Nuffield Department of Medicine, University of Oxford, The Peter Medawar Building for Pathogen Research, South Parks Road, Oxford OX1 3SY, United Kingdom.
Infect Immun. 2011 Aug;79(8):3328-37. doi: 10.1128/IAI.01133-10. Epub 2011 May 31.
Convincing correlates of protective immunity against tuberculosis have been elusive. In BALB/c mice, intranasal immunization with a replication-deficient recombinant adenovirus expressing Mycobacterium tuberculosis antigen 85A (adenovirus-85A) induces protective lower respiratory tract immunity against pulmonary challenge with Mycobacterium tuberculosis, while intradermal immunization with adenovirus-85A does not. Here we report that intranasal immunization with adenovirus-85A induces expression of the chemokine receptor CXCR6 on lung CD8 T lymphocytes, which is maintained for at least 3 months. CXCR6-positive antigen-specific T cell numbers are increased among bronchoalveolar lavage-recoverable cells. Similarly, intranasal immunization with recombinant antigen 85A with adjuvant induces CXCR6 expression on lung CD4 cells in BALB/c and C57BL/6 mice, while a synthetic ESAT6(1-20) peptide with adjuvant induces CXCR6 expression in C57BL/6 mice. Parenteral immunization fails to do so. Upregulation of CXCR6 is accompanied by a transient elevation of serum CXCL16 after intranasal immunization, and lung cells cultured ex vivo from mice immunized intranasally show increased production of CXCL16. Administration of CXCL16 and cognate antigen intranasally to mice previously immunized parenterally increases the number of antigen-specific T lymphocytes in the bronchoalveolar lavage-recoverable population, which mediates inhibition of the early growth of Mycobacterium tuberculosis after challenge. We conclude that expression of CXCR6 on lung T lymphocytes is a correlate of local protective immunity against Mycobacterium tuberculosis after intranasal immunization and that CXCR6 and CXCL16 play an important role in the localization of T cells within lung tissue and the bronchoalveolar lavage-recoverable compartment.
针对结核分枝杆菌保护性免疫的明确相关因素一直难以捉摸。在 BALB/c 小鼠中,鼻腔内接种复制缺陷型重组腺病毒表达结核分枝杆菌抗原 85A(腺病毒-85A)可诱导针对结核分枝杆菌肺部攻击的保护性下呼吸道免疫,而皮内接种腺病毒-85A 则没有。在这里,我们报告鼻腔内接种腺病毒-85A 可诱导肺 CD8 T 淋巴细胞上趋化因子受体 CXCR6 的表达,至少可维持 3 个月。支气管肺泡灌洗液可回收细胞中 CXCR6 阳性的抗原特异性 T 细胞数量增加。同样,用佐剂鼻腔内接种重组抗原 85A 也可诱导 BALB/c 和 C57BL/6 小鼠肺 CD4 细胞上 CXCR6 的表达,而用佐剂鼻腔内接种合成的 ESAT6(1-20) 肽可诱导 C57BL/6 小鼠肺 CD4 细胞上 CXCR6 的表达。而皮下免疫则不能。鼻腔内免疫后 CXCR6 的上调伴随着血清 CXCL16 的短暂升高,体外培养的肺细胞显示 CXCL16 的产生增加。经鼻给予 CXCL16 和同源抗原可增加经皮下免疫的小鼠支气管肺泡灌洗液可回收群体中抗原特异性 T 淋巴细胞的数量,这介导了挑战后结核分枝杆菌早期生长的抑制。我们得出结论,鼻腔内免疫后肺 T 淋巴细胞上 CXCR6 的表达是针对结核分枝杆菌局部保护性免疫的一个相关因素,而 CXCR6 和 CXCL16 在 T 细胞在肺组织和支气管肺泡灌洗液可回收区的定位中发挥重要作用。