Flow cytometric visualisation of cytokine production by CD3-CD56+ NK cells and CD3+CD56+ NK-T cells in whole blood

Mendes, R.; Bromelow, K V; Westby, Michael; Galea‐Lauri, Joanna; Smith, Ian; O’Brien, Mary; Souberbielle, Bernard

doi:10.1002/(sici)1097-0320(20000101)39:1<72::aid-cyto10>3.0.co;2-r

Cited by 47 publications

(22 citation statements)

References 38 publications

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“…For instance, elevated frequency of peripheral CD56 ϩ T cells was reported in other inflammatory conditions such as uveitis, which is often associated with IBD (40). These observations link peripheral CD56 ϩ T cells to mucosal immune dysregulation and suggest pathological significance for mechanisms modulating CD56 ϩ T cell frequency (50). Although perturbations in CD56 ϩ T cell frequency may not be unique to IBD, specific modulation of CD56 ϩ T cell trafficking or effector function may represent targets for gut-specific therapeutic intervention (51).…”

Section: Cd56mentioning

confidence: 95%

CD56 Marks an Effector T Cell Subset in the Human Intestine

Cohavy

Targan

2007

The Journal of Immunology

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T cells are key mediators of intestinal immunity, and specific T cell subsets can have differing immunoregulatory roles in animal models of mucosal inflammation. In this study, we describe human CD56+ T cells as a morphologically distinct population expressing a mature, nonproliferative phenotype that is frequent in the gut. Enhanced potential for IFN-γ and TNF synthesis suggested a proinflammatory function, and we directly demonstrate effector function mediated by direct T-T interaction with responder cells in vitro. CD56+ T cells from peripheral blood responded to the gut-related CD2 signal, and were necessary for effective CD2-mediated proliferation of peripheral blood CD56− T cells. Our findings associate CD56+ T cells with the intestinal immune compartment and suggest a putative effector function in human mucosal immunity.

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Section: Cd56mentioning

confidence: 95%

CD56 Marks an Effector T Cell Subset in the Human Intestine

Cohavy

Targan

2007

The Journal of Immunology

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“…13 Intracellular staining was carried out according to a modified method as described by Mendes et al 14 Briefly, DC were fixed in 0.5 ml of fixing solution (2% paraformaldehyde in PBS). After washing, the cells were permeabilised with 0.5 ml of 1 Â permeabilising solution (BD) and incubated for 15 min followed by washing in buffer (0.1% saponin, 0.2% bovine serum albumin and 0.1% sodium azide).…”

Section: Flow Cytometry and Immunophenotypingmentioning

confidence: 99%

Dendritic cells loaded with apoptotic tumour cells induce a stronger T-cell response than dendritic cell–tumour hybrids in B-CLL

et al. 2003

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Dendritic cells (DC) are professional (specialised) antigenpresenting cells that can capture antigen from apoptotic tumour cells and induce MHC class I-and II-restricted responses. Also, DC fused with tumour cells may be effective for immune response induction. Both cell preparations may be considered as vaccine candidates in a therapeutic approach. We examined autologous T-cell activation by DC that had endocytosed leukaemic B-cell apoptotic bodies (Apo-DC) and compared it to the T-cell stimulatory capacity of DC that were fused with tumour cells. Following incubation, 22.676.2 (mean7s.e.m.) of DC had endocytosed leukaemic cells, while the frequency of DC-leukaemic cell hybrids was 10.572.6%. Apo-DC and hybrid cells both demonstrated the ability to stimulate a tumour-specific T-cell immune response in vitro. A T-cell proliferation response was also observed in four out of five CLL patients when using Apo-DC. However, fusion hybrids lacked the ability to elicit a proliferative response. Apo-DC also induced an IFN-c response, as did hybrid cells. The cytokine response induced by Apo-DC was significantly higher than that induced by fusion (Po0.05). This study shows that endocytosed apoptotic tumour cells induced a significantly stronger T-cell response than DC hybrids; and as such should be a better candidate for vaccine production.

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“…Cells were stimulated with 50 ng PMA (Sigma, USA) and 1 μg/ml Ionomycin (Sigma, USA). 10 μg/ml brefeldin A (Sigma, USA) was added as secretion inhibitor [17]. Cells were cultured in incubator for 6 h at 37°C with 5% CO 2.…”

Section: Cytokine Productionmentioning

confidence: 99%