Background During the last decade, it was observed that peripheral blood lymphocyte subset distribution was altered in autoimmune diseases such as systemic lupus erythematosus (SLE), primary Sjögren's syndrome (pSS), mixed connective tissue disease, multiple sclerosis, and ANCA-associated vasculitis.
Objectives Accordingly, our aim was to evaluate in the follow-up of patients with venous thromboembolism (VTE) whether lymphocyte distribution is altered in well-characterized primary antiphospholipid syndrome (pAPS) patients.
Methods A prospective, descriptive and comparative study was conducted at Brest University Medical School (France) from June to October 2013. Cases of pAPS VTE patients were selected from the data base EDITH (Study of Determinants Interactions of venous thrombosis), which is a monocentric case-control cohort. From this data base, eleven pAPS VTE patients selected during their follow-up were included and matched with non-APS VTE patients, autoimmune disease patients (Sjögren's syndrome and systemic lupus erythematosus) and controls. Using a 4 colors flow cytometer, peripheral blood B cell subsets (B1, transitional, naïve, and memory), T cell subsets (CD3, CD4, CD8) and NK-cells were explored.
Results In contrast to non-APS VTE patients and controls, pAPS VTE patients displayed total CD3 and CD8 naïve (CD45RA+ CD27+) T cell reduction, and disturbance in B cell homeostasis with increased proportions of B1 cells, transitional B cells (CD24++ CD38++) and naïve B cells (IgD+CD27-), while unswitched (IgD+CD27+) and switched (IgD-CD27+) memory B cells were reduced. The unswitch memory B cell percentage, and even better the naïve/unswitched memory B cell ratio were both effective to distinguish pAPS VTE patients from non-APS VTE patients, and from patients with autoimmune diseases. Interestingly, the absolute number of CD4 T cells was positively correlated with IgG anti-cardiolipin antibody levels.
Conclusions In summary, this study, although conducted with a limited number of well characterized pAPS patients, revealed two major points. First, disturbances in B cell homeostasis that can be used as a signature for pAPS, and second an association between the CD4+ T cell subset and the production of IgG aCL Ab. Future studies shall address whether these perturbations would be helpful for the diagnosis and/or for the therapeutic management and follow-up of these patients.
Disclosure of Interest None declared