Journal
JOURNAL OF IMMUNOLOGY
Volume 180, Issue 11, Pages 7553-7557Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.180.11.7553
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- NICHD NIH HHS [K08 HD051584-01, K08 HD051584, K08HD51584, K08 HD051584-04, K08 HD051584-02, K08 HD051584-03] Funding Source: Medline
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Infection with attenuated Listeria monocytogenes (Lm) is a robust in vivo model for examining how Ag-specific T cells are primed, and subsequent challenge with virulent Lm allows for the protective effects of T cell priming to be quantified. Herein, we investigated the role of programmed death ligand 1 (PDL-1) in T cell priming and immunity conferred after primary infection with Lm Delta actA followed by virulent Lm challenge. In striking contrast to the inhibitory role of PDL-1 on T cell immunity in other infection models, marked reductions in the magnitude of T cell expansion and the kinetics of T cell proliferation were observed with PDL-1 blockade after primary Lm AactA infection. More importantly, PDL-1 blockade beginning before primary infection and maintained throughout the experiment resulted in delayed bacterial clearance and T cell expansion after secondary challenge with virulent Lm. These results indicate that for immunity to intracellular bacterial infection, PDL-1 plays an important stimulatory role for priming and expansion of protective T cells.
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