TCRγδ+CD8αβ+ T cell in health and disease: a novel and functionally active subpopulation of T-cells enriched within the gut

M. Kadivar, J. Petersson, Vasileios Bekiaris, J. Marsal, L. Svensson

Research output: Contribution to journalConference abstract in journalResearchpeer-review

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Abstract

γδ T-cells have been implicated in the pathogenesis of immune-mediated diseases such asinflammatory bowel disease (IBD). However, a potential role of different immune cell subsets in IBD and also in the process of mucosal healing upon treatment is unknown. γδ T-cells have been divided into CD8αα+ and CD8- T-cells. By using flow cytometry and RT-PCR, we described for the first time anovel subset of human γδ T-cells expressing CD8αβ heterodimers on their surface. We found thatthese TCRγδ+CD8αβ+ T-cell subset exist in both human peripheral blood as well as in the gut, however they were differentially enriched within the gut. TCRγδ+CD8αβ+ T-cells displayed highcytotoxic activity by expressing Fas Ligand on their surface and also producing Granzyme B and Perforin. We showed that these cells can produce INFγ and TNFα but they did not show the ability toproduce IL-17 in healthy individuals. In patients with IBD, we found a decrease in the percentage ofintestinal CD8αβ+ γδ T-cells compared to healthy controls. Moreover, the percentage of TCRγδ+CD8αβ+ T-cells out of γδ T-cells showed a negative correlation with Crohn's disease activity.Three months of anti-TNFα (adalimumab) therapy increased the percentage of TCRγδ+CD8αβ+ T-cellsclose to the level of healthy controls. These results suggest that TCRγδ+CD8αβ+ T-cells might possiblyplay a role in gut inflammation and also intestinal wound healing after anti-TNFα treatment. These results are likely to have implications for the development of novel therapies to treat mucosal inflammatory diseases.
Original languageEnglish
JournalEuropean Journal of Immunology
Volume46
Issue numberSuppl. 1
Pages (from-to)154-154
ISSN0014-2980
Publication statusPublished - 2016
Event ICI 2016 International Congress of Immunology - Melbourne, Australia
Duration: 21 Aug 201626 Aug 2016

Conference

Conference ICI 2016 International Congress of Immunology
CountryAustralia
CityMelbourne
Period21/08/201626/08/2016

Cite this

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title = "TCRγδ+CD8αβ+ T cell in health and disease: a novel and functionally active subpopulation of T-cells enriched within the gut",
abstract = "γδ T-cells have been implicated in the pathogenesis of immune-mediated diseases such asinflammatory bowel disease (IBD). However, a potential role of different immune cell subsets in IBD and also in the process of mucosal healing upon treatment is unknown. γδ T-cells have been divided into CD8αα+ and CD8- T-cells. By using flow cytometry and RT-PCR, we described for the first time anovel subset of human γδ T-cells expressing CD8αβ heterodimers on their surface. We found thatthese TCRγδ+CD8αβ+ T-cell subset exist in both human peripheral blood as well as in the gut, however they were differentially enriched within the gut. TCRγδ+CD8αβ+ T-cells displayed highcytotoxic activity by expressing Fas Ligand on their surface and also producing Granzyme B and Perforin. We showed that these cells can produce INFγ and TNFα but they did not show the ability toproduce IL-17 in healthy individuals. In patients with IBD, we found a decrease in the percentage ofintestinal CD8αβ+ γδ T-cells compared to healthy controls. Moreover, the percentage of TCRγδ+CD8αβ+ T-cells out of γδ T-cells showed a negative correlation with Crohn's disease activity.Three months of anti-TNFα (adalimumab) therapy increased the percentage of TCRγδ+CD8αβ+ T-cellsclose to the level of healthy controls. These results suggest that TCRγδ+CD8αβ+ T-cells might possiblyplay a role in gut inflammation and also intestinal wound healing after anti-TNFα treatment. These results are likely to have implications for the development of novel therapies to treat mucosal inflammatory diseases.",
author = "M. Kadivar and J. Petersson and Vasileios Bekiaris and J. Marsal and L. Svensson",
year = "2016",
language = "English",
volume = "46",
pages = "154--154",
journal = "European Journal of Immunology",
issn = "0014-2980",
publisher = "Wiley - V C H Verlag GmbH & Co. KGaA",
number = "Suppl. 1",

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TCRγδ+CD8αβ+ T cell in health and disease: a novel and functionally active subpopulation of T-cells enriched within the gut. / Kadivar, M.; Petersson, J.; Bekiaris, Vasileios; Marsal, J.; Svensson, L.

In: European Journal of Immunology, Vol. 46, No. Suppl. 1, 2016, p. 154-154.

Research output: Contribution to journalConference abstract in journalResearchpeer-review

TY - ABST

T1 - TCRγδ+CD8αβ+ T cell in health and disease: a novel and functionally active subpopulation of T-cells enriched within the gut

AU - Kadivar, M.

AU - Petersson, J.

AU - Bekiaris, Vasileios

AU - Marsal, J.

AU - Svensson, L.

PY - 2016

Y1 - 2016

N2 - γδ T-cells have been implicated in the pathogenesis of immune-mediated diseases such asinflammatory bowel disease (IBD). However, a potential role of different immune cell subsets in IBD and also in the process of mucosal healing upon treatment is unknown. γδ T-cells have been divided into CD8αα+ and CD8- T-cells. By using flow cytometry and RT-PCR, we described for the first time anovel subset of human γδ T-cells expressing CD8αβ heterodimers on their surface. We found thatthese TCRγδ+CD8αβ+ T-cell subset exist in both human peripheral blood as well as in the gut, however they were differentially enriched within the gut. TCRγδ+CD8αβ+ T-cells displayed highcytotoxic activity by expressing Fas Ligand on their surface and also producing Granzyme B and Perforin. We showed that these cells can produce INFγ and TNFα but they did not show the ability toproduce IL-17 in healthy individuals. In patients with IBD, we found a decrease in the percentage ofintestinal CD8αβ+ γδ T-cells compared to healthy controls. Moreover, the percentage of TCRγδ+CD8αβ+ T-cells out of γδ T-cells showed a negative correlation with Crohn's disease activity.Three months of anti-TNFα (adalimumab) therapy increased the percentage of TCRγδ+CD8αβ+ T-cellsclose to the level of healthy controls. These results suggest that TCRγδ+CD8αβ+ T-cells might possiblyplay a role in gut inflammation and also intestinal wound healing after anti-TNFα treatment. These results are likely to have implications for the development of novel therapies to treat mucosal inflammatory diseases.

AB - γδ T-cells have been implicated in the pathogenesis of immune-mediated diseases such asinflammatory bowel disease (IBD). However, a potential role of different immune cell subsets in IBD and also in the process of mucosal healing upon treatment is unknown. γδ T-cells have been divided into CD8αα+ and CD8- T-cells. By using flow cytometry and RT-PCR, we described for the first time anovel subset of human γδ T-cells expressing CD8αβ heterodimers on their surface. We found thatthese TCRγδ+CD8αβ+ T-cell subset exist in both human peripheral blood as well as in the gut, however they were differentially enriched within the gut. TCRγδ+CD8αβ+ T-cells displayed highcytotoxic activity by expressing Fas Ligand on their surface and also producing Granzyme B and Perforin. We showed that these cells can produce INFγ and TNFα but they did not show the ability toproduce IL-17 in healthy individuals. In patients with IBD, we found a decrease in the percentage ofintestinal CD8αβ+ γδ T-cells compared to healthy controls. Moreover, the percentage of TCRγδ+CD8αβ+ T-cells out of γδ T-cells showed a negative correlation with Crohn's disease activity.Three months of anti-TNFα (adalimumab) therapy increased the percentage of TCRγδ+CD8αβ+ T-cellsclose to the level of healthy controls. These results suggest that TCRγδ+CD8αβ+ T-cells might possiblyplay a role in gut inflammation and also intestinal wound healing after anti-TNFα treatment. These results are likely to have implications for the development of novel therapies to treat mucosal inflammatory diseases.

M3 - Conference abstract in journal

VL - 46

SP - 154

EP - 154

JO - European Journal of Immunology

JF - European Journal of Immunology

SN - 0014-2980

IS - Suppl. 1

ER -