Role of CD5⁺ B-1 cells in EAE pathogenesis

Abstract

Hybridoma cell lines producing natural autoantibodies (NAA), generated from A.SW mice with progressive experimental autoimmune encephalomyelitis (P-EAE), have been shown to cause demyelination and renal pathology when injected into naïve mice. To investigate the relative contribution of these antibodies to disease pathogenesis, B-1 cells, the major producers of NAA, were depleted by hypotonic shock. Depletion of B-1 cells during the effector phase of EAE significantly decreased the severity of demyelination and overall pathology in the brain. There was also a decreased incidence of P-EAE and a decrease in clinical score. Depletion during the induction phase of the disease resulted in an increase in the incidence of P-EAE and in the clinical score. Overall, B-1 cells were found to modulate EAE pathogenesis.

• Autoantibodies
• Autoimmunity
• CNS-demyelinating disease
• CNS disease pathology
• Multiple sclerosis

Acknowledgements

The authors would like to thank Jane E. Libbey, MS, and Nikki J. Kirkman, BS, for many helpful discussions and Faris Hasanovic, J. Wes Peterson, Bryan A. Moore, Victor Gappmeier and Daniel G. Smith for excellent technical assistance. We are grateful to Ms Kathleen Borick for preparation of the manuscript. This work was supported by NIH grant 5R01NS040350.