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Max Löhning

Researcher at Charité

Publications -  88
Citations -  9343

Max Löhning is an academic researcher from Charité. The author has contributed to research in topics: Cytotoxic T cell & Immune system. The author has an hindex of 41, co-authored 72 publications receiving 8560 citations. Previous affiliations of Max Löhning include Leibniz Association & University of Zurich.

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The alarmin IL-33 promotes regulatory T-cell function in the intestine

TL;DR: It is shown in mice that the IL-33 receptor ST2 is preferentially expressed on colonic Treg cells, where it promotes Treg function and adaptation to the inflammatory environment, and suggests that the balance between IL- 33 and IL-23 may be a key controller of intestinal immune responses.
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P- and E-selectin mediate recruitment of T-helper-1 but not T-helper-2 cells into inflamed tissues

TL;DR: It is shown that Th1 cells, but not Th2 cells, are able to bind to P- selectin and E-selectin, indicating that selective recruitment is an additional level of regulation for both effector function profile and character of a local immune response.
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Stat6-independent GATA-3 autoactivation directs IL-4-independent Th2 development and commitment.

TL;DR: Introducing GATA-3 into Stat6-deficient T cells completely restored Th2 development, inducing c-Maf, Th2-specific DNase I hypersensitive sites in the IL-4 locus, and Th2 cytokine expression and creating a feedback pathway stabilizing Th2 commitment.
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T1/ST2 is preferentially expressed on murine Th2 cells, independent of interleukin 4, interleukin 5, and interleukin 10, and important for Th2 effector function

TL;DR: Potential target genes preferentially expressed in Th2 cells, expressing interleukin (IL)-4, IL-5, and/or IL-10, but not interferon-gamma are identified and one such gene, T1/ST2, is expressed stably on both Th2 clones and Th2-polarized cells activated in vivo or in vitro.
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Eosinophils are required for the maintenance of plasma cells in the bone marrow

TL;DR: It is demonstrated that bone marrow eosinophils localized together with plasma cells and were the key providers of plasma cell survival factors and depletion of eosInophils induced apoptosis in long-lived bone marrow plasma cells.