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      Intestinal lymphatic vasculature: structure, mechanisms and functions

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      Journal: Nature Reviews Gastroenterology & Hepatology
      Publisher: Springer Nature

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          Abstract

          The intestinal lymphatic vasculature has a range of functions, from maintenance of interstitial fluid balance to transport of antigens, cells, dietary lipids and fat-soluble vitamins. In this Review, Petrova and Bernier-Latmani provide an in-depth overview of intestinal lymphatics, including their roles in human diseases.

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          Regional specialization within the intestinal immune system.

          Allan M Mowat, William Agace (2014)
          The intestine represents the largest compartment of the immune system. It is continually exposed to antigens and immunomodulatory agents from the diet and the commensal microbiota, and it is the port of entry for many clinically important pathogens. Intestinal immune processes are also increasingly implicated in controlling disease development elsewhere in the body. In this Review, we detail the anatomical and physiological distinctions that are observed in the small and large intestines, and we suggest how these may account for the diversity in the immune apparatus that is seen throughout the intestine. We describe how the distribution of innate, adaptive and innate-like immune cells varies in different segments of the intestine and discuss the environmental factors that may influence this. Finally, we consider the implications of regional immune specialization for inflammatory disease in the intestine.
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            CCR7 governs skin dendritic cell migration under inflammatory and steady-state conditions.

            Lars Ohl, Mariette Mohaupt, Niklas Czeloth … (2004)
            The CC chemokine receptor CCR7 has been identified as a key regulator of homeostatic B and T cell trafficking to secondary lymphoid organs. Data presented here demonstrate that CCR7 is also an essential mediator for entry of both dermal and epidermal dendritic cells (DC) into the lymphatic vessels within the dermis while this receptor is dispensable for the mobilization of Langerhans cells from the epidermis to the dermis. Moreover, a distinct population of CD11c(+)MHCII(high) DC showing low expression of the costimulatory molecules CD40, CD80, and CD86 in wild-type animals was virtually absent in skin-draining lymph nodes of CCR7-deficient mice under steady-state conditions. We provide evidence that these cells represent a semimature population of DC that is capable of initiating T cell proliferation under conditions known to induce tolerance. Thus, our data identify CCR7 as a key regulator that governs trafficking of skin DC under both inflammatory and steady-state conditions.
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              Origin of the lamina propria dendritic cell network.

              Milena Bogunovic, Florent Ginhoux, Julie Helft … (2009)
              CX(3)CR1(+) and CD103(+) dendritic cells (DCs) in intestinal lamina propria play a key role in mucosal immunity. However, the origin and the developmental pathways that regulate their differentiation in the lamina propria remain unclear. We showed that monocytes gave rise exclusively to CD103(-)CX(3)CR1(+) lamina propria DCs under the control of macrophage-colony-stimulating factor receptor (M-CSFR) and Fms-like thyrosine kinase 3 (Flt3) ligands. In contrast, common DC progenitors (CDP) and pre-DCs, which give rise to lymphoid organ DCs but not to monocytes, differentiated exclusively into CD103(+)CX(3)CR1(-) lamina propria DCs under the control of Flt3 and granulocyte-macrophage-colony-stimulating factor receptor (GM-CSFR) ligands. CD103(+)CX(3)CR1(-) DCs but not CD103(-)CX(3)CR1(+) DCs in the lamina propria constitutively expressed CCR7 and were the first DCs to transport pathogenic Salmonella from the intestinal tract to the mesenteric lymph nodes. Altogether, these results underline the diverse origin of the lamina propria DC network and identify mucosal DCs that arise from pre-DCs as key sentinels of the gut immune system.
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                Author and article information

                Journal
                Title: Nature Reviews Gastroenterology & Hepatology
                Abbreviated Title: Nat Rev Gastroenterol Hepatol
                Publisher: Springer Nature
                ISSN (Print): 1759-5045
                ISSN (Electronic): 1759-5053
                Publication date Created: June 28 2017
                Publication date (Print): June 28 2017
                Volume:
                Issue:
                Article
                DOI: 10.1038/nrgastro.2017.79
                PubMed ID: 28655884
                SO-VID: 3b28ab7a-ae5a-4c9a-9ecb-d75f19a45cf8
                Copyright © © 2017
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