Willis-Carr J I, St Pierre R L
J Immunol. 1978 Apr;120(4):1153-9.
Dietary vitamin B6 (pyridoxine) deficiency in young Lewis rats results in a reduction of T lymphocyte numbers and defects of cellular immunocompetence. In vitro studies of thymic epithelial (TE) cells, responsible for inducing T lymphocyte differentiation, revealed that maintenance on a vitamin B6 deficient diet for 2 weeks resulted in a severe defect in TE cell function. When the deficient animals were returned to a normal diet, TE cell function was restored. Exposure of lymphoid precursors from neonatally thymectomized or vitamin B6-deficient donors to normal TE monolayers resulted in their conversion to functional T lymphocytes, as measured by their response in MLR and to mitogens. However, TE monolayers from vitamin B6-deficient animals were unable to effect such a maturation of T lymphocytes. Therefore, it is suggested that the defect in cellular immunocompetence following this dietary deficiency is due, at least in part, to the inability of TE cells to effect the differentiation of T lymphocyte precursors to functional T lymphocytes. The dietary deficiency does not, however, impair lymphoid precursors, which can be stimulated to further differentiation by exposure to normal TE cell monolayers.
幼年Lewis大鼠饮食中维生素B6（吡哆醇）缺乏会导致T淋巴细胞数量减少和细胞免疫能力缺陷。对负责诱导T淋巴细胞分化的胸腺上皮（TE）细胞进行的体外研究表明，持续2周的维生素B6缺乏饮食会导致TE细胞功能严重缺陷。当缺乏维生素B6的动物恢复正常饮食后，TE细胞功能得以恢复。将新生胸腺切除或维生素B6缺乏供体的淋巴前体暴露于正常TE单层细胞中，通过其在混合淋巴细胞反应（MLR）和对有丝分裂原的反应来衡量，结果显示它们会转化为功能性T淋巴细胞。然而，来自维生素B6缺乏动物的TE单层细胞无法促使T淋巴细胞发生这种成熟。因此，有人提出，这种饮食缺乏后细胞免疫能力的缺陷至少部分是由于TE细胞无法促使T淋巴细胞前体分化为功能性T淋巴细胞。不过，饮食缺乏并不会损害淋巴前体，通过暴露于正常TE细胞单层细胞，淋巴前体可被刺激进一步分化。
