I am trying to investigate the effect of a mutation in a common signalling pathway on IgA production.
One experiment I would like to do is to stimulate (CD40L, APRIL/BAFF + IL10 +LPS) primary naive B cells to produce IgA and see what happens to IgA levels when I interfere with the pathway.
I have EBV transformed B cell lines from the patient that we originally discovered the mutation in, sadly this patient is now deceased so I can't get new samples.
Can these cell lines be stimulated in the same way as primary B cells? Or does the transformation process means they are now in effect IgM+ memory B cells?
I am asking as I may be able to compare the lines from this patient vs controls and the added bonus of lots of cells means I can do genetic analysis.
It would be great to get some thoughts on this.
Thanks
Epstein–Barr virus (EBV) infection may initiate production of autoantibodies and development of cancer and autoimmune diseases. Here we
outline phenotypic and functional changes in B cells of patients with
rheumatoid arthritis (RA) related to EBV infection. The B-cell phenotype
was analysed in blood and bone marrow (BM) of RA patients who had
EBV transcripts in BM (EBV+, n = 13) and in EBV (n = 22) patients
with RA. The functional effect of EBV was studied in the sorted CD25+
and CD25 peripheral B cells of RA patients (n = 18) and healthy controls (n = 9). Rituximab treatment results in enrichment of CD25+ B cells
in peripheral blood (PB) of EBV+ RA patients. The CD25+ B-cell subset
displayed a more mature phenotype accumulating IgG-expressing cells. It
was also enriched with CD27+ and CD95+ cells in PB and BM. EBV stimulation of the sorted CD25+ B cells in vitro induced a polyclonal IgG and
IgM secretion in RA patients, while CD25+ B cells of healthy subjects did
not respond to EBV stimulation. CD25+ B cells were enriched in PB and
synovial fluid of RA patients. EBV infection affects the B-cell phenotype
in RA patients by increasing the CD25+ subset and by inducing their
immunoglobulin production. These findings clearly link CD25+ B cells to
the EBV-dependent sequence of reactions in the pathogenesis of RA.
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