Alejandro Gómez-Gómez MD PhD
Alejandro is a rheumatologist at Hospital Vall d’Hebron in Barcelona. His research focuses on Sjögren’s disease and other immune-mediated diseases using multi-omics approaches. He is also interested in studying inflammatory uveitis and recently obtained his PhD with a thesis on the immunosuppressive treatment of non-infectious uveitis. He is a member of the Spanish Society of Rheumatology and the EMEUNET Visibility & Global Affairs sub-committee.
| Oral 0832 | Saturday, 16.11.23 15.00 Abstracts: Pediatric Rheumatology – Basic Science Presenting author: S McCuaig (USA) Title: Spatial Transcriptomic Assessment of Histologically Damaged and Unaffected Glomeruli in Class III Pediatric Lupus Nephritis Reveals Distinct Transcriptional Programs  This study used spatial transcriptomics to examine differences between histologically damaged and unaffected glomeruli in pediatric lupus nephritis (pSLE). Damaged glomeruli showed distinct transcriptional signatures, with increased expression of markers like CD68, C5AR1, and ITGA11, suggesting roles in complement activation and fibrosis. Remarkably, IFN gene response does not associate with local glomerular damage in pSLE. These findings highlight potential biomarkers and therapeutic targets for treating lupus nephritis. |
| Oral 1645 | Sunday, 17.11.24 09.00 Plenary II Presenting author: M Casal-Dominguez (UK) Title: Antisynthetase Autoantibodies Disrupt the Function of Their Target Aminoacyl-tRNA Synthetases in Muscle Cells This study examined whether antisynthetase syndrome autoantibodies impair the function of aminoacyl-tRNA synthetases. RNA sequencing of muscle biopsies from antisynthestase (AS) patients revealed an AS-specific gene set, overexpressed in patients with anti-Jo1 autoantibodies. Internalization of anti-Jo1 antibodies into muscle cells activated the NFKB pathway and increased expression of inflammation-related genes, similar to the effects of histidinol, an enzyme inhibitor. These findings suggest AS autoantibodies disrupt enzyme function and trigger inflammatory pathways. |
| Oral 2530 | Monday, 18.11.24 09.00 Plenary III Presenting author: TI Papadimitriou (Netherlands) Title: Single-cell Multi-omics Analysis of Reactive Lymph Nodes, Affected Tissues, and Blood Reveals a Naive-like CD4+TRAIL+ T Cell Population That Differentially Directs Effector Anti-nuclear Antigen Reactive Responses in Patients with Sjogren’s Syndrome and Systemic Sclerosis This study explores the mechanisms underlying distinct clinical manifestations of Sjögren’s syndrome (SjS) and systemic sclerosis (SSc) by identifying autoreactive T and B cells. Expanded ANA-reactive T-cell clones were found in both diseases, but SjS showed increased SSA/B-reactive Th2/Th17 populations and effector T cells, while SSc had predominantly Scl70-reactive CD4+ TRAIL+ T cells. Targeting this immune-regulatory axis may aid in developing tolerogenic treatments for systemic autoimmune diseases. |
| Oral 2536 | Monday, 18.11.23 13.00 Abstracts: Genetics, Genomics & Proteomics Presenting author: K Bu (USA) Title: Trans-Disease Microbial Biomarkers of Protection and Pathogenesis in Autoimmune Conditions: Results from the AMP AIM Consortium This study analyzed the gut microbiomes of 126 patients with six autoimmune and immune-mediated diseases (AIMDs) compared to healthy controls. AIMD patients had reduced microbial diversity and distinct compositions, with specific taxa enriched in each disease. P. faecium, a short-chain fatty acid producer, was depleted across all AIMDs and negatively correlated with inflammation. These findings suggest that while pathogenic microbes are disease-specific, protective mechanisms may be shared across AIMDs. |
| Oral 2593 | Monday, 18.11.24 15.00 Abstracts: Cytokines & Cell Trafficking Presenting author: M Bollmann (Sweden) Title: A Long-term Synovial Tissue 3D Model Incorporating Fibroblasts, Macrophages, Endothelial Cells, and Other Immune Cells Such as Innate Lymphoid Cells Enables Animal Model-Independent Rheumatoid Arthritis Research This study presents two long-term 3D culture systems that replicate rheumatoid arthritis (RA) synovial tissue, incorporating fibroblasts, macrophages, endothelial cells, and innate lymphoid cells. The models mimic synovial architecture and inflammatory responses, with different markers expressed. These systems provide a physiologically relevant platform for studying RA pathophysiology, cell interactions, and testing therapies, offering an alternative to traditional 2D cultures and animal models. |