Human pleural B-cells regulate IFN-? production by local T-cells and NK cells in a Mycobacterium tuberculosis-induced delayed hypersensitivity reaction

Articulo

Autoría:

SCHIERLOH, LUIS PABLO ; LANDONI, VERONICA INES ; BALBOA, LUCIANA ; Musella, Rosa María ; Castagnino, Jorge ; Moraña, Eduardo ; de Casado, Graciela C. ; Palmero, Domingo ; Sasiain, María del Carmen

Fecha:

2014

Editorial y Lugar de Edición:

Portland Press

Revista:

CLINICAL SCIENCE (LONDON, ENGLAND : 1979), vol. 127 (pp. 391-403) Portland Press

Resumen

DTH (delayed type hypersensitivity) reactions are secondary cellular immune responses that appear 24–72 h after antigen exposure. Tuberculous pleurisy is a common manifestation of extrapulmonary TB (tuberculosis) and is considered a human model of Th1-mediated DTH. In order to identify functional cross-talk among cellular populations sited in this inflammatory microenvironment, we analysed phenotypic and functional features of human B-cells isolated from the PF (pleural fluid) of TB patients. Freshly isolated PF-B-cells displayed a lower expression of CD20, CD1d and HLA-DR, and a higher expression of CD95, CD38, CD25, CXCR3 (CXC chemokine receptor 3) and CXCR4 (CXC chemokine receptor 4) than their PB (peripheral blood) counterparts, suggesting a non-classical in situ activation. Although memory PF-T-cell frequencies were increased, the frequencies of memory PF-B-cells were not. We demonstrated that, upon stimulation with ?-irradiated M. tuberculosis, mycobacterially secreted proteins or a lectin mitogen, PF-B-cells had a strong activation and produced IL-10 by a mechanism that was dependent on bystander activation of CD19? PF cells. Besides, within PF cells, B-cells diminished in vitro M. tuberculosis-induced IFN (interferon)-? production by T-cells and NK (natural killer) cells in an IL-10-dependent manner. Finally, we found that the lower the frequency of B-cells, the higher the ratio of IFN-?/IL-10 within PF. Thus our results suggest that B-cells can regulate a human DTH reaction induced by M. tuberculosis.

Palabras Clave

B CellsInterferon GammaTuberculosis

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http://hdl.handle.net/11336/29414