<i>Mycobacterium tuberculosis</i>-Induced Gamma Interferon Production by Natural Killer Cells Requires Cross Talk with Antigen-Presenting Cells Involving Toll-Like Receptors 2 and 4 and the Mannose Receptor in Tuberculous Pleurisy

Schierloh, Pablo; Yokobori, Noemí; Alemán, Mercedes; Landoni, Verónica Inés; Geffner, Laura; Musella, Rosa M.; Castagnino, Jorge; Baldini, Matías; Abbate, Eduardo; Barrera, Silvia de la; Sasiain, María C.

doi:10.1128/iai.00381-07

Cited by 55 publications

(67 citation statements)

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“…Herein, by using short-time monokine-stimulated primary NK cells, we found that these cells have the capacity to up-regulate T-bet and IFN-g expression driving Th1 polarization of CD4 1 cells and to induce CD69 expression on CD4 1 T cells in an ICAM-1-dependent fashion. In addition, we also found that NK cells form conjugates with T cells in an ICAM-1 dependent way, as previously observed with Plasmodium falciparum-infected erythrocytes [50] and with [10,11,36], we were able to show that endogenous up-regulation of ICAM-1 by pass the requirement of in vitro NK pre-activation and was indeed sufficient to enhance CD69 expression in PF-T cells.In summary, we demonstrate that ICAM-1/LFA-1 are differentially expressed between PB-and PF-NK cells being CD56 bright ICAM-1 high cells the major NK population within TB-PF, and also the producers of . Moreover, herein we provide evidence of another mechanism mediated by endogenously activated NK cells, specifically, T-cell costimulation through ICAM-1.…”

supporting

confidence: 88%

“…Functionally, CD56 bright cells are effective cytokine producers, whereas CD56 dim cells are efficient effectors of natural and Ab-dependent target cell lysis. Recently, we have described that an endogenously activated pleural fluid NK (PF-NK) population is a major source of IFN-g in response to Mtb [10,11]. Consistently, PF-NK are enriched in CD56 bright cells, as has been observed in other chronic inflammatory sites [12,13] or in tumor-affected tissues [14].…”

supporting

confidence: 53%

“…Exclusion criteria included positive HIV test or the presence of concurrent infectious diseases. TB-PF together with PB samples were obtained during therapeutic thoracentesis as described previously [10]. A total of 17 PF were studied (average age 5 29 year, range 5 20-46 year) and among them, six had pulmonary disease according to chest X-ray findings.…”

Section: Patients and Healthy Blood Donorsmentioning

confidence: 99%

“…We have previously described that upon in vitro stimulation with Mtb, a large percentage of PF-NK produce IFN-g [10,11]. To evaluate whether a relationship between ICAM-1 expression and Mtb-induced IFN-g response by PF-NK cells could be ascribed, PFMC were incubated for 24 h with or without Mtb and, thereafter, ICAM-1 and IFN-g co-expression was assessed on NK cells.…”

Section: Nk Cells From Tuberculous Pleural Fluid Express High Icam-1 mentioning

confidence: 99%

“…According to its cytotoxic effector function [41], CD56 dim from PB and PF expressed high LFA-1 levels, whereas NK-mediated helper functions may be related to the high ICAM-1 levels on CD56 bright [42]. Accordingly, IFN-g production was also ascribed to CD56 bright subset [10]. These data lead us to explore functional consequences on NK-T cells interactions.…”

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NK cells from tuberculous pleurisy express high ICAM‐1 levels and exert stimulatory effect on local T cells

et al. 2009

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Tuberculous pleurisy, one of the most common manifestations of extrapulmonary tuberculosis, is characterized by a T-cell-mediated hypersensitivity reaction along with a Th1 immune profile. In this study, we investigated functional cross-talk among T and NK cells in human tuberculous pleurisy. We found that endogenously activated pleural fluidderived NK cells express high ICAM-1 levels and induce T-cell activation ex vivo through ICAM-1. Besides, upon in vitro stimulation with monokines and PAMP, resting peripheral blood NK cells increased ICAM-1 expression leading to cellular activation and Th1 polarization of autologous T cells. Furthermore, these effects were abolished by anti-ICAM-1 Ab. Hence, NK cells may contribute to the adaptive immune response by a direct cellcontact-dependent mechanism in the context of Mycobacterium tuberculosis infection.Key words: ICAM-1 . NK cells . Pleurisy . Th1 . Tuberculosis Supporting Information available online IntroductionPleuritis is the most frequent clinical manifestation of extrapulmonary tuberculosis (TB) among young adults, and is normally considered a relatively benign form of disease since it may resolve without chemotherapy [1]. Tuberculous pleurisy is caused by a severe delayed-type hypersensitivity reaction in response to the rupture of a subpleural focus of Mycobacterium tuberculosis (Mtb) infection, but it may also be developed as a complication of primary pulmonary TB [2,3]. This pleural effusion is characterized by a strong granulomatous inflammatory response to Mtb together with high levels of . NK cells are CD56 1 CD16 1/À /CD3 À CD19 À lymphocytes of the innate immune system whose function is controlled by an array of germline-encoded activator/inhibitory receptors [5,6]. Two subsets of NK cells have been identified in humans according to CD56 expression differing in phenotype and function, and also in terms of chemokine receptors and adhesion molecules expression [7,8,9]. Functionally, CD56 bright cells are effective cytokine producers, whereas CD56 dim cells are efficient effectors of natural and Ab-dependent target cell lysis. Recently, we have described that an endogenously activated pleural fluid NK (PF-NK) population is a major source of IFN-g in response to Mtb [10,11]. Consistently, PF-NK are enriched in CD56 bright cells, as has been observed in other chronic inflammatory sites [12,13] or in tumor-affected tissues [14]. Together with the classical NK functions (i.e. cytotoxicity and cytokine production), novel skills have recently been described in niche-specific and in vitro-activated human NK cells. These unconventional capabilities include [16,17,18] and direct pathogen recognition [19,20]. In this regard, a novel innate immune cell population called Interferon-producing killer dendritic cells has been recently described in mice [21,22].ICAM-1/CD54 is the major ligand of costimulatory a L b 2 integrin (CD11a/CD18), commonly known as lymphocyte function-associated antigen (LFA-1) [23,24]. The surface enhancement of ICAM-1 on endothelial, APC and...

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supporting

confidence: 88%

supporting

confidence: 53%

Section: Patients and Healthy Blood Donorsmentioning

confidence: 99%

Section: Nk Cells From Tuberculous Pleural Fluid Express High Icam-1 mentioning

confidence: 99%

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confidence: 99%

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