Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.07.21.214809v1?rss=1 Authors: Christian, D. A., Adams, T. A., Smith, T. E., Shallberg, L. A., Theisen, D. J., Phan, A. T., Abraha, M., Perry, J., Ruthel, G., Clark, J. T., Murphy, K. M., Kedl, R. M., Hunter, C. A. Abstract: The omentum in the peritoneal cavity contains fat associated lymphoid clusters (FALCs) whose role in the response to microbial challenge are poorly understood. After intraperitoneal immunization with Toxoplasma gondii, type I dendritic cells (cDC1) were critical to induce innate sources of IFN-{gamma} required to recruit monocytes to the FALCs. The migration of infected peritoneal macrophages into T and B cell rich areas of the FALCs allowed the TCR-induced activation of parasite-specific T cells. Unexpectedly, cDC1 were not required for T cell priming but rather supported the expansion of parasite-specific CD8+ T cells. An agent-based mathematical model predicted that the lack of cDC1 would impact the early proliferative burst, and we confirmed that cDC1 were required for optimal T cell expression of nutrient uptake receptors and cell survival. These studies highlight that cDC1 in the FALCs have distinct roles in the co-ordination of the innate and adaptive responses to microbial challenge. Copy rights belong to original authors. Visit the link for more info