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Dendritic cells infected with Listeria monocytogenes undergo a maturation response distinct from neighboring uninfected dendritic cells
Author(s) -
Cook Anne Stanner
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.675.20
Subject(s) - cd86 , cd40 , cd80 , listeria monocytogenes , dendritic cell , immune system , biology , priming (agriculture) , antigen , population , microbiology and biotechnology , intracellular parasite , antigen presenting cell , t cell , immunology , in vitro , cytotoxic t cell , bacteria , medicine , biochemistry , genetics , germination , botany , environmental health
Dendritic Cells (DC) are considered the sentinels of the immune system due to their ability to activate naïve T‐cells, which is dependent on their maturation state. Listeria monocytogenes ( L.m .) induces a maturation response marked by costimulatory molecules, cytokines, and T cell priming in a population DC if bacteria enter the cytosol. However, microscopic examination of L.m.‐ infected DC both in vitro and in vivo revealed that a larger percentage of uninfected DC expressed CD86 than infected DC. Two color flow cytometric analysis of fluorescently labeled L.m. vs. intracellular IL‐12 confirmed that the majority of infected cells failed to express IL‐12 while the majority of uninfected cells produced IL‐12. However, infected DC expressed IL‐6, TNFα, and CD40, while uninfected DC expressed CD86, CD80, and IL‐12. Based on these findings, we hypothesize that Lm infected DC undergo a different maturation response than neighboring uninfected DC. Consistent with this hypothesis, we have shown that uninfected DC can be stimulated to produce IL‐12 and CD86 when treated with supernatant from Lm ‐treated DC. Additionally, uninfected DC required less antigen to stimulate naïve CD 8+ T cells than infected DC. These data illustrate the cooperative nature of the immune response to a bacterial infection. Research supported by NIH/NIAD grant 1R01AI057770‐01A1