Immunophenotypic characterization of peripheral T lymphocytes in Mycobacterium tuberculosis infection and disease
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2002-04-01
Autores
Rodrigues, Denise do Socorro da Silva 
Medeiros, Eduardo Alexandrino Servolo de
Weckx, Lily Yin
Salomão, Reinaldo
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The cellular immune response probably plays a pivotal role in determining the clinical outcome after exposure to Mycobacterium tuberculosis. We used multi-parameter flow-cytometry to evaluate the distribution of T-lymphocyte subsets during infection and disease caused by M. tuberculosis. Samples were obtained from 71 volunteers to identify the T CD4(+) and CD8(+) lymphocyte numbers, and the activation plus memory/naive phenotypes, as defined by CD38, HLA-DR, CD45RA and CD27 markers. Subjects were divided into 18 healthy volunteers without detectable reaction to purified protein derivative (PPD-), 18 health care workers with a recent conversion to PPD, 20 patients with active pulmonary tuberculosis (TBC) and 15 patients with treated TBC at 6 months of therapy. By multiple-comparison analyses, the T CD4(+) lymphocyte number of the TBC group was lower than the PPD- group (P < 0.05). Ibis difference was apparently lost after treatment. the higher and the lower number of naive T CD4(+) cells was observed in the PPD- and TB C group, respectively. CD8(+) T lymphocytes were also statistically different among the four groups (P = 0.0002), lower in the TBC group (P < 0.05). CD8(+) T lymphocyte activation was evaluated by the CD38 and HLA-DR surface expression. the percentage distribution of these markers was statistically different between the four groups (P = 0.0055). TBC patients had a higher percentage of CD38(+) cells and mean fluorescence index, suggesting an overall increase of cell activation. These results suggest that peripheral T lymphocytes reflect cellular activation during TBC, along with possible redistribution of naive, memory/effector and late differentiated memory/effector phenotypes in the peripheral blood after infection and disease caused by M. tuberculosis.
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Clinical and Experimental Immunology. Oxford: Blackwell Publishing Ltd, v. 128, n. 1, p. 149-154, 2002.