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Expansion of CCR5+ CD4+ T-lymphocytes in the course of active pulmonary tuberculosis

¹ Dept of Biology, University of Roma "Tor Vergata", and ² Division of Respiratory Medicine, University of Roma "Tor Vergata" at the INMI L. Spallanzani-IRCCS, Roma, Italy.

CORRESPONDENCE: M. Fraziano, Dept of Biology, University of Roma "Tor Vergata", Via della Ricerca Scientifica 00133, Roma, Italy. Fax: 39 672594224. E-mail: fraziano@bio.uniroma2.it

Keywords: CCR3, CCR5, lymphocytes, Mycobacterium tuberculosis, tuberculosis

Received: September 16, 2003
Accepted May 28, 2004

The present study was supported in part by Italian Ministry of University (MIUR 60%) and by the IV Research Program on AIDS (Grant N. 50D.05) of the Italian Institute ofHealth. S.K. Garg was supported by a UNESCO-ROSTE study fellowship.

Nonsyncytium inducing, macrophage tropic HIV strains predominate in the course of active tuberculosis (TB). The present study assesses the expression of CCR5 in CD4+ T-lymphocytes from blood and bronchoalveolar lavage (BAL) of TB patients, non-TB lung disease controls and healthy controls.

Memory (CD45RO+), recently activated (CD69+), proliferating (Ki67+) CCR5+ or CCR3+ CD4+ T-lymphocytes were determined by multiparametric flow cytometry analysis.

Results show that BAL CD4+ T-lymphocytes expressing CCR5 or CCR3 were significantly increased when compared to peripheral blood both in patients and in healthy controls. However, the data show that the proportions of peripheral blood CCR5+ CD4+ and CCR3+ CD4+ T-lymphocytes and BAL CCR5+ CD4+ T-lymphocytes, but not BAL CCR3+ CD4+ T-lymphocytes, were significantly increased in TB patients. Furthermore, the observation that BAL CCR5+ CD4+ T-lymphocytes from TB patients expressed early activation markers, were not proliferating and showed down-regulation of CCR5 expression suggests recruitment and trapping at the site of disease.

Altogether, these results suggest that the lower respiratory tract mucosa may provide cellular targets accessible for efficient transmission of macrophage tropic HIV-1 variants and that tuberculosis may enhance this phenomenon.

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