美国特鲁多研究所的科学家们的一项最新发现可能将有助于结核病的预防。Andrea Cooper博士的研究小组发现了肺部一种淋巴组织的发育和抵御疾病之间的联系。
该研究的论文发表在最新一期的《Journal of Immunology》杂志上。
肺结核是一种致死性的感染疾病，其主要是由肺结核分支杆菌所引起。该病菌通常会造成肺部损伤，还可以影响身体的其它组织器官。它可通过肺结核病人的咳嗽、喷嚏或唾液等途径，经由空气传播感染其它人。如果不进行及时的治疗，其可造成超过50%的感染人群死亡。
Cooper博士说道：“在我们进行的实验中，一种特定细胞因子的缺失可导致肺部淋巴组织的发育不全。这会导致肺部缺少一种能将血液中循环的免疫细胞聚集在感染区域的分子的表达。尽管过去这种淋巴组织已经在肺结核病人肺部受损区域被人们发现，但这是由我们首次证实了其介导的免疫反应在保护肺部不受肺结核病菌感染中具有重要的作用。”
通过研究该免疫系统的不同组分如何有效控制肺结核病菌的感染，公共卫生健康的研究者可以更有效的结合疫苗、免疫治疗和药物来保护人们的身体不受病菌感染。由于目前的疫苗还没有靶向该新发现的免疫组织细胞，因此未来可以基于此开发出新的比现在更有效的疫苗。
相关英文论文摘要：
IL-23 Is Required for Long-Term Control of Mycobacteriumtuberculosis and B Cell Follicle Formation in the Infected Lung
IL-23 is required for the IL-17 response to infection with Mycobacterium tuberculosis, but is not required for the early control of bacterial growth. However, mice deficient for the p19 component of IL-23 (Il23a−/−) exhibit increased bacterial growth late in infection that is temporally associated with smaller B cell follicles in the lungs. Cxcl13 is required for B cell follicle formation and immunity during tuberculosis. The absence of IL-23 results in decreased expression of Cxcl13 within M. tuberculosis-induced lymphocyte follicles in the lungs, and this deficiency was associated with increased cuffing of T cells around the vessels in the lungs of these mice. Il23a−/− mice also poorly expressed IL-17A and IL-22 mRNA. These cytokines were able to induce Cxcl13 in mouse primary lung fibroblasts, suggesting that these cytokines are likely involved in B cell follicle formation. Indeed, IL-17RA–deficient mice generated smaller B cell follicles early in the response, whereas IL-22–deficient mice had smaller B cell follicles at an intermediate time postinfection; however, only Il23a−/− mice had a sustained deficiency in B cell follicle formation and reduced immunity. We propose that in the absence of IL-23, expression of long-term immunity to tuberculosis is compromised due to reduced expression of Cxcl13 in B cell follicles and reduced ability of T cells to migrate from the vessels and into the lesion. Further, although IL-17 and IL-22 can both contribute to Cxcl13 production and B cell follicle formation, it is IL-23 that is critical in this regard.
英文论文链接：https://www.jimmunol.org/content/early/2011/10/14/jimmunol.1101377
