Effects of Vitamin B6 Deficiency on the Composition and Functional Potential of T Cell Populations

The immune system is critical in preventing infection and cancer, and malnutrition can weaken different aspects of the immune system to undermine immunity. Previous studies suggested that vitamin B6 deficiency could decrease serum antibody production with concomitant increase in IL4 expression. Howe...

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Bibliographic Details
Published in:	Journal of immunology research 2017-01, Vol.2017, p.2197975-12
Main Authors:	Qian, Bingjun, Shen, Shanqi, Zhang, Jianhua, Jing, Pu
Format:	Article
Language:	eng
Subjects:	Animals Cell Differentiation Cytokines Cytokines - genetics Diet Down-Regulation Food safety Gene expression Immune system Interferon-gamma - genetics Interferon-gamma - secretion Interleukin-2 - genetics Interleukin-2 - secretion Interleukin-4 - genetics Interleukin-4 - secretion Kinases Laboratory animals Lymphocyte Activation Lymphocytes Malnutrition Metabolism Mice Nutrition research Pyridoxal Phosphate - analogs & derivatives Pyridoxal Phosphate - blood Signal transduction Studies Suppressor of Cytokine Signaling 1 Protein - genetics T-Box Domain Proteins - genetics T-Lymphocytes - immunology T-Lymphocytes - physiology Vitamin B 6 Deficiency - blood Vitamin B 6 Deficiency - immunology Vitamin B 6 Deficiency - metabolism Xanthurenates - blood
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Summary:	The immune system is critical in preventing infection and cancer, and malnutrition can weaken different aspects of the immune system to undermine immunity. Previous studies suggested that vitamin B6 deficiency could decrease serum antibody production with concomitant increase in IL4 expression. However, evidence on whether vitamin B6 deficiency would impair immune cell differentiation, cytokines secretion, and signal molecule expression involved in JAK/STAT signaling pathway to regulate immune response remains largely unknown. The aim of this study is to investigate the effects of vitamin B6 deficiency on the immune system through analysis of T lymphocyte differentiation, IL-2, IL-4, and INF-γ secretion, and SOCS-1 and T-bet gene transcription. We generated a vitamin B6-deficient mouse model via vitamin B6-depletion diet. The results showed that vitamin B6 deficiency retards growth, inhibits lymphocyte proliferation, and interferes with its differentiation. After ConA stimulation, vitamin B6 deficiency led to decrease in IL-2 and increase in IL-4 but had no influence on IFN-γ. Real-time PCR analysis showed that vitamin B6 deficiency downregulated T-bet and upregulated SOCS-1 transcription. This study suggested that vitamin B6 deficiency influenced the immunity in organisms. Meanwhile, the appropriate supplement of vitamin B6 could benefit immunity of the organism.
ISSN:	2314-8861 2314-7156