Abstract
BACKGROUND: CD200, a cell-surface immunoglobulin-like molecule expressed by immune and stromal cells, dampens the pro-inflammatory activity of tissue-resident innate cells via its receptor, CD200R. This interaction appears critical for peripheral immune tolerance, particularly in the airways where excessive inflammation is undesirable. Vitamin D contributes to pulmonary health and promotes regulatory immune pathways, therefore its influence on CD200 and CD200R was investigated.
METHODS: CD200 and CD200R expression were assessed by qPCR and immunoreactivity of human lymphoid, myeloid and epithelial cells following 1α,25-dihydroxyvitamin D3 (1α,25VitD3) exposure in vitro and in peripheral T cells following 1α,25VitD3 oral ingestion in vivo. The effect of 1α25VitD3 was also assessed in human airway-resident cells.
RESULTS: 1α25VitD3 potently upregulated CD200 on peripheral human CD4+ T cells in vitro, and in vivo there was a trend towards upregulation in healthy, but not asthmatic individuals. CD200R expression was not modulated in any cells studied. CD200 induction was observed to a lesser extent in CD8+ T cells and not in B cells or airway epithelium. T cells isolated from the human airway also responded strongly to 1α25VitD3 to upregulate CD200.
CONCLUSIONS: The capacity of 1α,25-dihydroxyvitamin D3 to induce CD200 expression by peripheral and respiratory tract T cells identifies an additional pathway via which vitamin D can restrain inflammation in the airways to maintain respiratory health.
Original language | English |
---|---|
Pages (from-to) | 574-81 |
Number of pages | 8 |
Journal | Thorax |
Volume | 67 |
Issue number | 7 |
DOIs | |
Publication status | Published - Jul 2012 |
Keywords
- Antigens, CD
- Asthma
- Cells, Cultured
- Child
- Flow Cytometry
- Humans
- Immune Tolerance
- Immunity, Cellular
- Polymerase Chain Reaction
- RNA, Messenger
- Respiratory Mucosa
- T-Lymphocytes
- Up-Regulation
- Vitamin D
- Vitamins
- Comparative Study
- Journal Article
- Research Support, Non-U.S. Gov't