Role of NK Cells in Tuberculous Pleurisy as Innate Promoters of Local Type 1 Immunity with Potential Application on Differential Diagnosis

Human pleural B-cells regulate IFN-γ production by local T-cells and NK cells in aMycobacterium tuberculosis-induced delayed hypersensitivity reaction

“…Among the chemokine receptors assessed, the percentages of CXCR3 + cells and CXCR4 MFI (mean fluorescence intensity) were increased in PF-B-cells (Figure 2A), whereas no significant differences in CCR1, CCR2, CCR5 and CX 3 CR1 expression were detected (results not shown). Then, we determined whether Bcells were also activated in PF, as in other pleural cell populations [9][10][11][12][13][14][15][16]. Compared with PB-B-cells, PF-B-cells had higher CD95/Fas, CD38, CD25 and CD45R0 expression and lower CD32 and CD1d expression (Figure 2B), indicating B-cell activation [24][25][26].…”

“…For the cancer patients, one had an adenoma, one had a mesothelioma and three were of undetermined origin. by abundant PMNs (polymorphonuclear cells) and M s (macrophages), followed by NK (natural killer) cells, γ /δ T-cell and Th cells, together with accumulation of their soluble mediators [9][10][11][12][13][14][15][16]. This local inflammatory response is considered as a DTH (delayed type hypersensitivity) reaction in which CD4 + T-cells are the major effector population, making tuberculous pleurisy a relevant model for studying human DTH reactions [12,17].…”

“…Physical examination, complete blood cell count, electrolytes, chest X-ray, HIV test, ADA (adenosine deaminase) and LDH (lact-ate dehydrogenase) in PF were performed by the institutions. The diagnosis of tuberculous pleurisy was based on a positive Ziehl-Nielsen stain or Lowestein-Jensen culture from PF and/or histopathology of pleural biopsy, and was confirmed further by an M. tuberculosis-induced IFN (interferon)-γ response [15] and an ADA-positive test [8]. None of the patients had multidrugresistant TB.…”

“…It has been demonstrated that the frequencies of CD4 + T-cells are increased in tuberculous PF, whereas PMNs, NK cells and monocytes are decreased compared with PB [9][10][11][13][14][15][16]. Thus, to determine the B-cell frequency in both compartments, freshly isolated PBMCs and PFMCs derived from patients with pleurisy (TB and no-TB), as well as PBMCs from healthy subjects, were stained with anti-CD19 and anti-CD3 mAbs and analysed by FACS.…”

“…Next, we investigated whether PF-B-cells modulated a previously characterized M. tuberculosis-evoked ex vivo response [15,16]. To assess this, IFN-γ production was measured in PFMCs and CD19 + -depleted PFMCs stimulated with M. tuberculosis antigens.…”