Research on B cells identifes subset

[tatt]

http://onlinelibrary.wiley.com/doi/10.1111/cei.12749/abstract

Far too technical for me. I think this is is not particularly great news but not entirely bad as they did find something different in ME. Whether that difference is actually likely to have any relevance to rituximab is the bit that's beyond me.

 

[Cort]

http://onlinelibrary.wiley.com/doi/10.1111/cei.12749/abstract

Far too technical for me. I think this is is not particularly great news but not entirely bad as they did find something different in ME. Whether that difference is actually likely to have any relevance to rituximab is the bit that's beyond me.

The immune system is so darn complicated.

It does appear to impact Rituximab therapy although I have no clue how. Interestingly the changes were negatively associated with duration, which if I'm reading this right, suggests that more changes were found in the early duration patients ((???)

Summary

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a heterogeneous condition of unknown etiology characterized by multiple symptoms including fatigue, post-exertional malaise and cognitive impairment, lasting for at least 6 months. Recently, two clinical trials of B-cell depletion therapy with rituximab (anti-CD20) reported convincing improvement in symptoms. A possible but undefined role for B-cells has therefore been proposed. Studies of the relative percentages of B-cell subsets in patients with ME/CFS have not revealed any reproducible differences from healthy controls (HC). In order to explore whether more subtle alterations in B-cell subsets related to B-cell differentiation exist in ME/CFS patients we used flow cytometry to immunophenotype CD19+ B-cells. The panel utilized IgD, CD27 and CD38 (classical B-cell subsets) together with additional markers. A total of 38 patients fulfilling Canadian, Centre for Disease Control, and Fukuda ME/CFS criteria and 32 age/sex-matched HC were included.

We found no difference in percentages of classical subsets between ME/CFS patients and HC.

However, we observed an increase in frequency (p<0.01) and expression (MFI; p=0.03) of CD24 on total B-cells, confined to IgD+ subsets. Within memory subsets, a higher frequency of CD21+CD38- B-cells (>20%) was associated with the presence of ME/CFS (Odds ratio: 3.47 (1.15-10.46); p=0.03) compared with HC and there was a negative correlation with disease duration.

In conclusion, we identified possible changes in B-cell phenotype in patients with ME/CFS. These may reflect altered B-cell function and if confirmed in other patient cohorts, could provide a platform for studies based on clinical course or responsiveness to rituximab-therapy. This article is protected by copyright. All rights reserved.