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Early Life Programming of Mesenteric Lymph Node Stromal Cell Identity by the Lymphotoxin Pathway Regulates Mucosal Immune Responses in the Adult

ABSTRACT: Early Life Programming of Mesenteric Lymph Node Stromal Cell Identity by the Lymphotoxin Pathway Regulates Mucosal Immune Responses in the Adult

PROVIDER: PRJNA575894 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10233179.fastq.gz	Fastqsanger.gz
	SRR10233180.fastq.gz	Fastqsanger.gz
	SRR10233181.fastq.gz	Fastqsanger.gz
	SRR10233182.fastq.gz	Fastqsanger.gz
	SRR10233183.fastq.gz	Fastqsanger.gz

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Early Life Programming of Mesenteric Lymph Node Stromal Cell Identity by the Lymphotoxin Pathway Regulates Mucosal Immune Responses in the Adult (Stromal cells)

Project description:Early Life Programming of Mesenteric Lymph Node Stromal Cell Identity by the Lymphotoxin Pathway Regulates Mucosal Immune Responses in the Adult (Stromal cells)

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Early Life Programming of Mesenteric Lymph Node Stromal Cell Identity by the Lymphotoxin Pathway Regulates Mucosal Immune Responses in the Adult (B cells)

Project description:Early Life Programming of Mesenteric Lymph Node Stromal Cell Identity by the Lymphotoxin Pathway Regulates Mucosal Immune Responses in the Adult (B cells)

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Early Life Programming of Mesenteric Lymph Node Stromal Cell Identity by the Lymphotoxin Pathway Regulates Mucosal Immune Responses in the Adult (Stromal cells)

Project description:Redundant mechanisms support IgA responses to intestinal antigens. These include multiple priming sites (mesenteric lymph nodes (MLN), Peyer's patches and isolated lymphoid follicles) and various cytokines that promote class switch to IgA, even in the absence of T cells. In spite of these back-up mechanisms, vaccination against enteric pathogens such as Rotavirus has limited success in some populations.Genetic and environmental signals experienced during early life are known to influence mucosal immunity, yet the mechanisms for how these exposures operate remain unclear. Here we used Rotavirus infection to follow antigen-specific IgA responses through time and in different gut compartments. Using genetic and pharmacological approaches, we tested the role of a pathway known to support IgA responses (Lymphotoxin - LT) at different developmental stages. We found that LT-beta receptor (LTβR) signalling in early life programs intestinal IgA responses in adulthood by affecting antibody class switch recombination to IgA and subsequent generation of IgA antibody-secreting cells within an intact MLN. In addition, early life LTβR signalling dictates the phenotype and function of MLN stromal cells in order to support IgA responses in the adult. Collectively, our studies uncover new mechanistic insights into how early life LTβR signalling impacts mucosal immune responses during adulthood.

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Early Life Programming of Mesenteric Lymph Node Stromal Cell Identity by the Lymphotoxin Pathway Regulates Mucosal Immune Responses in the Adult (B cells)

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Single cell sequencing of the effects of blocking lymphotoxin alpha in the mesenteric lymph node and spleen

Project description:TNFDARE+/- mice develop TNF-driven transmural ileitis and mesenteric inflammation, and lose body mass, reminiscent of human Crohn’s disease. Here, we report that B cells regulate body mass and intestinal permeability during ileitis in a manner that is linked to lymphotoxin (LT)-a but not LTb, whereas B cell LTab2 promoted mesenteric TLS that suppressed lymphatic outflow. Using genetic approaches and neutralizing reagents, we connect LTa3, a ligand for TNFRs, expressed by activated follicular B cells to their appearance in draining lymph nodes and the generation or persistence of IgA+ ileal plasma cells. Some of the same B cells also expressed TNF. Opposite to LTa, expression of TNF by B cells was disadvantageous to the development of IgA+ ileal plasma cells, suggesting counterbalancing interplay between LTa3 and TNF in ileitis. These data highlight a multi-faceted role of B cells in ileitis that includes an unexpected role for B cell-derived LTa3 in the maintenance of body weight.

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