The vitamin D receptor turns off chronically activated T cells

Area of Science:

• Immunology
• Endocrinology
• Cell Biology

Background:

• 1,25(OH)2D3 inhibits T helper (TH) 1 and TH 17 cell proliferation and cytokine production.
• TH 1 and TH 17 cells are implicated in the pathogenesis of immune-mediated diseases.
• 1,25(OH)2D3 treatment ameliorates immune-mediated diseases but does not affect infectious diseases.

Purpose of the Study:

• To review the role of vitamin D in regulating T cell responses.
• To explain the paradoxical effects of 1,25(OH)2D3 in immune-mediated versus infectious diseases.
• To highlight vitamin D as a late-acting regulator of T cell function.

Main Methods:

• Review of existing literature on vitamin D and T cell immunology.
• Analysis of T cell activation pathways and vitamin D receptor (VDR) expression.
• Correlation of T cell responses with disease states and vitamin D treatment.

Main Results:

• Resting T cells lack VDR expression and are unresponsive to vitamin D.
• VDR expression increases late after T cell activation.
• Vitamin D acts to inhibit T cell proliferation and cytokine production in chronic T cell activation scenarios.

Conclusions:

• Vitamin D is a critical late-stage regulator of T cell responses.
• The timing of VDR expression explains why vitamin D benefits immune-mediated diseases but not infections.
• Vitamin D plays a key role in resolving inflammation by dampening T cell activity.