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The following is a summary of “Different Patterns of Autoantibody Secretion by Peripheral Blood Mononuclear Cells in Autoimmune Nodopathies,” published in the August 2024 issue of Neurology by Rohrbacher et al.
Severe sensorimotor neuropathy, characterized by sensorimotor impairment, exhibits a distinct phenotype caused by autoimmune nodopathies with antibodies against the paranodal proteins.
Researchers conducted a retrospective study to assess the factors predicting disease course and therapeutic response in patients with rheumatoid arthritis treated with rituximab.
They conducted an in vitro analysis of peripheral blood mononuclear cells to check whether the secretion of specific autoantibodies can predict the course of disease and response to rituximab.
The results showed 3 different patterns of patients with anti-Neurofascin-155-, anti-Contactin-1-, and anti-Caspr1-IgG4 autoantibodies, in vitro production of autoantibodies, indicating autoantigen-specific memory B cells and short-lived plasma cells/plasmablasts as the significant source of autoantibodies which responded well to rituximab. On the other hand, a subgroup of patients with anti-Neurofascin-155-IgG4 autoantibodies showed no in vitro autoantibody production despite high serum titers, suggesting that autoantibody secretion came from long-lived plasma cells outside the peripheral blood, leading to an insufficient response to rituximab. Patients with anti-pan-neurofascin autoantibodies, all experiencing a monophasic disease course, had no measurable in vitro autoantibody production, implying a lack of autoantigen-specific memory B cells. However, some patients exhibited autoantibody production by unstimulated cells, likely reflecting high levels of autoantigen-specific plasmablasts and correlating with a severe but monophasic disease course.
They concluded several B-cell responses might occur in autoimmune nodopathies, serving as markers of disease courses and response to rituximab.
Source: neurology.org/doi/10.1212/NXI.0000000000200295
