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MyD88 Signaling Regulates Steady-State Migration of Intestinal CD103(+) Dendritic Cells Independently of TNF-alpha and the Gut Microbiota

Artikel i vetenskaplig tidskrift
Författare K. Hagerbrand
Jessica Westlund
Ulf Yrlid
W. Agace
B. Johansson-Lindbom
Publicerad i Journal of Immunology
Volym 195
Nummer/häfte 6
Sidor 2888-2899
ISSN 0022-1767
Publiceringsår 2015
Publicerad vid Institutionen för biomedicin, avdelningen för mikrobiologi och immunologi
Sidor 2888-2899
Språk en
Länkar dx.doi.org/10.4049/jimmunol.1500210
Ämnesord RECEPTOR-DEFICIENT MICE, MESENTERIC LYMPH-NODES, T-CELL, LAMINA PROPRIA, AFFERENT LYMPH, RETINOIC-ACID, IN-VIVO, EPITHELIAL-CELLS, PEYERS-PATCHES, IMMUNITY, Immunology
Ämneskategorier Immunologi inom det medicinska området

Sammanfattning

Intestinal homeostasis and induction of systemic tolerance to fed Ags (i.e., oral tolerance) rely on the steady-state migration of small intestinal lamina propria dendritic cells (DCs) into draining mesenteric lymph nodes (MLN). The majority of these migratory DCs express the a integrin chain CD103, and in this study we demonstrate that the steady-state mobilization of CD103(+) DCs into the MLN is in part governed by the IL-1R family/TLR signaling adaptor molecule MyD88. Similar to mice with complete MyD88 deficiency, specific deletion of MyD88 in DCs resulted in a 50-60% reduction in short-term accumulation of both CD103(+)CD11b(+) and CD103(+)CD11b(-) DCs in the MLN. DC migration was independent of caspase-1, which is responsible for the inflammasome-dependent proteolytic activation of IL-1 cytokine family members, and was not affected by treatment with broad-spectrum antibiotics. Consistent with the latter finding, the proportion and phenotypic composition of DCs were similar in mesenteric lymph from germ-free and conventionally housed mice. Although TNF-alpha was required for CD103(+) DC migration to the MLN after oral administration of the TLR7 agonist R848, it was not required for the steady-state migration of these cells. Similarly, TLR signaling through the adaptor molecule Toll/IL-1R domain-containing adapter inducing IFN-beta and downstream production of type I IFN were not required for steady-state CD103(+) DC migration. Taken together, our results demonstrate that MyD88 signaling in DCs, independently of the microbiota and TNF-alpha, is required for optimal steady-state migration of small intestinal lamina propria CD103(+) DCs into the MLN.

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