Glucocorticoid-resistant Th17 cells are selectively attenuated by cyclosporine A

Lauren P. Schewitz-Bowers; Philippa J.P. Lait; David A. Copland; Ping Chen; Wenting Wu; Ashwin D. Dhanda; Barbara P. Vistica; Emily L. Williams; Baoying Liu; Shayma Jawad; Zhiyu Li; William Tucker; Sima Hirani; Yoshiyuki Wakabayashi; Jun Zhu; Nida Sen; Becky L. Conway-Campbell; Igal Gery; Andrew D. Dick; Lai Wei; Robert B. Nussenblatt; Richard W.J. Lee

doi:10.1073/pnas.1418316112

Glucocorticoid-resistant Th17 cells are selectively attenuated by cyclosporine A

Lauren P. Schewitz-Bowers
, Philippa J.P. Lait
, David A. Copland
, Ping Chen
, Wenting Wu
, Ashwin D. Dhanda
, Barbara P. Vistica
, Emily L. Williams
, Baoying Liu
, Shayma Jawad
, Zhiyu Li
, William Tucker
, Sima Hirani
, Yoshiyuki Wakabayashi
, Jun Zhu
, Nida Sen
, Becky L. Conway-Campbell
, Igal Gery
, Andrew D. Dick
, Lai Wei

Robert B. Nussenblatt^*, Richard W.J. Lee

^*Corresponding author for this work

Peninsula Medical School

Research output: Contribution to journal › Article › peer-review

Abstract

Significance Cyclosporine A was one of the first drugs used in clinical practice to successfully rescue glucocorticoid-resistant inflammatory diseases. In this article we extend the characterization of glucocorticoid-resistant human Th17 cells, and demonstrate that this effector memory T-cell subset is reciprocally attenuated by cyclosporine A. This therapeutic paradigm was confirmed in a murine model of autoimmunity, refining our understanding of cyclosporine A’s effect on the adaptive immune response. These data support the rationale for Th17-targeting therapies in the treatment of glucocorticoid-resistant inflammation.

Original language	English
Pages (from-to)	4080-4085
Number of pages	0
Journal	Proceedings of the National Academy of Sciences
Volume	112
Issue number	13
Early online date	16 Mar 2015
DOIs	https://doi.org/10.1073/pnas.1418316112
Publication status	Published - 31 Mar 2015

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10.1073/pnas.1418316112

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Schewitz-Bowers, L. P., Lait, P. J. P., Copland, D. A., Chen, P., Wu, W., Dhanda, A. D., Vistica, B. P., Williams, E. L., Liu, B., Jawad, S., Li, Z., Tucker, W., Hirani, S., Wakabayashi, Y., Zhu, J., Sen, N., Conway-Campbell, B. L., Gery, I., Dick, A. D., ... Lee, R. W. J. (2015). Glucocorticoid-resistant Th17 cells are selectively attenuated by cyclosporine A. Proceedings of the National Academy of Sciences, 112(13), 4080-4085. https://doi.org/10.1073/pnas.1418316112

@article{b3fa15cc386544c4b48bf8aecb8bd76a,

title = "Glucocorticoid-resistant Th17 cells are selectively attenuated by cyclosporine A",

abstract = "Significance Cyclosporine A was one of the first drugs used in clinical practice to successfully rescue glucocorticoid-resistant inflammatory diseases. In this article we extend the characterization of glucocorticoid-resistant human Th17 cells, and demonstrate that this effector memory T-cell subset is reciprocally attenuated by cyclosporine A. This therapeutic paradigm was confirmed in a murine model of autoimmunity, refining our understanding of cyclosporine A{\textquoteright}s effect on the adaptive immune response. These data support the rationale for Th17-targeting therapies in the treatment of glucocorticoid-resistant inflammation.",

author = "Schewitz-Bowers, \{Lauren P.\} and Lait, \{Philippa J.P.\} and Copland, \{David A.\} and Ping Chen and Wenting Wu and Dhanda, \{Ashwin D.\} and Vistica, \{Barbara P.\} and Williams, \{Emily L.\} and Baoying Liu and Shayma Jawad and Zhiyu Li and William Tucker and Sima Hirani and Yoshiyuki Wakabayashi and Jun Zhu and Nida Sen and Conway-Campbell, \{Becky L.\} and Igal Gery and Dick, \{Andrew D.\} and Lai Wei and Nussenblatt, \{Robert B.\} and Lee, \{Richard W.J.\}",

year = "2015",

month = mar,

day = "31",

doi = "10.1073/pnas.1418316112",

language = "English",

volume = "112",

pages = "4080--4085",

journal = "Proceedings of the National Academy of Sciences",

issn = "0027-8424",

publisher = "National Academy of Sciences",

number = "13",

}

Schewitz-Bowers, LP, Lait, PJP, Copland, DA, Chen, P, Wu, W, Dhanda, AD, Vistica, BP, Williams, EL, Liu, B, Jawad, S, Li, Z, Tucker, W, Hirani, S, Wakabayashi, Y, Zhu, J, Sen, N, Conway-Campbell, BL, Gery, I, Dick, AD, Wei, L, Nussenblatt, RB & Lee, RWJ 2015, 'Glucocorticoid-resistant Th17 cells are selectively attenuated by cyclosporine A', Proceedings of the National Academy of Sciences, vol. 112, no. 13, pp. 4080-4085. https://doi.org/10.1073/pnas.1418316112

TY - JOUR

T1 - Glucocorticoid-resistant Th17 cells are selectively attenuated by cyclosporine A

AU - Schewitz-Bowers, Lauren P.

AU - Lait, Philippa J.P.

AU - Copland, David A.

AU - Chen, Ping

AU - Wu, Wenting

AU - Dhanda, Ashwin D.

AU - Vistica, Barbara P.

AU - Williams, Emily L.

AU - Liu, Baoying

AU - Jawad, Shayma

AU - Li, Zhiyu

AU - Tucker, William

AU - Hirani, Sima

AU - Wakabayashi, Yoshiyuki

AU - Zhu, Jun

AU - Sen, Nida

AU - Conway-Campbell, Becky L.

AU - Gery, Igal

AU - Dick, Andrew D.

AU - Wei, Lai

AU - Nussenblatt, Robert B.

AU - Lee, Richard W.J.

PY - 2015/3/31

Y1 - 2015/3/31

N2 - Significance Cyclosporine A was one of the first drugs used in clinical practice to successfully rescue glucocorticoid-resistant inflammatory diseases. In this article we extend the characterization of glucocorticoid-resistant human Th17 cells, and demonstrate that this effector memory T-cell subset is reciprocally attenuated by cyclosporine A. This therapeutic paradigm was confirmed in a murine model of autoimmunity, refining our understanding of cyclosporine A’s effect on the adaptive immune response. These data support the rationale for Th17-targeting therapies in the treatment of glucocorticoid-resistant inflammation.

AB - Significance Cyclosporine A was one of the first drugs used in clinical practice to successfully rescue glucocorticoid-resistant inflammatory diseases. In this article we extend the characterization of glucocorticoid-resistant human Th17 cells, and demonstrate that this effector memory T-cell subset is reciprocally attenuated by cyclosporine A. This therapeutic paradigm was confirmed in a murine model of autoimmunity, refining our understanding of cyclosporine A’s effect on the adaptive immune response. These data support the rationale for Th17-targeting therapies in the treatment of glucocorticoid-resistant inflammation.

U2 - 10.1073/pnas.1418316112

DO - 10.1073/pnas.1418316112

M3 - Article

SN - 0027-8424

VL - 112

SP - 4080

EP - 4085

JO - Proceedings of the National Academy of Sciences

JF - Proceedings of the National Academy of Sciences

IS - 13

ER -

Glucocorticoid-resistant Th17 cells are selectively attenuated by cyclosporine A

Abstract

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