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      Transcriptional profiling of stroma from inflamed and resting lymph nodes defines immunological hallmarks

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          Abstract

          Lymph node stromal cells (LNSCs) closely regulate immunity and self-tolerance, yet key aspects of their biology remain poorly illuminated. Comparative transcriptomic analyses of murine LNSC subsets revealed expression of important immune mediators, growth factors, and novel structural components. Pairwise analyses of ligands and cognate receptors across hematopoietic and stromal subsets suggested a complex web of cross-talk. Compared with skin and thymic fibroblasts, fibroblastic reticular cells (FRCs) were enriched in genes relevant to cytokine signaling. LNSCs from inflamed lymph nodes upregulated acute phase response genes, chemokines, and antigen presentation genes. Poorly studied podoplanin −CD31 − LNSCs showed similarities to FRCs, but lacked IL-7 expression, and were identified as myofibroblastic integrin α7 + pericytes. Together these data comprehensively describe the transcriptional characteristics of LNSC subsets.

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          Fibroblastic reticular cells in lymph nodes regulate the homeostasis of naive T cells.

          Alexander Link, Tobias K. Vogt, Stéphanie Favre … (2007)
          Interleukin 7 is essential for the survival of naive T lymphocytes. Despite its importance, its cellular source in the periphery remains poorly defined. Here we report a critical function for lymph node access in T cell homeostasis and identify T zone fibroblastic reticular cells in these organs as the main source of interleukin 7. In vitro, T zone fibroblastic reticular cells were able to prevent the death of naive T lymphocytes but not of B lymphocytes by secreting interleukin 7 and the CCR7 ligand CCL19. Using gene-targeted mice, we demonstrate a nonredundant function for CCL19 in T cell homeostasis. Our data suggest that lymph nodes and T zone fibroblastic reticular cells have a key function in naive CD4(+) and CD8(+) T cell homeostasis by providing a limited reservoir of survival factors.
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            LPS-TLR4 Signaling to IRF-3/7 and NF-κB Involves the Toll Adapters TRAM and TRIF

            Katherine A Fitzgerald, Daniel C. Rowe, Betsy J Barnes … (2003)
            Toll–IL-1–resistance (TIR) domain–containing adaptor-inducing IFN-β (TRIF)–related adaptor molecule (TRAM) is the fourth TIR domain–containing adaptor protein to be described that participates in Toll receptor signaling. Like TRIF, TRAM activates interferon regulatory factor (IRF)-3, IRF-7, and NF-κB-dependent signaling pathways. Toll-like receptor (TLR)3 and 4 activate these pathways to induce IFN-α/β, regulated on activation, normal T cell expressed and secreted (RANTES), and γ interferon–inducible protein 10 (IP-10) expression independently of the adaptor protein myeloid differentiation factor 88 (MyD88). Dominant negative and siRNA studies performed here demonstrate that TRIF functions downstream of both the TLR3 (dsRNA) and TLR4 (LPS) signaling pathways, whereas the function of TRAM is restricted to the TLR4 pathway. TRAM interacts with TRIF, MyD88 adaptor–like protein (Mal)/TIRAP, and TLR4 but not with TLR3. These studies suggest that TRIF and TRAM both function in LPS-TLR4 signaling to regulate the MyD88-independent pathway during the innate immune response to LPS.
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              The conduit system transports soluble antigens from the afferent lymph to resident dendritic cells in the T cell area of the lymph node.

              Michael Sixt, Nobuo Kanazawa, Manuel Selg … (2005)
              Resident dendritic cells (DC) within the T cell area of the lymph node take up soluble antigens that enter via the afferent lymphatics before antigen carrying DC arrive from the periphery. The reticular network within the lymph node is a conduit system forming the infrastructure for the fast delivery of soluble substances from the afferent lymph to the lumen of high endothelial venules (HEVs). Using high-resolution light microscopy and 3D reconstruction, we show here that these conduits are unique basement membrane-like structures ensheathed by fibroblastic reticular cells with occasional resident DC embedded within this cell layer. Conduit-associated DC are capable of taking up and processing soluble antigens transported within the conduits, whereas immigrated mature DC occur remote from the reticular fibers. The conduit system is, therefore, not a closed compartment that shuttles substances through the lymph node but represents the morphological equivalent to the filtering function of the lymph node.
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                Author and article information

                Journal
                Journal ID (nlm-journal-id): 100941354
                Journal ID (pubmed-jr-id): 21750
                Journal ID (nlm-ta): Nat Immunol
                Journal ID (iso-abbrev): Nat. Immunol.
                Title: Nature immunology
                ISSN (Print): 1529-2908
                ISSN (Electronic): 1529-2916
                Publication date Nihms-submitted: 25 February 2012
                Publication date (Electronic): 01 April 2012
                Publication date PMC-release: 01 November 2012
                Volume: 13
                Issue: 5
                Pages: 499-510
                Affiliations
                [1 ]Department of Cancer Immunology and AIDS, Dana Farber Cancer Institute, Boston, MA 02115, USA
                [2 ]Division of Medical Sciences, Harvard Medical School, Boston, MA 02115, USA
                [3 ]School of Engineering and Applied Sciences, Harvard University, Cambridge, MA 02138, USA
                [4 ]The Immune Disease Institute and Program in Cellular and Molecular Medicine, Children’s Hospital, Department of Pediatrics and Department of Pathology, Harvard Medical School, Boston, MA, USA
                [5 ]Brigham and Women’s Hospital, Boston MA 02115, USA
                [6 ]Department of Medicine, Division of Rheumatology, Immunology and Allergy, Harvard Medical School, Boston, MA 02115, USA
                [7 ]Department of Microbiology and Immunobiology, Harvard Medical School, Boston, MA 02115, USA
                Author notes
                Correspondence: Shannon J. Turley shannon_turley@ 123456dfci.harvard.edu Tel: 617.632.4990 Fax: 617.582.7999
                [‡]

                These authors contributed equally to this work.

                Article
                Manuscript ID: NIHMS357437
                DOI: 10.1038/ni.2262
                PMC ID: 3366863
                PubMed ID: 22466668
                SO-VID: 89943c18-4a59-40e1-86c5-c26d1d031502
                License:

                Users may view, print, copy, download and text and data- mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use: http://www.nature.com/authors/editorial_policies/license.html#terms

                History
                Funding
                Funded by: National Institute of General Medical Sciences : NIGMS
                Award ID: R01 GM038903-25 || GM
                Categories
                Subject: Article

                ScienceOpen disciplines: Immunology
                Data availability:
                ScienceOpen disciplines: Immunology

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