ Treg cells was higher in patients with cavitary lesions compared to patients without cavitary lesions, the difference was statistically insignificant. However, the mean percentage of CD4+CD25+ Treg cells was lower in patients with extrapulmonary TB in relation to patients who had purely pulmonary disease, the difference was statistically insignificant.
IL-10 mRNA expression was lower in patients with cavitary lesions compared to patients with no cavitary lesions, and in patients with extrapulmonary manifestations with respect to patients with no extrapulmonary manifestations, the difference was statistically insignificant.
In conclusion, CD4+CD25+ Treg cells are expanded in peripheral blood of patients with pulmonary TB, accounting, at least in part, for suppressed specific T cell responses during active pulmonary TB. Negative modulation of effector cells requires a direct cell to cell contact between Treg cells and their targets while IL-10 doesn’t appear to play a major role. These cells may represent an important strategy used by M.tuberculosis to evade protective immunity of the host. The fact that these cells display antigen specificity provides hope for novel targeted immune interventions to circumvent these pathogenic strategies.