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14 results on '"Narayan, Sharmal"'

4. Increased interleukin-10 production by ASC-deficient CD4+ T cells impairs bystander T-cell proliferation

Author

Narayan Sharmal, Kolly Laeticia, So Alexander, and Busso Nathalie

Subjects
CD4-Positive T-Lymphocytes, endocrine system, CD3 Complex, animal diseases, T-Lymphocytes, chemical and pharmacologic phenomena, Cell Count, CD8-Positive T-Lymphocytes, Lymphocyte Activation, T-Lymphocytes, Regulatory, Interferon-gamma, Mice, CD28 Antigens, Antigens, CD, NLR Family, Pyrin Domain-Containing 3 Protein, Immune Tolerance, Animals, Cell Proliferation, Mice, Knockout, Tumor Necrosis Factor-alpha, Arthritis, Interleukins, Antibodies, Monoclonal, hemic and immune systems, Original Articles, Bystander Effect, eye diseases, Coculture Techniques, Interleukin-10, CARD Signaling Adaptor Proteins, Mice, Inbred C57BL, Cytoskeletal Proteins, Culture Media, Conditioned, Cytokines, Lymph Nodes, Apoptosis Regulatory Proteins, Carrier Proteins, Spleen
Abstract

Apoptosis associated speck like protein containing a caspase recruitment domain (ASC) is an important component of the inflammasome functioning as an adaptor protein that facilitates the recruitment and activation of procaspases that in turn promote the maturation of interleukin 1beta (IL 1beta) and IL 18. Despite initial focus on the inflammatory properties of ASC there is emerging evidence that highlights the importance of ASC in facilitating adaptive immune responses. However the cellular and molecular basis for the involvement of ASC in adaptive immunity remains largely unexplored. We have previously demonstrated that activated ASC deficient T cells have dampened proliferative responses. We have therefore explored the underlying cellular mechanism(s) by which ASC regulates T cell proliferation. We show that under activating conditions (anti CD3/CD28 stimulation) in bulk T cell cultures the presence of ASC( / ) CD4(+) T cells is sufficient to suppress the proliferative responses of neighbouring T cells. Furthermore ASC( / ) CD4(+) T cells upon activation exhibit a suppressive cytokine profile with elevated production of IL 10 and reduced secretion of T helper type 1 cytokines interferon gamma and IL 2. This increase in IL 10 secretion within the activated ASC( / ) CD4(+) T cell compartment was not associated with a proportional increase in conventional Foxp3(+) regulatory T (Treg) cells. Interestingly when equal numbers of fluorescence activated cell sorted ASC(+/+) and ASC( / ) Treg cells (CD4(+) CD44(intermediate/high) CD25(+)) were activated in vitro the ASC( / ) fraction produced significantly more IL 10 than their wild type counterparts suggesting that ASC( / ) Treg cells have greater suppressive capacity. Collectively these results imply that the ASC may influence the development and functioning of Treg cells.

Published
2011

7. Erratum: Octacalcium phosphate crystals induce inflammation in vivo through interleukin-1 but independent of the NLRP3 inflammasome in mice

Author

Narayan, Sharmal, primary, Pazar, Borbola, additional, Ea, Hang-Korng, additional, Kolly, Laeticia, additional, Bagnoud, Nathaliane, additional, Chobaz, Véronique, additional, Lioté, Frédéric, additional, Vogl, Thomas, additional, Holzinger, Dirk, additional, Kai-Lik So, Alexander, additional, and Busso, Nathalie, additional

Published
2011
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14. Increased interleukin-10 production by ASC-deficient CD4+ T cells impairs bystander T-cell proliferation.

Author

Narayan, Sharmal, Kolly, Laeticia, So, Alexander, and Busso, Nathalie

Subjects
*INTERLEUKIN-10, *T cells, *CELL proliferation, *APOPTOSIS, *IMMUNITY, *CYTOKINES, *INTERFERONS, *CD4 antigen
Abstract

Summary Apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC) is an important component of the inflammasome, functioning as an adaptor protein that facilitates the recruitment and activation of procaspases that in turn promote the maturation of interleukin-1β (IL-1β) and IL-18. Despite initial focus on the inflammatory properties of ASC there is emerging evidence that highlights the importance of ASC in facilitating adaptive immune responses. However, the cellular and molecular basis for the involvement of ASC in adaptive immunity remains largely unexplored. We have previously demonstrated that activated ASC-deficient T cells have dampened proliferative responses. We have therefore explored the underlying cellular mechanism(s) by which ASC regulates T-cell proliferation. We show that under activating conditions (anti-CD3/CD28 stimulation) in bulk T-cell cultures the presence of ASC−/− CD4+ T cells is sufficient to suppress the proliferative responses of neighbouring T cells. Furthermore, ASC−/− CD4+ T cells upon activation exhibit a suppressive cytokine profile, with elevated production of IL-10 and reduced secretion of T helper type 1 cytokines, interferon-γ and IL-2. This increase in IL-10 secretion within the activated ASC−/− CD4+ T-cell compartment was not associated with a proportional increase in conventional Foxp3+ regulatory T (Treg) cells. Interestingly, when equal numbers of fluorescence-activated cell sorted ASC+/+ and ASC−/− Treg cells (CD4+ CD44intermediate/high CD25+) were activated in vitro, the ASC−/− fraction produced significantly more IL-10 than their wild-type counterparts, suggesting that ASC−/− Treg cells have greater suppressive capacity. Collectively, these results imply that the ASC may influence the development and functioning of Treg cells. [ABSTRACT FROM AUTHOR]

Published
2011
Full Text
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