最近一项研究解释了为什么维生素D是抵抗结核病的一个强有力的武器。这些发现有助于临床试验以测试维生素D补充剂是否可在高危人群中帮助人们抵抗结核病。研究人员一直怀疑，这种重要的维生素是通过免疫系统来产生其功效的，但他们对其过程却一直不清楚。
结核菌
Robert Modlin及其同事研究发现，维生素D会促使免疫系统的两个主要分支—即先天性免疫及适应性免疫同步抵御结核病。先天性免疫是机体的第一道抵御病原体的防线，它们是发生最早感染征兆时在棋盘上随时可被调动的卒子。相反，适应性免疫细胞只会对特殊的病原体发动进攻，而机体需要时间来生产这些定制的免疫细胞。
研究人员发现，维生素D会促使适应性免疫细胞（叫做T细胞）释放一种叫做IFN-gamma的分子，该分子转而会激活先天免疫细胞（叫做巨噬细胞）来进攻入侵的结核菌。这种巨噬细胞接着会释放一种抗菌肽cathelicidin。这一过程需要一定量的维生素D，但并非每个人体内都有足够的维生素D供应。例如，在皮肤颜色较黑的人群中维生素D缺乏更为常见。因此，非洲裔美国人更易罹患结核病及其它潜在的传染病。
该研究团队对一组非裔美国人与一组白人进行了比较并发现，那些有着足够量维生素D的白人可通过IFN-gamma产生cathelicidin，而在体内维生素D含量较低的非洲裔美国人中则不能做到这一点。这些结果表明，维生素D是先天和适应性免疫在抵抗结核病的时候所共同需要的，而服用维生素D补充剂可能会使皮肤颜色较黑的人群及其他高危人群受益。
相关英文论文摘要：
Vitamin D Is Required for IFN-γ–Mediated Antimicrobial Activity of Human Macrophages
Control of tuberculosis worldwide depends on our understanding of human immune mechanisms, which combat the infection. Acquired T cell responses are critical for host defense against microbial pathogens, yet the mechanisms by which they act in humans remain unclear. We report that T cells, by the release of interferon-γ (IFN-γ), induce autophagy, phagosomal maturation, the production of antimicrobial peptides such as cathelicidin, and antimicrobial activity against Mycobacterium tuberculosis in human macrophages via a vitamin D–dependent pathway. IFN-γ induced the antimicrobial pathway in human macrophages cultured in vitamin D–sufficient sera, but not in sera from African-Americans that have lower amounts of vitamin D and who are more susceptible to tuberculosis. In vitro supplementation of vitamin D–deficient serum with 25-hydroxyvitamin D3 restored IFN-γ–induced antimicrobial peptide expression, autophagy, phagosome-lysosome fusion, and antimicrobial activity. These results suggest a mechanism in which vitamin D is required for acquired immunity to overcome the ability of intracellular pathogens to evade macrophage-mediated antimicrobial responses. The present findings underscore the importance of adequate amounts of vitamin D in all human populations for sustaining both innate and acquired immunity against infection.
