B Cell Dynamics and Transitional B Cells in Long COVID Zoia R. Korobova, Natalia A. Arsentieva, Natalia E. Liubimova, Oleg K. Batsunov, Anastasia A. Butenko, Albina E. Kokoeva, Natalia G. Kucherenko, Victor A. Kashchenko, Ekaterina V. Boeva, Anna O. Norka, Anastasia A. Knizhnikova, Vadim V. Rassokhin, Nikolay A. Belyakov, Areg A. Totolian Background Long COVID is characterized by persistent symptoms following acute SARS-CoV-2 infection. This study aims to evaluate immune system markers, including antigen-specific antibodies, B cell subsets, and Th2-related cytokines, in individuals with long COVID and to investigate their potential impact on the development of this condition. Methods We analyzed blood plasma from 63 individuals diagnosed with long COVID based on clinical presentation and 47 healthy individuals with COVID-19 history but no clinical symptoms. Antigen-specific IgG antibodies were measured using commercial ELISA kits. Lymphocyte subpopulations were assessed via flow cytometry and a gating strategy based on CD27 and CD38. Th2 cytokines (IL-4, IL-5, IL-13) were quantified using the xMAP multiplex assay. Results We noted no significant differences in IgG levels between groups. Notably, individuals with long COVID demonstrated a higher percentage of naive mature B cells (CD27−CD38+), while transitional (CD27−CD38+++) and double-negative (DN, CD27−CD38- cells were significantly reduced. Elevated levels of IL-5 and IL-13 were observed in long COVID patients. Classification analysis revealed that the percentage of transitional B cells (CD27−CD38+++) was a strong predictor of long COVID. Conclusions Our findings highlight alterations in B cell dynamics among individuals with long COVID, which may contribute to autoimmune processes. Link | PDF (Current Issues in Molecular Biology) [Open Access]
What’s the significance of different amounts of immune cells in the blood? Is this just pure speculation?
Others with more background in immunology would be able to provide a more detailed answer, but generally, the final phenotype of an immune cell from a progenitor state (or less “matured”) is a finely tuned regulatory process. It’s influenced by a variety of other factors, including signaling from other immune cells in response to things like infection, checkpoints to try to kill the cell if it recognizes a self-antigen (i.e. if it binds to the organism’s own tissue as in autoimmunity), or other biological changes associated with aging. So a less differentiated immune cell may be pushed to become one type of specialized immune cell over another based on environmental signals. It’s common for studies to report cell type frequencies as a sort of proxy measurement to show that there’s some abnormality in signaling that defines immune trajectory. They’re really just saying “we see a skew in B-cell subpopulations that is reminiscent of what we see in some autoimmune diseases, so there might be some similar underlying mechanism.” But in my non-expert opinion, this is pretty vague speculation about the “why” if they don’t have more direct evidence of autoimmunity.
Yes. You nearly always find some shift or other of B cell subsets - which probably means B cells in blood at different stages of maturation are a bit more or less busy for any one of a thousand reasons. It might be secondary to sitting on a settee or eating less broccoli or getting up later. In the autoimmune disease we know well studies like this do not show anything very exciting.
