B7-H1 (programmed cell death ligand 1) is required for the development of multifunctional Th1 cells and immunity to primary, but not secondary, Salmonella infection.
B7-H1 (programmed cell death ligand 1) is required for the development of multifunctional Th1 cells and immunity to primary, but not secondary, Salmonella infection.
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DOI：
10.4049/jimmunol.1000743
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发表时间：
2010-08-15
期刊：
影响因子：
--
通讯作者：
McSorley SJ
中科院分区：
文献类型：
--
作者：
Lee SJ;O'Donnell H;McSorley SJ
Robust antibody and CD4 T cell responses are required for the resolution of Salmonella infection in susceptible mice. Here we examined the role of B7-H1 (PD-L1) in resistance to primary Salmonella infection. Infected B7-H1-deficient mice had significantly higher bacterial burdens at day 21 and day 35 after infection compared to wild-type mice, demonstrating that B7-H1 plays an important role in immunity to Salmonella. B7-H1-deficient and wild-type mice both generated Salmonella-specific IgM and IgG2c antibody responses to infection and clonal expansion of endogenous and adoptively transferred Salmonella-specific CD4 T cells was similar in both groups. However, although Salmonella-specific IFN-γ producing Th1 CD4 T cells were generated in Salmonella-infected B7-H1-deficient mice, these cells did not expand to the level observed in wild-type mice. Furthermore, fewer multifunctional Th1 cells that simultaneously secreted IFN-γ, TNF-α, and IL-2 were detected in Salmonella-infected B7-H1-deficient mice. Together, these data demonstrate that B7-H1 is required for the generation of multifunctional Th1 responses and optimal protective immunity to primary Salmonella infection.
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影响因子：
32.4
作者：
Dong, HD;Zhu, GF;Chen, LP
通讯作者：
Chen, LP
鼠伤寒沙门氏菌通过穿透和破坏佩耶斑块的专门上皮细胞来引起鼠的感染。
影响因子：
15.3
作者：
Jones, Bradley D.;Ghori, Nafisa;Falkow, Stanley
通讯作者：
Falkow, Stanley
DOI：
10.4049/jimmunol.0900772
发表时间：
2009-07-15
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Griffin A;Baraho-Hassan D;McSorley SJ
通讯作者：
McSorley SJ
影响因子：
3.1
作者：
McSorley, SJ;Jenkins, MK
通讯作者：
Jenkins, MK
影响因子：
32.4
作者：
McSorley, SJ;Asch, S;Jenkins, MK
通讯作者：
Jenkins, MK