Influence of Cdx2 and TaqI Gene Variants on Vitamin D Modulated Intracellular Chemokine Positive T-Cell Subsets in Pulmonary Tuberculosis.

PURPOSE

We studied the effect of 1,25(OH)D (vitamin D) on intracellular chemokine-positive T-cell subsets in whole blood cultures of healthy controls and patients with pulmonary tuberculosis.

METHODS

Genotyping was performed by the polymerase chain reaction-restriction fragment length polymorphism method. The regulatory role of the Cdx2 and 3'UTR TaqI gene variants on chemokine-positive T-cell subsets was studied from culture filtrate antigen stimulated with or without vitamin D treated whole blood cultures of 60 healthy controls and 50 patients with pulmonary tuberculosis.

FINDINGS

Vitamin D significantly suppressed monocyte chemoattractant protein 1, macrophage inhibitory protein (MIP)-1α, MIP-1β, regulated on activation, normal T-cell expressed and secreted (RANTES), and interferon-γ inducible protein 10 (IP-10)-positive T-cell subsets compared with culture filtrate antigen stimulated cells without vitamin D treatment. In the Cdx2 AA genotype, vitamin D decreased MIP-1α, MIP-1β, and RANTES-positive T cells compared with the GG genotype. Whereas in the TaqI tt genotype, decreased MIP-1β and RANTES and increased IP-10-positive T cells were observed compared with the TT genotype in vitamin D treated cells (p < 0.05).

IMPLICATIONS

This study suggests that vitamin D may regulate the chemokine-positive T cells through the Cdx2 AA and TaqI tt genotypes. This could be helpful to regulate chemokine-mediated inflammatory response during active disease condition. Hence, vitamin D supplementation along with tuberculosis drugs may be useful for faster recovery from the disease.