BOTH ANTI-CD11A (LFA-I) AND ANTI-CD11B (MAC-1) THERAPY DELAY THE ONSET AND DIMINISH THE SEVERITY OF EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS

Experimental autoimmune encephalomyelitis (EAE) is a demyelinating dis ease of the central nervous system (CNS) induced in rodents by activat ed CD4(+) T cells specific for various myelin proteins such as myelin basic protein and proteolipid protein. The disease is characterized by breach of the blood-brain barrier, perivascular infiltration of leuko cytes into the CNS, local inflammation and demyelination in the form o f plaques. In this study, we evaluated the effect of administration of antibodies to two members of the beta 2 integrin sub-family of adhesi on molecules, CD11a and CD11b, on the onset and progression of EAE. CD 11a and CD11b are involved in cell-cell interactions leading to T cell and macrophage extravasation to inflammatory sites and T cell activat ion. our results show that anti-CD11a antibodies could completely bloc k the induction of EAE and anti-CD11b antibodies significantly delayed the onset and diminished the severity of clinical signs of EAE even w hen injections were initiated at the first appearance of clinical sign s.