Increased Susceptibility to Apoptosis of CD56dimCD16+ NK Cells Induces the Enrichment of IFN-γ-Producing CD56bright Cells in Tuberculous Pleurisy

Schierloh, Pablo; Yokobori, Noemí; Alemán, Mercedes; Musella, Rosa M.; Beigier-Bompadre, Macarena; Saab, María A.; Alves, Leandro Procópio; Abbate, Eduardo; Barrera, Silvia de la; Sasiain, María C.

doi:10.4049/jimmunol.175.10.6852

Cited by 85 publications

(120 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%

“…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%

“…Next, the cells were positively selected with anti-CD56 mAb employing GAM-coated MACS s following manufacture's instructions (Miltenyi Biotec, Bergisch Gladbach, Germany). Typical procedure yield less than 5% of contaminating CD3 1 /CD19 1 /CD14 1 cells even in the scarce NK population from PF [11]. …”

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

confidence: 99%

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confidence: 99%

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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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“…Thus, CD56 bright NK cells are highly enriched and activated within synovial fluid from patients with psoriatic arthritis and rheumatoid arthritis (RA),122, 123 as well as in inflamed tissues in tuberculosis 124. Similarly, MAIT cells are also well established to be recruited to sites of inflammation,81, 125 and have been found to be enriched in the synovial fluid of patients with ankylosing spondylitis126 and RA127.…”

Section: Functional Similarities Between Nk Cell and Cd8+ T‐cell Subsetsmentioning

confidence: 99%

Innate‐like CD8+ T‐cells and NK cells: converging functions and phenotypes

2018

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SummaryNew data in the worlds of both innate‐like CD8+ T‐cells and natural killer (NK) cells have, in parallel, clarified some of the phenotypes of these cells and also their associated functions. While these cells are typically viewed entirely separately, the emerging innate functions of T‐cells and, similarly, the adaptive functions of NK cells suggest that many behaviours can be considered in parallel. In this review we compare the innate functions of CD8+ T‐cells (especially mucosal‐associated invariant T‐cells) and those of NK cells, and how these relate to expression of phenotypic markers, especially CD161 and CD56.

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