We have been discussing whether Epstein Barr Virus could trigger MS, without the requirement for T cells.
It is thought that high-affinity (strong binding) isotype–switched (Antibodies such as IgG that develop from proteotypic IgD or IgM producing B cells) antibodies by B cells depends on signals from CD4+ Thelper cells. Antigen (Ag) binding to surface Ig molecules (BCRs) causes naive (mature) B cells to migrate to the border between the B cell follicle in lymph glands and T cell area (paracortex of the lymph gland) and present MHC class II–bound, Ag-derived peptides (p:MHCII) to Th cells that were previously activated by the same p:MHCII complex on dendritic cells. The Ag-specific B cells then receive signals from the Th cells, proliferate, and undergo isotype switching. Some of the activated B cell progeny become Ab-secreting plasmablasts (PBs), whereas others enter germinal centers (GCs) along with specialized T follicular helper (Tfh) cells and drive the formation of high-affinity memory B cells and long-lived plasma cells
In this study they removed differnt types of T cells
So in the mouse they could detect 20,000 naive B cells reactive to a target and this increased to 300,000 activated cells after immunization of these 40,000 were antibody producing plasma blasts. Now when they looked at the T cell requirement if they depleted the follicle helping cells you could make 22,000 plasma blasts and if you lack Th1 or Th17 you can still produce over 30,000 plasmablasts. So whilst T cells are important the subtypes are not absolutely required.
These results indicate that isotype-switched PB production requires a CD40-dependent form of cognate T cell help that does not depend on a single differentiated Th cell subset.
If you have no T cells only 400 plasma blasts were produced. Now this clearly shows you need T cells to get an optimal response, but without T cells you still have a response. Would 400 cells be enough to to trigger a problem that resulted in the eventualy involvement of T cell supported B cells? Now add EBV into the mix and this gives the B cells the CD40 signal that may come from the T cells and perhaps you could?
J Immunol. 2019 Jan 15;202(2):401-405. doi: 10.4049/jimmunol.1801349. Epub 2018 Dec 14.