The FDA label says “
The mechanism(s) by which glatiramer acetate exerts its effects in patients with MS are not fully understood. However, glatiramer acetate is thought to act by modifying immune processes that are believed to be responsible for the pathogenesis of MS.
These processes has changed over time so this paper made me smile
Here, they show that GA treatment revives antiviral T-cell responses and determines a shift in B-cell phenotypic distribution with an increase of naive and a reduction of memory cells.
However how well does it do the job? Because what ever it does it has to reflect how good it works in MS. I would say with the B memory cells it is just about right
Gisella Guerrera, Serena Ruggieri, Mario Picozza, Eleonora Piras, Francesca Gargano, Roberta Placido, Claudio Gasperini, Marco Salvetti, Maria Chiara Buscarinu, Luca Battistini, Giovanna Borsellino, Daniela F. AngeliniEBV-specific CD8 T lymphocytes and B cells during glatiramer acetate therapy in patients with MS Neurol Neuroimmunol Neuroinflamm Nov 2020, 7 (6) e876; DOI: 10.1212/NXI.0000000000000876
Objective Infection with Epstein-Barr virus (EBV) has been associated with clinical activity and risk of developing MS. The purpose of this study is to investigate the impact of glatiramer acetate (GA) therapy on EBV-specific immune responses and disease course.
Methods We characterized EBV-specific CD8 T lymphocytes and B cells during disease-modifying treatments in 2 groups of patients with MS. We designed a 2-pronged approach consisting of a cross-sectional study (39 untreated patients, 38 patients who had undergone 12 months of GA treatment, and 48 healthy donors compatible for age and sex with the patients with MS) and a 12-month longitudinal study (35 patients treated with GA). CD8 EBV-specific T cells and B lymphocytes were studied using pentamers and multiparametric flow cytometry.
Results We find that treatment with GA enhances viral recognition by inducing an increased number of circulating virus-specific CD8 T cells (p = 0.0043) and by relieving their features of exhaustion (p = 0.0053) and senescence (p < 0.0001, p = 0.0001). B cells, phenotypically and numerically tracked along the 1-year follow-up study, show a steady decrease in memory B-cell frequencies (p = 0.025), paralleled by an increase of the naive B subset.
Conclusion GA therapy acts as a disease-modifying therapy restoring homeostasis in the immune system, including anti-EBV responses