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GPR15-mediated T cell recruitment during acute viral myocarditis facilitated virus elimination and improved outcome

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GPR15-mediated T cell recruitment during acute viral myocarditis facilitated virus elimination and improved outcome. / Stoffers, Bastian; Wolf, Hanna; Bacmeister, Lucas; Kupsch, Svenja; Vico, Tamara; Marchini, Timoteo; Brehm, Maria A.; Yan, Isabell; Becher, P. Moritz; Ardeshirdavani, Armin; Escher, Felicitas; Kim, Sangwon V.; Klingel, Karin; Kirchhof, Paulus; Blankenberg, Stefan; Zeller, Tanja; Wolf, Dennis; Hilgendorf, Ingo; Westermann, Dirk; Lindner, Diana.

In: Nat Cardiovasc Res, Vol. 3, No. 1, 01.2024, p. 76 – 93.

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

Harvard

Stoffers, B, Wolf, H, Bacmeister, L, Kupsch, S, Vico, T, Marchini, T, Brehm, MA, Yan, I, Becher, PM, Ardeshirdavani, A, Escher, F, Kim, SV, Klingel, K, Kirchhof, P, Blankenberg, S, Zeller, T, Wolf, D, Hilgendorf, I, Westermann, D & Lindner, D 2024, 'GPR15-mediated T cell recruitment during acute viral myocarditis facilitated virus elimination and improved outcome', Nat Cardiovasc Res, vol. 3, no. 1, pp. 76 – 93. https://doi.org/10.1038/s44161-023-00401-z

APA

Stoffers, B., Wolf, H., Bacmeister, L., Kupsch, S., Vico, T., Marchini, T., Brehm, M. A., Yan, I., Becher, P. M., Ardeshirdavani, A., Escher, F., Kim, S. V., Klingel, K., Kirchhof, P., Blankenberg, S., Zeller, T., Wolf, D., Hilgendorf, I., Westermann, D., & Lindner, D. (2024). GPR15-mediated T cell recruitment during acute viral myocarditis facilitated virus elimination and improved outcome. Nat Cardiovasc Res, 3(1), 76 – 93. https://doi.org/10.1038/s44161-023-00401-z

Vancouver

Stoffers B, Wolf H, Bacmeister L, Kupsch S, Vico T, Marchini T et al. GPR15-mediated T cell recruitment during acute viral myocarditis facilitated virus elimination and improved outcome. Nat Cardiovasc Res. 2024 Jan;3(1):76 – 93. https://doi.org/10.1038/s44161-023-00401-z

Bibtex

@article{ca4c531121364c7d9ee79720a664ffd4,
title = "GPR15-mediated T cell recruitment during acute viral myocarditis facilitated virus elimination and improved outcome",
abstract = "Viral myocarditis is characterized by infiltration of mononuclear cells essential for virus elimination. GPR15 has been identified as a homing receptor for regulatory T cells in inflammatory intestine diseases, but its role in inflammatory heart diseases is still elusive. Here we show that GPR15 deficiency impairs coxsackievirus B3 elimination, leading to adverse cardiac remodeling and dysfunction. Delayed recruitment of regulatory T cells in GPR15-deficient mice was accompanied by prolonged persistence of cytotoxic and regulatory T cells. In addition, RNA sequencing revealed prolonged inflammatory response and altered chemotaxis in knockout mice. In line, we identified GPR15 and its ligand GPR15L as an important chemokine receptor–ligand pair for the recruitment of regulatory and cytotoxic T cells. In summary, the insufficient virus elimination might be caused by a delayed recruitment of T cells as well as delayed interferon-γ expression, resulting in a prolonged inflammatory response and an adverse outcome in GPR15-deficient mice.",
author = "Bastian Stoffers and Hanna Wolf and Lucas Bacmeister and Svenja Kupsch and Tamara Vico and Timoteo Marchini and Brehm, {Maria A.} and Isabell Yan and Becher, {P. Moritz} and Armin Ardeshirdavani and Felicitas Escher and Kim, {Sangwon V.} and Karin Klingel and Paulus Kirchhof and Stefan Blankenberg and Tanja Zeller and Dennis Wolf and Ingo Hilgendorf and Dirk Westermann and Diana Lindner",
note = "Cited by: 1",
year = "2024",
month = jan,
doi = "10.1038/s44161-023-00401-z",
language = "English",
volume = "3",
pages = "76 – 93",
journal = "Nat Cardiovasc Res",
issn = "2731-0590",
publisher = "Springer",
number = "1",

}

RIS

TY - JOUR

T1 - GPR15-mediated T cell recruitment during acute viral myocarditis facilitated virus elimination and improved outcome

AU - Stoffers, Bastian

AU - Wolf, Hanna

AU - Bacmeister, Lucas

AU - Kupsch, Svenja

AU - Vico, Tamara

AU - Marchini, Timoteo

AU - Brehm, Maria A.

AU - Yan, Isabell

AU - Becher, P. Moritz

AU - Ardeshirdavani, Armin

AU - Escher, Felicitas

AU - Kim, Sangwon V.

AU - Klingel, Karin

AU - Kirchhof, Paulus

AU - Blankenberg, Stefan

AU - Zeller, Tanja

AU - Wolf, Dennis

AU - Hilgendorf, Ingo

AU - Westermann, Dirk

AU - Lindner, Diana

N1 - Cited by: 1

PY - 2024/1

Y1 - 2024/1

N2 - Viral myocarditis is characterized by infiltration of mononuclear cells essential for virus elimination. GPR15 has been identified as a homing receptor for regulatory T cells in inflammatory intestine diseases, but its role in inflammatory heart diseases is still elusive. Here we show that GPR15 deficiency impairs coxsackievirus B3 elimination, leading to adverse cardiac remodeling and dysfunction. Delayed recruitment of regulatory T cells in GPR15-deficient mice was accompanied by prolonged persistence of cytotoxic and regulatory T cells. In addition, RNA sequencing revealed prolonged inflammatory response and altered chemotaxis in knockout mice. In line, we identified GPR15 and its ligand GPR15L as an important chemokine receptor–ligand pair for the recruitment of regulatory and cytotoxic T cells. In summary, the insufficient virus elimination might be caused by a delayed recruitment of T cells as well as delayed interferon-γ expression, resulting in a prolonged inflammatory response and an adverse outcome in GPR15-deficient mice.

AB - Viral myocarditis is characterized by infiltration of mononuclear cells essential for virus elimination. GPR15 has been identified as a homing receptor for regulatory T cells in inflammatory intestine diseases, but its role in inflammatory heart diseases is still elusive. Here we show that GPR15 deficiency impairs coxsackievirus B3 elimination, leading to adverse cardiac remodeling and dysfunction. Delayed recruitment of regulatory T cells in GPR15-deficient mice was accompanied by prolonged persistence of cytotoxic and regulatory T cells. In addition, RNA sequencing revealed prolonged inflammatory response and altered chemotaxis in knockout mice. In line, we identified GPR15 and its ligand GPR15L as an important chemokine receptor–ligand pair for the recruitment of regulatory and cytotoxic T cells. In summary, the insufficient virus elimination might be caused by a delayed recruitment of T cells as well as delayed interferon-γ expression, resulting in a prolonged inflammatory response and an adverse outcome in GPR15-deficient mice.

U2 - 10.1038/s44161-023-00401-z

DO - 10.1038/s44161-023-00401-z

M3 - SCORING: Journal article

VL - 3

SP - 76

EP - 93

JO - Nat Cardiovasc Res

JF - Nat Cardiovasc Res

SN - 2731-0590

IS - 1

ER -