期刊
MUCOSAL IMMUNOLOGY
卷 12, 期 6, 页码 1391-1403出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41385-019-0203-z
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资金
- Ministry of Education, Culture, Sports, Science, and Technology of Japan [23229004]
- Core Research for Evolutional Science and Technology Program of the Japan Science, and a Technology Agency
- Health Labor Sciences Research Grant from the Ministry of Health, Labor and Welfare of Japan
- Grants-in-Aid for Scientific Research [23229004] Funding Source: KAKEN
Our current study focused on elucidating the role of specific chemokine-receptor interactions in antigen (Ag)-specific immune cell migration from nasal to genital mucosal tissues. This cellular migration is critical to induce effective Ag-specific immune responses against sexually transmitted genital infections. In this study, nasal immunization with live attenuated HSV-2 TK- induced the upregulation of CCR5 expression in effector immune cells, including CD4(+) T cells, in Ag-priming sites and vaginal tissue. The CCR5 ligands CCL3, CCL4, and CCL5 all showed upregulated expression in vaginal tissue; in particular, CCL5 expression was highly enhanced in the stromal cells of vaginal tissue after nasal immunization. Intravaginal blockade of CCL5 by using neutralizing antibody diminished the number of HSV-2-specific effector cells in the vagina. Furthermore, loss of CCR5, a receptor for CCL5, impaired the migration of nasally primed Ag-specific effector cells from the airway to vagina. Effector cells adoptively transferred from CCR5-deficient mice failed to migrate into vaginal tissue, consequently increasing recipient mice's susceptibility to HSV-2 vaginal infection. These results indicate that the CCR5-CCL5 chemokine pathway is required for the migration and retention of nasally primed Ag-specific effector cells in vagina for providing protective immunity against HSV-2 infection.
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