[37] CD38, a cellular activation marker previously associated with HIV pathogenesis,[38]

presented a higher frequency in CD8+ T cells among RR/HIV individuals in the NS and ML-stimulated cells, a phenomenon not detected in the RR group. A higher frequency of CD38 in HIV/leprosy co-infected individuals, regardless of the lower viral load, has also been found in recent studies.[39] This activation marker profile can be attributed to the remaining viral production that persists in certain patients whether they are undergoing effective, long-term HAART learn more or not.[40] Furthermore, the increased frequency in T-cell activation markers in RR and RR/HIV might also be explained by the fact that immune activation could be determined by ML. As in recent

studies showing a higher frequency of CD8+ T cells in the borderline tuberculoid/HIV granuloma of HIV patients,[41] our data demonstrated a higher frequency of CD8+ T cells in RR/HIV granulomas. T-cell memory, a critical component of the adaptive immune CP673451 response, is characterized by an increase in the strength and speed of the reaction against previously encountered pathogens. In recent studies evaluating immune responses in patients with tuberculous pleurisy, it was demonstrated that early secreted antigen target (ESAT)-6 and culture filtrate protein (CFP)-10-specific T helper type 1, type 22 and type 17 cells presented a CD45RA− CD62L− CCR7+ CD27+ phenotype.[42] In addition, the presence of a CFP-10-specific population with a CD45RO+ CD62L− CCR7− CD27− phenotype has been described in patients with tuberculous pleurisy.[43] In bacillus Calmette–Guérin-immunized purified protein derivative-positive patients, it was found that IFN-γ-producing CD4+ cells presented a CD45RA− CCR7+/− CD62L− phenotype, which indicates that these cells are central/effector memory cells.[44] In a longitudinal study investigating the effect of HAART in patients co-infected with HIV/M. tuberculosis, it was seen that the HAART effect leads to expansion of central memory CD27+ CD45RA−

and CD27+ CCR5− CD4+ cells after 12 weeks followed MG-132 cell line by expansion of naive CD27+ CD45RA+ cells after 36 weeks. Terminally differentiated effector CD4+ CD27− CCR7− cells decreased by 12 weeks together with a proportional decline of purified protein derivative-specific CD4+IFN-γ+ cells.[45] The present study also showed that ML increased the frequency of central memory CD4+ T and CD8+ T cells in RR patients. RR/HIV patients likewise presented an increase in TCM CD4+ T cells along with higher numbers of TCM and TEM CD8+ T cells. An augmentation in the number of CD8+ T cells co-localizing with CD45RA in skin biopsies was seen as well, which may be indicative of an effector memory phenotype.