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T cell-derived protein S engages TAM receptor signaling in dendritic cells to control the magnitude of the immune response

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T cell-derived protein S engages TAM receptor signaling in dendritic cells to control the magnitude of the immune response. / Carrera Silva, Eugenio A; Chan, Pamela Y; Joannas, Leonel; Errasti, Andrea E; Gagliani, Nicola; Bosurgi, Lidia; Jabbour, Maurice; Perry, Anthony; Smith-Chakmakova, Faye; Mucida, Daniel; Cheroutre, Hilde; Burstyn-Cohen, Tal; Leighton, Jonathan A; Lemke, Greg; Ghosh, Sourav; Rothlin, Carla V.

In: IMMUNITY, Vol. 39, No. 1, 25.07.2013, p. 160-70.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Carrera Silva, EA, Chan, PY, Joannas, L, Errasti, AE, Gagliani, N, Bosurgi, L, Jabbour, M, Perry, A, Smith-Chakmakova, F, Mucida, D, Cheroutre, H, Burstyn-Cohen, T, Leighton, JA, Lemke, G, Ghosh, S & Rothlin, CV 2013, 'T cell-derived protein S engages TAM receptor signaling in dendritic cells to control the magnitude of the immune response', IMMUNITY, vol. 39, no. 1, pp. 160-70. https://doi.org/10.1016/j.immuni.2013.06.010

APA

Carrera Silva, E. A., Chan, P. Y., Joannas, L., Errasti, A. E., Gagliani, N., Bosurgi, L., Jabbour, M., Perry, A., Smith-Chakmakova, F., Mucida, D., Cheroutre, H., Burstyn-Cohen, T., Leighton, J. A., Lemke, G., Ghosh, S., & Rothlin, C. V. (2013). T cell-derived protein S engages TAM receptor signaling in dendritic cells to control the magnitude of the immune response. IMMUNITY, 39(1), 160-70. https://doi.org/10.1016/j.immuni.2013.06.010

Vancouver

Carrera Silva EA, Chan PY, Joannas L, Errasti AE, Gagliani N, Bosurgi L et al. T cell-derived protein S engages TAM receptor signaling in dendritic cells to control the magnitude of the immune response. IMMUNITY. 2013 Jul 25;39(1):160-70. https://doi.org/10.1016/j.immuni.2013.06.010

Bibtex

@article{03e0ae01be944749a6049aaaaccd0794,
title = "T cell-derived protein S engages TAM receptor signaling in dendritic cells to control the magnitude of the immune response",
abstract = "Dendritic cell (DC) activation is essential for the induction of immune defense against pathogens, yet needs to be tightly controlled to avoid chronic inflammation and exaggerated immune responses. Here, we identify a mechanism of immune homeostasis by which adaptive immunity, once triggered, tempers DC activation and prevents overreactive immune responses. T cells, once activated, produced Protein S (Pros1) that signaled through TAM receptor tyrosine kinases in DCs to limit the magnitude of DC activation. Genetic ablation of Pros1 in mouse T cells led to increased expression of costimulatory molecules and cytokines in DCs and enhanced immune responses to T cell-dependent antigens, as well as increased colitis. Additionally, PROS1 was expressed in activated human T cells, and its ability to regulate DC activation was conserved. Our results identify a heretofore unrecognized, homeostatic negative feedback mechanism at the interface of adaptive and innate immunity that maintains the physiological magnitude of the immune response.",
keywords = "Adaptive Immunity, Animals, Cells, Cultured, Colitis, Cytokines, Dendritic Cells, Flow Cytometry, Gene Expression, Humans, Immunoblotting, Lymphocyte Activation, Mice, Mice, Knockout, Mice, Transgenic, Protein S, Receptor Protein-Tyrosine Kinases, Reverse Transcriptase Polymerase Chain Reaction, Signal Transduction, T-Lymphocytes, Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't",
author = "{Carrera Silva}, {Eugenio A} and Chan, {Pamela Y} and Leonel Joannas and Errasti, {Andrea E} and Nicola Gagliani and Lidia Bosurgi and Maurice Jabbour and Anthony Perry and Faye Smith-Chakmakova and Daniel Mucida and Hilde Cheroutre and Tal Burstyn-Cohen and Leighton, {Jonathan A} and Greg Lemke and Sourav Ghosh and Rothlin, {Carla V}",
note = "Copyright {\textcopyright} 2013 Elsevier Inc. All rights reserved.",
year = "2013",
month = jul,
day = "25",
doi = "10.1016/j.immuni.2013.06.010",
language = "English",
volume = "39",
pages = "160--70",
journal = "IMMUNITY",
issn = "1074-7613",
publisher = "Cell Press",
number = "1",

}

RIS

TY - JOUR

T1 - T cell-derived protein S engages TAM receptor signaling in dendritic cells to control the magnitude of the immune response

AU - Carrera Silva, Eugenio A

AU - Chan, Pamela Y

AU - Joannas, Leonel

AU - Errasti, Andrea E

AU - Gagliani, Nicola

AU - Bosurgi, Lidia

AU - Jabbour, Maurice

AU - Perry, Anthony

AU - Smith-Chakmakova, Faye

AU - Mucida, Daniel

AU - Cheroutre, Hilde

AU - Burstyn-Cohen, Tal

AU - Leighton, Jonathan A

AU - Lemke, Greg

AU - Ghosh, Sourav

AU - Rothlin, Carla V

N1 - Copyright © 2013 Elsevier Inc. All rights reserved.

PY - 2013/7/25

Y1 - 2013/7/25

N2 - Dendritic cell (DC) activation is essential for the induction of immune defense against pathogens, yet needs to be tightly controlled to avoid chronic inflammation and exaggerated immune responses. Here, we identify a mechanism of immune homeostasis by which adaptive immunity, once triggered, tempers DC activation and prevents overreactive immune responses. T cells, once activated, produced Protein S (Pros1) that signaled through TAM receptor tyrosine kinases in DCs to limit the magnitude of DC activation. Genetic ablation of Pros1 in mouse T cells led to increased expression of costimulatory molecules and cytokines in DCs and enhanced immune responses to T cell-dependent antigens, as well as increased colitis. Additionally, PROS1 was expressed in activated human T cells, and its ability to regulate DC activation was conserved. Our results identify a heretofore unrecognized, homeostatic negative feedback mechanism at the interface of adaptive and innate immunity that maintains the physiological magnitude of the immune response.

AB - Dendritic cell (DC) activation is essential for the induction of immune defense against pathogens, yet needs to be tightly controlled to avoid chronic inflammation and exaggerated immune responses. Here, we identify a mechanism of immune homeostasis by which adaptive immunity, once triggered, tempers DC activation and prevents overreactive immune responses. T cells, once activated, produced Protein S (Pros1) that signaled through TAM receptor tyrosine kinases in DCs to limit the magnitude of DC activation. Genetic ablation of Pros1 in mouse T cells led to increased expression of costimulatory molecules and cytokines in DCs and enhanced immune responses to T cell-dependent antigens, as well as increased colitis. Additionally, PROS1 was expressed in activated human T cells, and its ability to regulate DC activation was conserved. Our results identify a heretofore unrecognized, homeostatic negative feedback mechanism at the interface of adaptive and innate immunity that maintains the physiological magnitude of the immune response.

KW - Adaptive Immunity

KW - Animals

KW - Cells, Cultured

KW - Colitis

KW - Cytokines

KW - Dendritic Cells

KW - Flow Cytometry

KW - Gene Expression

KW - Humans

KW - Immunoblotting

KW - Lymphocyte Activation

KW - Mice

KW - Mice, Knockout

KW - Mice, Transgenic

KW - Protein S

KW - Receptor Protein-Tyrosine Kinases

KW - Reverse Transcriptase Polymerase Chain Reaction

KW - Signal Transduction

KW - T-Lymphocytes

KW - Journal Article

KW - Research Support, N.I.H., Extramural

KW - Research Support, Non-U.S. Gov't

U2 - 10.1016/j.immuni.2013.06.010

DO - 10.1016/j.immuni.2013.06.010

M3 - SCORING: Journal article

C2 - 23850380

VL - 39

SP - 160

EP - 170

JO - IMMUNITY

JF - IMMUNITY

SN - 1074-7613

IS - 1

ER -