CD56bright NK Cells Are Enriched at Inflammatory Sites and Can Engage with Monocytes in a Reciprocal Program of Activation

Dalbeth, Nicola; Gundle, R; Davies, Robert J. O.; Lee, Gary; McMichael, Andrew J.; Callan, Margaret

doi:10.4049/jimmunol.173.10.6418

Cited by 262 publications

(260 citation statements)

References 27 publications

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“…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.…”

supporting

confidence: 53%

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: 53%

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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“…The fraction of CD4 þ CD28 À T lymphocytes is increased in RA vasculitis in comparison with other clinical forms of RA. 14,16,17 Both T and NK cells are involved in RA pathology, [1][2][3][4] but their contribution to different manifestations of the disease is largely unknown. Moreover, the mechanisms of KIR inhibitory and activatory functions in T cells are different from those in NK cells.…”

Section: Discussionmentioning

confidence: 99%

“…However, RA is a multifactorial disease, and several other genes are implicated in susceptibility to this condition. 2 Recently, the involvement of natural killer (NK) cells 4,5 and NKT cells 6 in RA was also described. NK cells kill target cells that have no or substantially reduced cellsurface expression of HLA class I molecules due to viral infection or malignant transformation and immunoselection.…”

Section: Introductionmentioning

confidence: 99%

Associations of killer cell immunoglobulin-like receptor genes with complications of rheumatoid arthritis

et al. 2007

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We investigated whether killer cell immunoglobulin-like receptor (KIR) genes are risk factor(s) for rheumatoid arthritis (RA) and its clinical manifestations. One hundred and seventy-seven RA patients and 243 healthy individuals were tested for the presence of 11 KIR genes using PCR-SSP method. The frequencies of KIRs in patients with RA were similar to the frequencies in controls. However, RA patients positive for KIR2DL3 and negative for KIR2DS3 had earlier disease diagnosis. Additionally, KIR2DL2 and KIR2DS2 were significantly more frequent among RA patients with extra-articular manifestations and in its subgroup with vasculitis than in controls and in patients without these complications. Furthermore, the frequencies of KIR2DS1 and KIR3DS1 were lower in patients without bone erosions compared with healthy individuals. Relationships between the presence or absence of autoantibodies (rheumatoid factor and anti-cyclic citrullinated peptide) and KIR frequencies were also evaluated, but no significant differences were observed. These results suggest that particular clinical manifestations of RA may have different genetic backgrounds with respect to KIR genotype.

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“…CD56 bright NK cells express high levels of cytokine receptors, which enables these cells to produce abundant IFN γ and proliferate in response to cytokines such as IL‐2, IL‐15, IL‐12, IL‐18 and IFN α 48, 53. As CD56 bright NK cells are the dominant NK cell population in tissues including lymph nodes and inflammatory sites, this allows them to interact with DCs and T‐cells at these sites 54, 55, 56, 57. In contrast, CD56 bright NK cells secrete little IFN γ in response to target cell recognition mediated by receptors such as NKG2D, even though the receptor is equally expressed by CD56 bright and CD56 dim cells 58.…”

Section: Subsets Of Nk Cellsmentioning

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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CD56bright NK Cells Are Enriched at Inflammatory Sites and Can Engage with Monocytes in a Reciprocal Program of Activation

Cited by 262 publications

References 27 publications

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

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

Associations of killer cell immunoglobulin-like receptor genes with complications of rheumatoid arthritis

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

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