Abstract
Experimental autoimmune encephalomyelitis (EAE), a well‐accepted experimental model for multiple sclerosis in humans, is a paralytic disease mediated by CD4+ T cells specific for myelin basic protein (MBP). Several approaches to immune‐specific therapy of EAE as a model for other organ‐specific autoimmune diseases have previously been reported. We now show that macrophages (MΦ) or B cells, as antigen‐presenting cells, when pulsed with MBP and intraperitoneally (but not intravenously) inoculated after the encephalitogenic challenge, are highly effective in blocking the development of EAE. Moreover, MΦ pulsed with an organ tissue homogenate, mouse spinal cord homogenate, can also present the relevant target antigen, MBP, and are as effective as MBP‐pulsed MΦ in blocking the development of EAE. This capacity of the MΦ to identify and present the relevant target antigen indicates that this approach is also applicable to organ‐specific autoimmune diseases other than EAE, regardless of how much is known about their etiological agent or specific target antigen. Nonviable glutaraldehyde‐fixed MBP‐pulsed MΦ or membranes derived from MBP‐pulsed MΦ retain their capacity to block the development of EAE.