Abstract

Experimental autoimmune encephalomyelitis (EAE) and/or tuberculin sensitivity were transferred to histocompatible recipients with myelin basic protein-stimulated and/or PPD stimulated guinea pig lymph node T cells previously separated by depletion of B cells ("panning") on rabbit anti-guinea pig Ig antibody-coated Petri plates. The depletion was augmented by complement-mediated lysis using mouse anti-guinea pig B-cell monoclonal antibody (31D2), rabbit anti-mouse Ig, and rabbit complement. B cells did not transfer EAE nor provide protection against active immunization with guinea pig spinal cord antigen.

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