Different Cytokine Production and Effector/Memory Dynamics of αβ+ or γδ+ T-Cell Subsets in the Peripheral Blood of Patients with Active Pulmonary Tuberculosis

Abstract

Immunity to M.tuberculosis (MTB) infection consists of interactions between various T-cell subsets that control the infection and prevent further reactivation. We analysed the effector/memory T-cell dynamics and cytokines production in the peripheral blood of patients with pulmonary tuberculosis (TB). We observed that the frequency of CD4+ T-cell effectors was significantly increased during active TB, confirming a major role of this T-cell subset in TB immunity. Pre-terminally differentiated CD8+ T-lymphocytes were increased in the peripheral blood as well. In contrast, we observed a reduced number of effector mycobacteria-reactive gammadelta+ T-lymphocytes with a specific defects in reacting to mycobacterial nonpeptidic antigens, suggesting that this innate response is rapidly lost during TB infection. Nevertheless, the frequency of gammadelta+ T-cells effectors in TB patients was higher than the alphabeta+ T-cell response to peptide from MTB-ESAT-6 protein and quantitatively similar to PPD reactivity. Thus, alphabeta+ and gammadelta+ T-cell differentiation and function are differently triggered by active TB infection.

Expression of Proliferating Cell Nuclear Antigen (PCNA) in Multiple Myeloma: Its Relationship to Bone Marrow Microvessel Density and other Factors of Disease Activity

“…The evidence of IL-6 as the major growth factor for myeloma cells is supported primarily by the observation of enhanced proliferative activity induced by IL-6 in short term cultures (20,(38)(39)(40). In our study, high levels ofIL-6 were associated with proliferative activity as assessed by the PCNA ofbone marrow plasma cells in pretreatment patients.…”

Diversity of γδ T-cell antigens

“…71,72 A cd response to ESAT-6 was also observed in patients with active pulmonary tuberculosis. 73 Others reported that ESAT-6 directly induces purified cd T effector memory cells from tuberculin skin testpositive patients to produce IFN-c, and that CD4 1 ab T cells regulate this response. 74 However, this observation has been challenged and it requires further investigation.…”

CD4+ CD25high Foxp3+ regulatory T cells downregulate human Vδ2+ T‐lymphocyte function triggered by anti‐CD3 or phosphoantigen

“…In contrast to acute systemic infections such as malaria, in tuberculosis (TB) the number and function of Vd2 + T cells are downregulated. [19][20][21][22] A variety of mechanisms have been proposed for the decrease in Vd2 + T-cell function in TB, including redistribution to the lung parenchyma, lack of CD4 + T helper activity, activation-induced cell death and immune suppression. 14,23 Regulatory T cells (Tregs) have a major role in suppressing other immune cells such as CD4…”