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 WeiRobert 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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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",

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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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