Disruption of the β2-integrin CD11d (αDβ2) gene fails to protect against experimental autoimmune encephalomyelitis

The fourth member of the β2-integrin family of adhesion molecules, CD11d (αDβ2), is expressed on a wide variety of immune cells, however its function in autoimmune diseases, including EAE remains unknown. We induced EAE in wild-type and CD11d−/− C57BL/6 mice using myelin oligodendrocyte glycoprotein (MOG35–55) peptide. The clinical course and histopathology of EAE were identical in both groups of mice throughout the disease course. There were no significant differences in the infiltration of leukocyte subsets into the central nervous system or in the production of cytokines from T cells isolated from the spleen or spinal cord from both groups of mice. Our data demonstrate that CD11d is not required for the development of EAE and, to date, is the only β2-integrin molecule whose deletion does not result in attenuated disease.