PB1371 - Positivity for Antiphospholipid Antibodies is Associated with Dysregulation of Circulating T Follicular Cells, but not B cells, In Thrombotic Primary Antiphospholipid Syndrome

Tuesday, June 25, 2024

13:45 – 14:45 ICT

Room: Exhibition Hall

Presenting Author(s)

PG

Pedro Gaspar, MD

Internal Medicine Department, Hospital Santa Maria, ULS Santa Maria, Lisbon, Portugal
Póvoa De Santa Iria, Lisboa, Portugal

Co-Author(s)

AC

Ana Rita Cruz-Machado

MD
Rheumatology and Metabolic Bone Diseases Department, ULS Santa Maria, Lisbon, Portugal
Lisboa, Lisboa, Portugal
FR

Filipa Ribeiro

PhD
Instituto de Medicina Molecular João Lobo Antunes, Centro Académico de Medicina de Lisboa, Faculdade de Medicina, Universidade de Lisboa, Lisbon, Portugal
Lisbon, Lisboa, Portugal
SP

Sandra Pascual-García

PhD
Department of Biotechnology, University of Alicante
Alicante, Comunidad Valenciana, Spain
VR

Válter R. Fonseca

MD, PhD
Instituto de Medicina Molecular João Lobo Antunes, Centro Académico de Medicina de Lisboa, Faculdade de Medicina, Universidade de Lisboa, Lisbon, Portugal
Lisbon, Lisboa, Portugal
VC

Vasco C. Romão

MD, PhD
Rheumatology and Metabolic Bone Diseases Department, ULS Santa Maria, Lisbon, Portugal
Lisbon, Lisboa, Portugal
LG

Luis Graca

Professor
Instituto de Medicina Molecular João Lobo Antunes, Centro Académico de Medicina de Lisboa, Faculdade de Medicina, Universidade de Lisboa, Lisbon, Portugal
Lisbon, Lisboa, Portugal

Background: Interaction between T and B cells are critical for antibody production, but their role and immunophenotypic characterization is scarcely studied in primary antiphospholipid syndrome (pAPS).

Aims: To address whether antiphospholipid antibody (aPL) profile dictates clinical, laboratory and immunological differences in pAPS.

Methods: We prospectively recruited 92 patients with thrombotic pAPS and 75 healthy donors (HD). Patients were categorized in two groups according to current aPL profile (IgM/IgG anti-cardiolipin [ACL], -ß2-glycoprotein [ß2GPI], -phosphatidylserine/prothrombin complex [PS/PT]; and IgG anti-Domain-1 of ß2GPI [D1-ß2GPI]): aPL+, positive for at least one aPL (n=43); and aPL-, negative for all aPL (i.e., positive for lupus anticoagulant [LA] in the past and/or currently) (n=49). We considered aPL < 30UQ as negative (ELISA immunoassays). Circulating T and B cells subsets were analysed by flow cytometry.

Results: Most patients were women (57.6%; median [IQR], age 50 (43-58.5) years; disease duration, 6 [3.5-14] years) (Table 1). Prevalence of LA (67.4%; 28.3%), ACL (44.6%; 28.3%), and ß2GPI (39.1%; 30.4%) positivity decreased over time. Anti-PS/PT and anti-D1-ß2GPI were present in 28.3% and 19.6% of patients. Clinical and laboratory characteristics were mostly comparable between aPL+ and aPL- patients (Table 1), as were the frequencies of Tfh and Treg cells (Fig. 1A-B). Within Tfh cells, activated-Tfh were increase in pAPS compared to HD, and in aPL+ patients (Fig. 1C). Within Treg cells, aPL+ patients had higher Tfr and Tfr/Tfh ratio compared to aPL- patients and HD (Fig. 1D-E). B cells subsets were similarly distributed between pAPS patients, HD, and specific aPL profile subgroups (Fig. 1F-J).

Conclusion(s): Despite clinical and laboratory similarities among aPL+ and aPL- pAPS patients, increased activated-Tfh and Tfr cells, and Tfr/Tfh ratio might indicate an active state of disease characterized by ongoing humoral response in aPL+ patients. aPL- patients displayed a similar T and B cell profile compared to HD.