Immunological association of inducible bronchus-associated lymphoid tissue organogenesis in Ag85B-rHPIV2 vaccine-induced anti-tuberculosis mucosal immune responses in mice.
Immunological association of inducible bronchus-associated lymphoid tissue organogenesis in Ag85B-rHPIV2 vaccine-induced anti-tuberculosis mucosal immune responses in mice.
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DOI:
10.1093/intimm/dxy046
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发表时间:
2018-09-25
影响因子:
4.4
通讯作者:
Kunisawa J
中科院分区:
文献类型:
--
作者:
Nagatake T;Suzuki H;Hirata SI;Matsumoto N;Wada Y;Morimoto S;Nasu A;Shimojou M;Kawano M;Ogami K;Tsujimura Y;Kuroda E;Iijima N;Hosomi K;Ishii KJ;Nosaka T;Yasutomi Y;Kunisawa J
We previously reported that Ag85B-expressing human parainfluenza type 2 virus (Ag85B-rHPIV2) was effective as a nasal vaccine against tuberculosis in mice; however, the mechanism by which it induces an immune response remains to be investigated. In the present study, we found that organogenesis of inducible bronchus-associated lymphoid tissue (iBALT) played a role in the induction of antigen-specific T cells and IgA antibody responses in the lung of mice intra-nasally administered Ag85B-rHPIV2. We found that expression of Ag85B was dispensable for the development of iBALT, suggesting that HPIV2 acted as an iBALT-inducing vector. When iBALT organogenesis was disrupted in Ag85B-rHPIV2-immunized mice, either by neutralization of the lymphotoxin pathway or depletion of CD11b+ cells, Ag85B-specific immune responses (i.e. IFN γ-producing T cells and IgA antibody) were diminished in the lung. Furthermore, we found that immunization with Ag85B-rHPIV2 induced neutrophil and eosinophil infiltration temporally after the immunization in the lung. Thus, our results show that iBALT organogenesis contributes to the induction of antigen-specific immune responses by Ag85B-rHPIV2 and that Ag85B-rHPIV2 provokes its immune responses without inducing long-lasting inflammation. A parainfluenza-based nasal vaccine induces formation of BALT in the lung
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DOI:
10.1084/jem.20090410
发表时间:
2009-10-26
期刊:
The Journal of experimental medicine
影响因子:
--
作者:
GeurtsvanKessel CH;Willart MA;Bergen IM;van Rijt LS;Muskens F;Elewaut D;Osterhaus AD;Hendriks R;Rimmelzwaan GF;Lambrecht BN
通讯作者:
Lambrecht BN
影响因子:
16.6
作者:
通讯作者:
--
影响因子:
15.3
作者:
Chvatchko, Y;KoscoVilbois, MH;Bonnefoy, JY
通讯作者:
Bonnefoy, JY
影响因子:
168.9
作者:
Fine, PEM;Ponnighaus, JM;Peto, R
通讯作者:
Peto, R
影响因子:
6.2
作者:
Fujkuyama Y;Tokuhara D;Kataoka K;Gilbert RS;McGhee JR;Yuki Y;Kiyono H;Fujihashi K
通讯作者:
Fujihashi K