Influence of Cdx2 and TaqI gene variants on vitamin D 3 modulated intracellular chemokine positive T-cell subsets in pulmonary tuberculosis.


Harishankar, M.; Selvaraj, P.


Clinical Therapeutics; 2017; 39: 946-957.     



Purpose: We studied the effect of 1,25(OH)2 D3 (vitamin D3 ) 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 D3 treated whole blood cultures of 60 healthy controls and 50 patients with pulmonary tuberculosis.


Findings: Vitamin D3 significantly suppressed monocyte chemoattractant protein 1, macrophage inhibitory protein (MIP)–1a, MIP-1ß, regulated on activation, normal T-cell expressed and secreted (RANTES), and interferon-? inducible protein 10 (IP-10)–positive T-cell subsets compared with culture filtrate antigen stimulated cells without vitamin D3 treatment. In the Cdx2 AA genotype, vitamin D3 decreased MIP-1a, MIP-1ß, and RANTES-positive T cells compared with the GG genotype. Whereas in the TaqI tt genotype, decreased MIP-1ß and RANTES and increased IP-10–positive T cells were observed compared with the TT genotype in vitamin D3 treated cells ( p < 0.05).


Implications: This study suggests that vitamin D3 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 D3 supplementation along with tuberculosis drugs may be useful for faster recovery from the disease.


Keywords: Chemokine; culture filtrate antigen; polymorphism; T cell; tuberculosis; vitamin D receptor.



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