Mannara et al. Passive Experimental Autoimmune Encephalomyelitis in C57BL/6 with MOG: Evidence of Involvement of B Cells. PLoS One. 2012;7(12):e52361. doi: 10.1371/journal.pone.0052361.
Experimental autoimmune encephalomyelitis (EAE) is the most relevant animal model to study demyelinating diseases such as multiple sclerosis. EAE can be induced by active (active EAE) or passive (at-EAE) transfer of activated T cells in several species and strains of rodents. However, histological features of at-EAE model in C57BL/6 are poorly described. The aim of this study was to characterize the neuroinflammatory and neurodegenerative responses of at-EAE in C57BL/6 mice by histological techniques and compare them with that observed in the active EAE model. To develop the at-EAE, splenocytes from active EAE female mice were harvested and cultured in presence of MOG(35-55) and IL-12, and then injected intraperitoneally in recipient female C57BL6/J mice. In both models, the development of EAE was similar except for starting before the onset of symptoms and presenting a higher EAE cumulative score in the at-EAE model. Spinal cord histological examination revealed an increased glial activation as well as more extensive demyelinating areas in the at-EAE than in the active EAE model. Although inflammatory infiltrates composed by macrophages and T lymphocytes were found in the spinal cord and brain of both models, B lymphocytes were significantly increased in the at-EAE model. The co-localization of these B cells with IgG and their predominant distribution in areas of demyelination would suggest that IgG-secreting B cells are involved in the neurodegenerative processes associated with at-EAE.
In immunological terminology. Passive transfer means the transfer of antibody. Adoptive transfer is the transfer of T cells, so the
Active EAE and adoptive EAE which they abbreviate to At-EAE.would be more appropriate than passive EAE. By inference of prescence they implicate antibodies in the demyelinating process. We know that antibodies against myelin can cause demyelination. However CD-20 agents that inhibit relapsing MS do not target the anti-body making B cells called plasma cells. The antibody was labelled as CD45R antibodies reactive with CD45RB also pick up T cells and it should have been CD45RA B220 variant.Which was used who knows as it was not in the methods. The question is why T cells specific for MOG cause more antibodies than when you immunize with MOG. The answer may be the bits of protein that were recognised. MOG35-55 contains a fragment that drives antibody responses, however this protein region called an epitope is not dominant in the whole protein so the default is to react to a different bit of MOG (myelin oligodendrocyte glycoprotein) that does not drive antibody responses. This happens in ABH mice also. Therefore the response to immunization with MOG35-55 is sub optimal, compared to an optimised T cell response..This is just a thought nd there may be other explanations. Do you have any?