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Autocrine vitamin D signaling switches off pro-inflammatory programs of TH1 cells

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Autocrine vitamin D signaling switches off pro-inflammatory programs of TH1 cells. / Chauss, Daniel; Freiwald, Tilo; McGregor, Reuben; Yan, Bingyu; Wang, Luopin; Nova-Lamperti, Estefania; Kumar, Dhaneshwar; Zhang, Zonghao; Teague, Heather; West, Erin E.; Vannella, Kevin M.; Ramos-Benitez, Marcos J.; Bibby, Jack; Kelly, Audrey; Malik, Amna; Freeman, Alexandra F.; Schwartz, Daniella M.; Portilla, Didier; Chertow, Daniel S.; John, Susan; Lavender, Paul; Kemper, Claudia; Lombardi, Giovanna; Mehta, Nehal N.; Cooper, Nichola; Lionakis, Michail S.; Laurence, Arian; Kazemian, Majid; Afzali, Behdad.

In: NAT IMMUNOL, Vol. 23, No. 1, 01.2022, p. 62–74.

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

Harvard

Chauss, D, Freiwald, T, McGregor, R, Yan, B, Wang, L, Nova-Lamperti, E, Kumar, D, Zhang, Z, Teague, H, West, EE, Vannella, KM, Ramos-Benitez, MJ, Bibby, J, Kelly, A, Malik, A, Freeman, AF, Schwartz, DM, Portilla, D, Chertow, DS, John, S, Lavender, P, Kemper, C, Lombardi, G, Mehta, NN, Cooper, N, Lionakis, MS, Laurence, A, Kazemian, M & Afzali, B 2022, 'Autocrine vitamin D signaling switches off pro-inflammatory programs of TH1 cells', NAT IMMUNOL, vol. 23, no. 1, pp. 62–74. https://doi.org/10.1038/s41590-021-01080-3

APA

Chauss, D., Freiwald, T., McGregor, R., Yan, B., Wang, L., Nova-Lamperti, E., Kumar, D., Zhang, Z., Teague, H., West, E. E., Vannella, K. M., Ramos-Benitez, M. J., Bibby, J., Kelly, A., Malik, A., Freeman, A. F., Schwartz, D. M., Portilla, D., Chertow, D. S., ... Afzali, B. (2022). Autocrine vitamin D signaling switches off pro-inflammatory programs of TH1 cells. NAT IMMUNOL, 23(1), 62–74. https://doi.org/10.1038/s41590-021-01080-3

Vancouver

Chauss D, Freiwald T, McGregor R, Yan B, Wang L, Nova-Lamperti E et al. Autocrine vitamin D signaling switches off pro-inflammatory programs of TH1 cells. NAT IMMUNOL. 2022 Jan;23(1):62–74. https://doi.org/10.1038/s41590-021-01080-3

Bibtex

@article{2e3095b087ef412eab9d1628fd58b268,
title = "Autocrine vitamin D signaling switches off pro-inflammatory programs of TH1 cells",
abstract = "The molecular mechanisms governing orderly shutdown and retraction of CD4+ type 1 helper T (TH1) cell responses remain poorly understood. Here we show that complement triggers contraction of TH1 responses by inducing intrinsic expression of the vitamin D (VitD) receptor and the VitD-activating enzyme CYP27B1, permitting T cells to both activate and respond to VitD. VitD then initiated the transition from pro-inflammatory interferon-γ+ TH1 cells to suppressive interleukin-10+ cells. This process was primed by dynamic changes in the epigenetic landscape of CD4+ T cells, generating super-enhancers and recruiting several transcription factors, notably c-JUN, STAT3 and BACH2, which together with VitD receptor shaped the transcriptional response to VitD. Accordingly, VitD did not induce interleukin-10 expression in cells with dysfunctional BACH2 or STAT3. Bronchoalveolar lavage fluid CD4+ T cells of patients with COVID-19 were TH1-skewed and showed de-repression of genes downregulated by VitD, from either lack of substrate (VitD deficiency) and/or abnormal regulation of this system.",
author = "Daniel Chauss and Tilo Freiwald and Reuben McGregor and Bingyu Yan and Luopin Wang and Estefania Nova-Lamperti and Dhaneshwar Kumar and Zonghao Zhang and Heather Teague and West, {Erin E.} and Vannella, {Kevin M.} and Ramos-Benitez, {Marcos J.} and Jack Bibby and Audrey Kelly and Amna Malik and Freeman, {Alexandra F.} and Schwartz, {Daniella M.} and Didier Portilla and Chertow, {Daniel S.} and Susan John and Paul Lavender and Claudia Kemper and Giovanna Lombardi and Mehta, {Nehal N.} and Nichola Cooper and Lionakis, {Michail S.} and Arian Laurence and Majid Kazemian and Behdad Afzali",
year = "2022",
month = jan,
doi = "10.1038/s41590-021-01080-3",
language = "English",
volume = "23",
pages = "62–74",
journal = "NAT IMMUNOL",
issn = "1529-2908",
publisher = "NATURE PUBLISHING GROUP",
number = "1",

}

RIS

TY - JOUR

T1 - Autocrine vitamin D signaling switches off pro-inflammatory programs of TH1 cells

AU - Chauss, Daniel

AU - Freiwald, Tilo

AU - McGregor, Reuben

AU - Yan, Bingyu

AU - Wang, Luopin

AU - Nova-Lamperti, Estefania

AU - Kumar, Dhaneshwar

AU - Zhang, Zonghao

AU - Teague, Heather

AU - West, Erin E.

AU - Vannella, Kevin M.

AU - Ramos-Benitez, Marcos J.

AU - Bibby, Jack

AU - Kelly, Audrey

AU - Malik, Amna

AU - Freeman, Alexandra F.

AU - Schwartz, Daniella M.

AU - Portilla, Didier

AU - Chertow, Daniel S.

AU - John, Susan

AU - Lavender, Paul

AU - Kemper, Claudia

AU - Lombardi, Giovanna

AU - Mehta, Nehal N.

AU - Cooper, Nichola

AU - Lionakis, Michail S.

AU - Laurence, Arian

AU - Kazemian, Majid

AU - Afzali, Behdad

PY - 2022/1

Y1 - 2022/1

N2 - The molecular mechanisms governing orderly shutdown and retraction of CD4+ type 1 helper T (TH1) cell responses remain poorly understood. Here we show that complement triggers contraction of TH1 responses by inducing intrinsic expression of the vitamin D (VitD) receptor and the VitD-activating enzyme CYP27B1, permitting T cells to both activate and respond to VitD. VitD then initiated the transition from pro-inflammatory interferon-γ+ TH1 cells to suppressive interleukin-10+ cells. This process was primed by dynamic changes in the epigenetic landscape of CD4+ T cells, generating super-enhancers and recruiting several transcription factors, notably c-JUN, STAT3 and BACH2, which together with VitD receptor shaped the transcriptional response to VitD. Accordingly, VitD did not induce interleukin-10 expression in cells with dysfunctional BACH2 or STAT3. Bronchoalveolar lavage fluid CD4+ T cells of patients with COVID-19 were TH1-skewed and showed de-repression of genes downregulated by VitD, from either lack of substrate (VitD deficiency) and/or abnormal regulation of this system.

AB - The molecular mechanisms governing orderly shutdown and retraction of CD4+ type 1 helper T (TH1) cell responses remain poorly understood. Here we show that complement triggers contraction of TH1 responses by inducing intrinsic expression of the vitamin D (VitD) receptor and the VitD-activating enzyme CYP27B1, permitting T cells to both activate and respond to VitD. VitD then initiated the transition from pro-inflammatory interferon-γ+ TH1 cells to suppressive interleukin-10+ cells. This process was primed by dynamic changes in the epigenetic landscape of CD4+ T cells, generating super-enhancers and recruiting several transcription factors, notably c-JUN, STAT3 and BACH2, which together with VitD receptor shaped the transcriptional response to VitD. Accordingly, VitD did not induce interleukin-10 expression in cells with dysfunctional BACH2 or STAT3. Bronchoalveolar lavage fluid CD4+ T cells of patients with COVID-19 were TH1-skewed and showed de-repression of genes downregulated by VitD, from either lack of substrate (VitD deficiency) and/or abnormal regulation of this system.

UR - https://doi.org/10.1038/s41590-021-01080-3

U2 - 10.1038/s41590-021-01080-3

DO - 10.1038/s41590-021-01080-3

M3 - SCORING: Journal article

C2 - 34764490

VL - 23

SP - 62

EP - 74

JO - NAT IMMUNOL

JF - NAT IMMUNOL

SN - 1529-2908

IS - 1

ER -