To the top

Page Manager: Webmaster
Last update: 9/11/2012 3:13 PM

Tell a friend about this page
Print version

MyD88 Signaling Regulates… - University of Gothenburg, Sweden Till startsida
To content Read more about how we use cookies on

Contact form


Note! If you want an answer on a question you must specify your email address

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

Journal article
Authors K. Hagerbrand
Jessica Westlund
Ulf Yrlid
W. Agace
B. Johansson-Lindbom
Published in Journal of Immunology
Volume 195
Issue 6
Pages 2888-2899
ISSN 0022-1767
Publication year 2015
Published at Institute of Biomedicine, Department of Microbiology and Immunology
Pages 2888-2899
Language en
Subject categories Immunology in the medical area


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.

Page Manager: Webmaster|Last update: 9/11/2012

The University of Gothenburg uses cookies to provide you with the best possible user experience. By continuing on this website, you approve of our use of cookies.  What are cookies?

Denna text är utskriven från följande webbsida:
Utskriftsdatum: 2019-11-11