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Project areas  / Project area A

Project area A: Innate Immunity and accessory cells


Area A is devoted to basic research addressing cellular mechanisms in Innate Immunity, thereby focusing on neutrophils, dendritic cells, mast cells, natural killer cells, and thrombocytes, as well as on microbial modifiers of Innate Immunity and their respective receptors and receptor-related molecules.


  • Project A03 (Peschel/Autenrieth) analyzes the molecules involved in the immunomodulatory activities of S. aureus, in particular those of community-associated methicillin-resistant S. aureus (CA-MRSA). These are mediated by phenol-soluble modulin (PSM) peptide toxins, which interact with neutrophils via the formyl peptide receptor 2 (FPR2), a G-protein coupled receptor. The in vivo roles of FPR2 and its agonists/antagonists in connecting innate and adaptive immune responses, the impact of PSMs on TLR2 ligands, and the in vivo relevance of PSM-modulated DCs in mouse models will be elucidated.

  • Project A06 (Biedermann) investigates the therapeutic potential of IgE-activated Mast cells (MC) for tumor immunotherapy. To this end, interactions between MCs and myeloid derived suppressor cells (MDSCs) and consequences for T-cell responses will be characterized both in vitro and in vivo. Screening assays will be used to detect tumor antigens that are prone to elicit IgE-production in order to identify therapeutic targets. Moreover, using our in vivo melanoma models, including MC-deficient mice, MC-specific activation by IgE and the interplay of MCs and MDSCs in anti-tumor immune responses will be elucidated.



  • Project A07 (Salih/Kopp) has demonstrated that both platelet-derived soluble factors such as TGF-β as well as transfer of platelet membrane molecules such as MHC class I and GITRL to cancer cells contribute to the escape of malignant cells from NK anti-tumor immunity. Now, several other immunoregulatory molecule systems for which an expression in platelets has been observed in our antecedent studies (e.g., OX40/OX40L, RANK/RANKL, RANTES, etc.) will be characterized regarding both their platelet and immune modifying properties in the upcoming funding period. These investigations serve to further characterize the basic mechanisms and immunomodulatory molecules that influence platelet-tumor-NK cell interaction.



  • Inflammatory bowel disease is the subject of our project A13, which is led by Julia Frick, who was recently appointed W2 professor. In previous work it was shown that the structure of LPS of commensal bacteria may determine whether a strain induces or prevents intestinal inflammation. Thus, a single lipid A fatty acid in the LPS molecule may account for the ability of E. coli to promote colitis. Now we will focus on LPS of commensal bacteria as a compound for prevention of inflammatory bowel disease (IBD) and the immunological mechanisms mediating the effects of these compounds.

  • Project, A14, is led by Dominik Hartl, who recently (2010) arrived from the LMU Munich. This project focuses on another important microbial polysaccharide, chitin, an essential component of exoskeletons of fungi, parasites and insects. Recent studies provided evidence that humans express a chitinase-like protein called YKL-40 (chitinase-3-like protein-1 (CHI3L1). The functional role of YKL-40 in inflammation and immunity is poorly defined. Based on preliminary studies from this group it is hypothesized that YKL-40 modulates immune responses through a novel innate/inflammasome-mediated anti-apoptotic pathway which will now be elucidated.



  • We are pleased to have recruited Alexander Weber from the DKFZ in Heidelberg as a new Junior Professor for Innate Immunity. Alexander Weber is the PI for project A15, which aims at analyzing the function of mutations and SNPs in molecules involved in TLR signaling such as MyD88 and IRAK. A specific hot-spot mutation in MyD88 has recently been reported in many different types of B cell malignancies, in particular diffuse large B-cell lymphoma (DLBCL, 30% of cases), mucosa-associated lymphoid tissue lymphoma (MALT, 10%), and chronic lymphocytic leukemia (CLL, >10%) and Waldenström macroglobulinemia (90%). Thus, this mutation (L265P) is thought to be causative in sustaining tumor cell proliferation. For this reason, targeted IRAK kinase inhibition will now be studied in molecular detail and in terms of therapeutic application. At the same time, this tumor-specific mutation may represent a suitable target for peptide-based T cell-mediated immunotherapy. This project thus nicely links innate immune signaling (area A) with oncogenesis mechanisms and a concrete immunotherapeutic approach (area C).





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