Publications by authors named "H Lorenz"
Article Synopsis
- ENPP1/CD203a is an enzyme that breaks down ATP and other nucleotides, influencing purinergic signaling and immune responses.
- The study investigates ENPP1 expression on immune cells using new heavy-chain antibodies and finds high levels in specific cells like CD141 dendritic cells and natural killer cells, while most T cells and B cells show low expression.
- This detailed analysis of ENPP1 expression will aid in understanding its role in immune regulation and could help identify ENPP1-related conditions and tumors for targeted treatments.
Objective: The high potential of CD19.CAR-T cells to treat autoimmune diseases such as Systemic Sclerosis (SSc) supposedly relies on the disappearance of autoantibodies. Here we investigated effects of CAR-T cells on the innate immune system which is an important contributor to pathology in SSc.
View Article and Find Full Text PDFThe model advanced training regulations define the content of advanced training to achieve the qualification of medical specialist in internal medicine and rheumatology. There are currently no criteria for issuing the authorization in advanced training. This position paper describes the criteria proposed by the German Society for Rheumatology and Clinical Immunology (DGRh), which should be the foundation for the issuance of authorization for advanced training in the field of internal medicine and rheumatology and for the assessment of the duration.
View Article and Find Full Text PDFBackground And Purpose: Irwin tests are key preclinical study elements for characterising drug-induced neurological side effects. This multicentre study aimed to assess the robustness of Irwin tests across multinational sites during three stages of protocol harmonisation. The projects were part of the Enhanced Quality in Preclinical Data framework, aiming to increase success rates in transition from preclinical testing to clinical application.
View Article and Find Full Text PDFObjective: Previous technical limitations prevented the proof of Fcγ-receptor (FcγR)-activation by soluble immune complexes (sICs) in patients. FcγRIIIa (CD16) is a risk factor in rheumatoid arthritis (RA). We aimed at determining the presence of CD16-activating sICs in RA and control diseases.
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