Dr. Pier Luigi Meroni is a full professor of Rheumatology at the University of Milan; he has been Head of the Department of Rheumatology for 10 years and he is now Director of the Immunorheumatology Research Laboratory – IRCCS Istituto Auxologico Italiano.
His clinical and scientific works focus on autoimmune/rheumatic diseases, particularly on the pathogenic role of serum autoantibodies.
He has published more than 500 papers in peer-reviewed journals. He has authored and edited 7 books and written 47 book chapters. h-index: 70 (Scopus), 131 (TIS,Top_Italian_Scientists_Biomedical_Sciences) n.8
His editorial activity is characterized by his inclusion in the editorial board of several journals in the field of rheumatology and autoimmunity.
He organized the IVth International Congress on Antiphospholipid Antibodies (Sirmione 1990) and he was co-chairman of the Vth International Congress on Autoimmunity (Sorrento 2006) and of the 12th International Congress on Anti-phospholipid Antibodies (Firenze 2007).
Dr. Meroni received the Roussel Prize in 1997 (Rome) for the studies on the age-associated immune-deficit, the EULAR Prize in 2005 (Vienna) for the researches on the infectious etiology of antiphospholipid syndrome and the AESKU Prize for life contribution to autoimmunity (2014 Nice). He was nominated ACR Master in 2014.
He has been Chairman and then member of the IUIS/WHO/AF/CDC Committee for the standardization of diagnostic tests for rheumatic diseases, Italian Representative of EASI (European Autoimmunity Standardization Initiative), founder of the IFCC Working Group Harmonization Autoimmune Serology Testing and president of the FIRMA (Forum Interdisciplinare Ricerca Malattie Autoimmuni).
EDUCATION
Medicine University of Milan
Specialization in Allergy and Clinical Immunology, University of Milan
Specialization in Hematology, University of Modena
RESEARCH INTERESTS
Pathogenic mechanisms and biomarkers of systemic autoimmune rheumatic diseases
Anti-β2GPI IgG display a broad reactivity against different β2GPI domains beyond domain 1: results from the APS ACTION and multi-center Italian cohorts Claudia Grossi, Caterina Bodio, Suresh Kumar, Elisa Bison, Ricard Cervera, et al. Frontiers in Immunology, 2026 Background Anti-β2glycoprotein I (β2GPI) antibodies are the hallmark of the antiphospholipid syndrome (APS). β2GPI consists of five domains, DI-DV. While DI is the primary target, the clinical relevance of antibodies against other domains remains uncertain. We analyzed two large anti-β2GPI IgG positive cohorts, to investigate whether different domain binding affects anti-β2GPI IgG assay testing and APS diagnosis. Methods The presence of anti-DI and anti-DIV/DV antibodies (by chemiluminescence (CLIA) and in-house ELISA, respectively) was searched in an APS ACTION (n.191) and Italian validation (n.105) cohorts. In the latter, we detected anti-β2GPI IgG reactivity by four assays (in-house and commercial ELISA, CLIA, and fluorescence enzyme immunoassay), and used a modified anti-β2GPI IgG in-house ELISA with recombinant single-domain-lacking β2GPI variants to evaluate domain-dependent reactivity. Results We confirmed anti-DI, anti-DIV/DV β2GPI IgG direct reactivity in classified and non-classifiable APS in the two cohorts, and found anti-DI/anti-DIV/DV double negative (38/191, 29/105) and anti-DIV/DV single-positive (6/191, 9/105) samples. Anti-β2GPI IgG discordant samples by the four methods had the highest presence of anti-DIV/DV single-positives and anti-DI/anti-DIV/DV double-negatives, compared to four-method concordant samples: 16% vs 2% and 45% vs 11% (p <0.0001), respectively. The single-domain molecule-based assay showed that the APS serum samples depended mainly on DI, DV, and DII, slightly on DIV, and not at all on DIII. Conclusions Serum IgG from both classified and non-classifiable APS may react with other β2GPI domains than DI and DIV-V. Anti-β2GPI domain selectivity can explain discordant results among diagnostic assays.
Distinct Effects of Complement C4A and C4B Copy Numbers in Systemic Sclerosis Serological and Clinical Subtypes Javier Martínez‐López, Carlos Rangel‐Peláez, Inmaculada Rodriguez‐Martin, Alfredo Guillen‐Del‐Castillo, Carmen P Simeón‐Aznar, et al. Arthritis and Rheumatology, 2026 Objective Complement component 4 (C4), encoded by C4A and C4B within the major histocompatibility complex (MHC) on chromosome 6, regulates the immune response and clears immune complexes. The variable copy number (CN) of C4 genes and retroviral human endogenous retrovirus K (HERV‐K) element influence its function. Given the relationship of C4 CN with systemic sclerosis (SSc) risk, we assessed associations with SSc clinical and serologic subtypes. Methods We compared imputed C4 CNs across SSc subgroups (4,049 anticentromere positive [ACA + ]; 2,200 anti–topoisomerase I [ATA + ]; 577 anti‐RNA polymerase [ARA + ]; 1,078 triple‐negative [TN] patients; 6,295 limited cutaneous SSc [lcSSc]; and 2,946 diffuse cutaneous SSc [dcSSc]) and 17,991 controls. We evaluated associations with SSc subtypes, identifying C4 ‐independent HLA alleles. Results Lower C4 CN and higher HERV‐K CN were associated with increased risk in all SSc subgroups. ATA + patients showed the strongest association, particularly with C4A (odds ratio = 1.88), and differences in C4A CN association were more pronounced between autoantibody subgroups (ATA + vs ACA + , P = 4 × 10 −11 ) than between clinical subgroups (dcSSc vs lcSSc, P = 1 × 10 −4 ). In ACA + patients, only low C4B CN showed a significant association to SSc risk ( P = 1.23 × 10 −5 ). We also observed sex‐biased associations: dcSSc, ATA + , and ARA + male patients showed stronger effects for C4A and ACA + and lcSSc female patients for C4B . Finally, our results suggest that the HLA alleles associated with SSc subgroups are independent of C4 CN. Conclusion This study highlights distinct genetic contributions of C4A and C4B in SSc subtypes susceptibility. Our findings suggest that lower C4 CNs, particularly C4A , increase the risk of the severe dcSSc subtype, potentially through a mechanism involving immune complex clearance. image
Direct simulation of hypertensive stress on endothelial cells: a streamlined model of in-vitro-hypertension Elena Raschi, Caterina Bodio, Chiara Brullo, Gianfranco Parati, Pier Luigi Meroni, et al. Frontiers in Physiology, 2026 Hypertension stands as one of the most significant preventable risk factors for cardiovascular disease, which is the leading cause of mortality worldwide. There is a disturbing gap, in preclinical research, between simplified cell culture and complex in vivo models. To contribute to bridge this gap, we have developed a simplified but realistic in vitro dynamic model of hypertension allowing the discrimination between mechanical pressure effects and Angiotensin II’s pharmacological action. We utilized an advanced bioreactor system capable of producing adjustable flow rates to culture human umbilical vein endothelial cells (HUVEC). This system allows for the investigation of the possible effects of Angiotensin II and/or an increase in intraluminal pressure (via the Live-Pa pressure-actuation device) exerted directly upon the HUVEC monolayer without simulating transmural pressure. Key hypertension-associated inflammatory markers, such as NF-kB, p38MAPK, Interleukins (IL)-6/8, and Endothelin-1 (ET-1), were subsequently assessed. Angiotensin II induced HUVEC NF-kB and p38MAPK phosphorylation, and elevated IL-6 and ET-1 secretion, with a trend in IL-8 increase. Live-Pa alone enhanced NF-kB and p38MAPK and influenced cytokine/chemokine secretion. Combined stimuli significantly augmented the inflammatory parameters as compared to unstimulated cells, suggesting a synergistic effect between chemical and mechanical stimuli. Overall, these in vitro results demonstrate both key consistencies (e.g., NF-kB and p38MAPK activation) and specific distinctions (e.g., no significant IL-6 increase in Live-Pa-exposed versus control HUVEC) when compared to published data from hypertensive versus normotensive animal models. The proposed advanced in vitro model may successfully reproduce some features of vascular function in hypertension and simulate hemodynamic conditions by controlled flow with adjustable pressure parameters. Crucially, this system allows discrimination between mechanical blood pressure effects and Angiotensin II’s pharmacological action on the endothelium, paving the way for understanding pathophysiological mechanisms and developing new therapies. Established methods make it possible that studies on cultured endothelial cells will be better comparable to the results of in vivo studies, thus directly supporting the 3Rs framework—Replacement, Reduction, and Refinement—which is essential for high-standard and ethical research.
