Vitamin D does not modulate NF-κB activity in Jurkat T cells

Amde Selassie Shifera; Deborah Leong; John A. Hardin

doi:10.1016/j.imlet.2010.04.001

Vitamin D does not modulate NF-κB activity in Jurkat T cells

Amde Selassie Shifera
, Deborah Leong
, John A. Hardin

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

4 Scopus citations

Abstract

The active form of vitamin D, 1α,25-dihydroxyvitamin D₃ [1α,25(OH)₂D₃], has been reported to influence the functioning of the immune system by targeting the activities of cellular signaling pathways, in addition to its direct genomic effects. One of the signaling pathways reported to be targeted by vitamin D is the NF-κB pathway, which is highly active in most immune cell types, including T cells. However, the effects of vitamin D on the NF-κB pathway in T cells are not fully understood. Therefore, we examined the effects of 1α,25(OH)₂D₃ on the NF-κB pathway in the Jurkat cell line, a human T cell line that constitutively expresses endogenous vitamin D receptor. We found that 1α,25(OH)₂D₃ does not inhibit the induction of IκBα degradation and the expression of an NF-κB-dependent reporter gene in Jurkat cells following treatment with PMA/ionomycin. Also, 1α,25(OH)₂D₃ did not suppress the activation of NF-κB by TNFα or PHA. Furthermore, we demonstrate that 1α,25(OH)₂D₃ does not block the induction of CD69, which is an NF-κB target gene and an early T cell activation marker. Therefore, we conclude that vitamin D does not modulate the activity of the NF-κB pathway in Jurkat cells.

Original language	English (US)
Pages (from-to)	151-158
Number of pages	8
Journal	Immunology Letters
Volume	131
Issue number	2
DOIs	https://doi.org/10.1016/j.imlet.2010.04.001
State	Published - Jul 2010
Externally published	Yes

Funding

Research in the laboratory of J.A.H. is supported by a grant from the Alliance for Lupus Research. A.S. was a Research Fellow supported by an NIAMS Rheumatology Training Grant , T32 AR050947 . We thank Dr. Laiping Xie for help in the conduct of our studies. We express our gratitude to Dr. Shao-Cong Sun (Pennsylvania State University) for the Jurkat cell line and to Dr. Sylvia Christakos (University of Medicine and Dentistry of New Jersey) for the CYP24A1-luciferase plasmid.

Funders	Funder number
National Institute for Arthritis and Musculoskeletal and Skin Diseases	T32AR050947
Alliance for Lupus Research	T32 AR050947

Keywords

CD69
Jurkat cells
NF-κB
T cells
Vitamin D

ASJC Scopus subject areas

Immunology and Allergy
Immunology

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10.1016/j.imlet.2010.04.001

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@article{81718b70c07842938b1d2d712dd2ec91,

title = "Vitamin D does not modulate NF-κB activity in Jurkat T cells",

abstract = "The active form of vitamin D, 1α,25-dihydroxyvitamin D3 [1α,25(OH)2D3], has been reported to influence the functioning of the immune system by targeting the activities of cellular signaling pathways, in addition to its direct genomic effects. One of the signaling pathways reported to be targeted by vitamin D is the NF-κB pathway, which is highly active in most immune cell types, including T cells. However, the effects of vitamin D on the NF-κB pathway in T cells are not fully understood. Therefore, we examined the effects of 1α,25(OH)2D3 on the NF-κB pathway in the Jurkat cell line, a human T cell line that constitutively expresses endogenous vitamin D receptor. We found that 1α,25(OH)2D3 does not inhibit the induction of IκBα degradation and the expression of an NF-κB-dependent reporter gene in Jurkat cells following treatment with PMA/ionomycin. Also, 1α,25(OH)2D3 did not suppress the activation of NF-κB by TNFα or PHA. Furthermore, we demonstrate that 1α,25(OH)2D3 does not block the induction of CD69, which is an NF-κB target gene and an early T cell activation marker. Therefore, we conclude that vitamin D does not modulate the activity of the NF-κB pathway in Jurkat cells.",

keywords = "CD69, Jurkat cells, NF-κB, T cells, Vitamin D",

author = "Shifera, \{Amde Selassie\} and Deborah Leong and Hardin, \{John A.\}",

note = "Funding Information: Research in the laboratory of J.A.H. is supported by a grant from the Alliance for Lupus Research. A.S. was a Research Fellow supported by an NIAMS Rheumatology Training Grant , T32 AR050947 . We thank Dr. Laiping Xie for help in the conduct of our studies. We express our gratitude to Dr. Shao-Cong Sun (Pennsylvania State University) for the Jurkat cell line and to Dr. Sylvia Christakos (University of Medicine and Dentistry of New Jersey) for the CYP24A1-luciferase plasmid.",

year = "2010",

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doi = "10.1016/j.imlet.2010.04.001",

language = "English (US)",

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AU - Shifera, Amde Selassie

AU - Leong, Deborah

AU - Hardin, John A.

N1 - Funding Information: Research in the laboratory of J.A.H. is supported by a grant from the Alliance for Lupus Research. A.S. was a Research Fellow supported by an NIAMS Rheumatology Training Grant , T32 AR050947 . We thank Dr. Laiping Xie for help in the conduct of our studies. We express our gratitude to Dr. Shao-Cong Sun (Pennsylvania State University) for the Jurkat cell line and to Dr. Sylvia Christakos (University of Medicine and Dentistry of New Jersey) for the CYP24A1-luciferase plasmid.

PY - 2010/7

Y1 - 2010/7

N2 - The active form of vitamin D, 1α,25-dihydroxyvitamin D3 [1α,25(OH)2D3], has been reported to influence the functioning of the immune system by targeting the activities of cellular signaling pathways, in addition to its direct genomic effects. One of the signaling pathways reported to be targeted by vitamin D is the NF-κB pathway, which is highly active in most immune cell types, including T cells. However, the effects of vitamin D on the NF-κB pathway in T cells are not fully understood. Therefore, we examined the effects of 1α,25(OH)2D3 on the NF-κB pathway in the Jurkat cell line, a human T cell line that constitutively expresses endogenous vitamin D receptor. We found that 1α,25(OH)2D3 does not inhibit the induction of IκBα degradation and the expression of an NF-κB-dependent reporter gene in Jurkat cells following treatment with PMA/ionomycin. Also, 1α,25(OH)2D3 did not suppress the activation of NF-κB by TNFα or PHA. Furthermore, we demonstrate that 1α,25(OH)2D3 does not block the induction of CD69, which is an NF-κB target gene and an early T cell activation marker. Therefore, we conclude that vitamin D does not modulate the activity of the NF-κB pathway in Jurkat cells.

AB - The active form of vitamin D, 1α,25-dihydroxyvitamin D3 [1α,25(OH)2D3], has been reported to influence the functioning of the immune system by targeting the activities of cellular signaling pathways, in addition to its direct genomic effects. One of the signaling pathways reported to be targeted by vitamin D is the NF-κB pathway, which is highly active in most immune cell types, including T cells. However, the effects of vitamin D on the NF-κB pathway in T cells are not fully understood. Therefore, we examined the effects of 1α,25(OH)2D3 on the NF-κB pathway in the Jurkat cell line, a human T cell line that constitutively expresses endogenous vitamin D receptor. We found that 1α,25(OH)2D3 does not inhibit the induction of IκBα degradation and the expression of an NF-κB-dependent reporter gene in Jurkat cells following treatment with PMA/ionomycin. Also, 1α,25(OH)2D3 did not suppress the activation of NF-κB by TNFα or PHA. Furthermore, we demonstrate that 1α,25(OH)2D3 does not block the induction of CD69, which is an NF-κB target gene and an early T cell activation marker. Therefore, we conclude that vitamin D does not modulate the activity of the NF-κB pathway in Jurkat cells.

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KW - NF-κB

KW - T cells

KW - Vitamin D

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JO - Immunology Letters

JF - Immunology Letters

IS - 2

ER -

Vitamin D does not modulate NF-κB activity in Jurkat T cells

Abstract

Funding

Keywords

ASJC Scopus subject areas

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