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- W4313404877 abstract "Abstract A major function of the microbiota is to shield the host from infection with pathogens via a process called colonization resistance. High affinity, T cell-dependent antibodies, produced through interaction between CD4 T follicular helper (Tfh) cells and germinal center (GC) B cells, can modulate gut microbiota diversity and function. We discovered that mice lacking maternal antibodies display increased levels of Tfh and GC B cells in gut draining lymphoid tissues such at the mesenteric lymph nodes and Peyer’s patches. This response is seen in the context of colonization by microbes as germ-free mice lacking maternal antibodies do not show increased Tfh and GC B cell responses. Given the importance of Tfh cells and TD antibody responses in regulating host-microbe interactions, we tested whether the elevation in Tfh and GC B cells seen in maternal antibody deficient pups alter susceptibility to colonization by the pathogen Salmonella typhimurium. We infected maternal antibody sufficient and deficient pups with the model pathogen Salmonella typhimurium via oral gavage. To block the Tfh and GC B cell response, we treated half of the pups from each group with anti-inducible T cell co-stimulator ligand (aICOSL) while the other half received an isotype control antibody. We found no difference in Salmonella typhimurium burden in the spleen, liver or cecum between maternal antibody sufficient or deficient pups treated aICOSL or isotype control antibody. Taken together, our data suggest that maternal antibodies and the subsequent rise in Tfh and GC B cells do not alter susceptibility to Salmonella typhimurium colonization later in life. Supported by AAI Careers in Immunology Fellowship" @default.
- W4313404877 created "2023-01-06" @default.
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- W4313404877 date "2022-05-01" @default.
- W4313404877 modified "2023-10-02" @default.
- W4313404877 title "Understanding the role of maternal antibodies on protection from enteric pathogens" @default.
- W4313404877 doi "https://doi.org/10.4049/jimmunol.208.supp.59.11" @default.
- W4313404877 hasPublicationYear "2022" @default.
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