@article{MilanezAlmeidaUlasPasztoietal.2015, author = {Milanez-Almeida, P. and Ulas, T. and Pasztoi, M. and Glage, S. and Schughart, K. and Lutz, M. B. and Schultze, J. L. and Huehn, J.}, title = {CD11b\(^{+}\)Ly6C\(^{++}\)Ly6G\(^{-}\) cells with suppressive activity towards T cells accumulate in lungs of influenza A virus-infected mice}, series = {European Journal of Microbiology and Immunology}, volume = {5}, journal = {European Journal of Microbiology and Immunology}, number = {4}, doi = {10.1556/1886.2015.00038}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-149583}, pages = {246-255}, year = {2015}, abstract = {Influenza A virus (IAV) infection causes an acute respiratory disease characterized by a strong inflammatory immune response and severe immunopathology. Proinflammatory mechanisms are well described in the murine IAV infection model, but less is known about the mechanisms leading to the resolution of inflammation. Here, we analyzed the contribution of CD11b\(^{+}\)Ly6C\(^{++}\)Ly6G\(^{-}\) cells to this process. An accumulation of CD11b\(^{+}\)Ly6C\(^{++}\)Ly6G\(^{-}\) cells within the lungs was observed during the course of IAV infection. Phenotypic characterization of these CD11b\(^{+}\)Ly6C\(^{++}\)Ly6G\(^{-}\) cells by flow cytometry and RNA-Seq revealed an activated phenotype showing both pro- and anti-inflammatory features, including the expression of inducible nitric oxide synthase (iNOS) by a fraction of cells in an IFN-γ-dependent manner. Moreover, CD11b\(^{+}\)Ly6C\(^{++}\)Ly6G\(^{-}\) cells isolated from lungs of IAV-infected animals displayed suppressive activity when tested in vitro, and iNOS inhibitors could abrogate this suppressive activity. Collectively, our data suggest that during IAV infection, CD11b\(^{+}\)Ly6C\(^{++}\)Ly6G\(^{-}\) cells acquire immunoregulatory function, which might contribute to the prevention of pathology during this life-threatening disease.}, language = {en} } @article{ShaikhVargasMokhtarietal.2021, author = {Shaikh, Haroon and Vargas, Juan Gamboa and Mokhtari, Zeinab and Jarick, Katja J. and Ulbrich, Maria and Mosca, Josefina Pe{\~n}a and Viera, Estibaliz Arellano and Graf, Caroline and Le, Duc-Dung and Heinze, Katrin G. and B{\"u}ttner-Herold, Maike and Rosenwald, Andreas and Pezoldt, Joern and Huehn, Jochen and Beilhack, Andreas}, title = {Mesenteric Lymph Node Transplantation in Mice to Study Immune Responses of the Gastrointestinal Tract}, series = {Frontiers in Immunology}, volume = {12}, journal = {Frontiers in Immunology}, issn = {1664-3224}, doi = {10.3389/fimmu.2021.689896}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-244869}, year = {2021}, abstract = {Mesenteric lymph nodes (mLNs) are sentinel sites of enteral immunosurveillance and immune homeostasis. Immune cells from the gastrointestinal tract (GIT) are constantly recruited to the mLNs in steady-state and under inflammatory conditions resulting in the induction of tolerance and immune cells activation, respectively. Surgical dissection and transplantation of lymph nodes (LN) is a technique that has supported seminal work to study LN function and is useful to investigate resident stromal and endothelial cell biology and their cellular interactions in experimental disease models. Here, we provide a detailed protocol of syngeneic mLN transplantation and report assays to analyze effective mLN engraftment in congenic recipients. Transplanted mLNs allow to study T cell activation and proliferation in preclinical mouse models. Donor mLNs proved viable and functional after surgical transplantation and regenerated blood and lymphatic vessels. Immune cells from the host completely colonized the transplanted mLNs within 7-8 weeks after the surgical intervention. After allogeneic hematopoietic cell transplantation (allo-HCT), adoptively transferred allogeneic CD4+ T cells from FVB/N (H-2q) mice homed to the transplanted mLNs in C57BL/6 (H-2b) recipients during the initiation phase of acute graft-versus-host disease (aGvHD). These CD4+ T cells retained full proliferative capacity and upregulated effector and gut homing molecules comparable to those in mLNs from unmanipulated wild-type recipients. Wild type mLNs transplanted into MHCII deficient syngeneic hosts sufficed to activate alloreactive T cells upon allogeneic hematopoietic cell transplantation, even in the absence of MHCII+ CD11c+ myeloid cells. These data support that orthotopically transplanted mLNs maintain physiological functions after transplantation. The technique of LN transplantation can be applied to study migratory and resident cell compartment interactions in mLNs as well as immune reactions from and to the gut under inflammatory and non-inflammatory conditions.}, language = {en} }