I noticed that researchers use MOG35-55 to induce a type of T cell-dependent EAE, while for both T cell and B cell-dependent EAE, they choose rhMOG. Some papers report that B cells also contribute to the disease process in rmMOG-induced EAE setting. If these two recombinant proteins both activate B cells, I want to know what's the difference between them.
Dear Echo Zhu
Please see the comparison below. There is a single amino acid substitution at position 42 of the MOG protein (position 7 of the peptide respectively) between the rodent (mouse/ rat) and human MOG protein from serine to proline.
rmMOG vs. rhMOG (aa 35-55)
rmMOG Met-Glu-Val-Gly-Trp-Tyr-Arg-Ser-Pro-Phe-Ser-Arg-Val-Val-His-Leu-Tyr-Arg-Asn-Gly-Lys
rhMOG Met-Glu-Val-Gly-Trp-Tyr-Arg-Pro-Pro-Phe-Ser-Arg-Val-Val-His-Leu-Tyr-Arg-Asn-Gly-Lys
The difference in B cell dependency of MOG induced EAE seems to majorly be attributed to immunization with full length (human) protein vs. the rodent peptide (in C57BL/6 mice), which may differ in other mouse strains (given their different MHCII) as per:
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If you're looking for an alternative model (especially in the chronic phase) check out our work on MBP induced EAE in the less commonly used RIIIS/J derived H2-r bearing B10.RIII mouse strains.
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All the best and good luck with your experiments,
Michael
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