Saskia Ziegler's research while affiliated with Universität Heidelberg and other places

... The deficiency of CalDAG-GEFI in neutrophils has been associated with impaired slow rolling, adhesion, and directionality of migration [138][139][140]. Furthermore, despite the regulatory behavior of migration in immune cells, Rap1 signaling is also critical in modulating the Ca 2+ -dependent regulation of Toll-like receptor (TLR) signaling [141][142][143]. In another study, murine neutrophils lacking CalDAG-GEF1/Rap1 were deficient in firmly adhering to the stimulated endothelial venules. ...

... amiRs are synthetically produced constructs that contain a short RNA sequence complementary to the miRNA sequence, linked to a short DNA sequence (poly CT) that serves as vehicle and allows the transition through the cell membrane. Importantly, amiRs are fully O-methylated and thereby not stimulatory and the DNA part is PTO (phosphothioate) modified to gain enhanced stability (30) (Figure S1 in Supplementary Material). In the experimental setup, monocytes isolated from blood of healthy donors were stimulated the day after isolation with GM-CSF, IL-4, and R848 (TLR7/8 ligand) to induce R848-stimulated suppressive APC. ...

... 15 Of note, among detected cytokines upon LPS + Poly(I:C) or LPS + R848 treatment, the highest concentrations were detected for the cytokines IL-6, TNF-α and the Th1-polarizing cytokine IL-12p70. 15 In line with this, it was previously [16][17][18][19] Of note, by the combination of two different danger signals plus FVIII, even lower concentrations of the danger signals, in particular LPS, were required to induce a synergistic DC activation and subsequent T cell activation. While we used an LPS concentration of 0.1 µg/ mL in our previous studies, 8,9 10-to 100-fold lower concentrations were required as soon as LPS was combined with 0.1 µg/mL R848 or 0.5 µg/mL poly(I:C). ...

... Additionally, SpA binds the heavychain variable region of the B-cell receptor (BCR), initiating supra-clonal expansion and the subsequent apoptosis of B1 and marginal zone (MZ) B cells [18,19], thereby dampening the humoral response against staphylococcal antigens. Moreover, SpA cross-links BCRs to activate and promote the generation of IL-10-producing immunosuppressive B cells [20]. This mechanism strengthens SA's ability to evade humoral immune responses. ...

... CD5 expression on B cells is a common feature of both RA and CLL [166], CD5 expression correlates with RAG activity in B cells of people with autoimmune disease [167], and RAG is expressed in B cells in the RA synovium [168]. In RA, the appearance of rheumatoid factor (RF, an antibody to Fc-IgG) correlates with the hypogalactosylation of IgG, occuring roughly two years after the appearance of antibodies to citrullinated proteins, but two years before RA diagnosis [169]. ...

... This could enhance the anti-tumor immune response. Apoptotic cells, on the other hand, typically do not release HMGB1 and are "immunologically silent", in contrast to necrotic cells [271,272]. Upon the administration of DOX, metastatic human melanoma SK-MEL-24 and human colon cancer LS174T cells undergo senescence; however, the less-metastatic cell lines SK-MEL-28 and DLD-1 prefer apoptosis following drug treatment. The expression of HMGB1 was found to be persistent in senescent B16-F10, SK-MEL-24, and LS174T cells that had been treated with DOX. ...