B cells expressing NgR1 and NgR3 are localized to EAE induced inflammatory infiltrates and are stimulated by BAFF
We have previously reported evidence that Nogo A activation of Nogo receptor 1 (NgR1) can drive axonal dystrophy during the neurological progression of experimental autoimmune encephalomyelitis (EAE) However, the B cell activating factor (BAFF/BlyS) may also be an important ligand of NgR during neuroinflammation. In the current study we define that NgR1 and its homologs may contribute to immune cell signaling during EAE. Meningeal B cells expressing NgR1 and NgR3 were identified within the lumbosacral spinal cords of ngr1+ EAE induced mice at clinical score 1. Furthermore, increased secretion of immunoglobulins that bound to central nervous system myelin were shown to be generated from isolated NgR1 and NgR3 expressing B cells of ngr1+ EAE induced mice. In vitro BAFF stimulation of NgR1 and NgR3 expressing B cells, directed them into the cell cycle DNA synthesis phase. However, when we antagonized BAFF signaling by co incubation with recombinant BAFF R, NgR1 Fc, or NgR3 peptides, the B cells remained in the G0/G1 phase. The data suggest that B cells express NgR1 and NgR3 during EAE, being localized to infiltrates of the meninges and that their regulation is governed by BAFF signaling.
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