Dr. Podojil’s work has focused on the role of costimulatory molecule expression and function on both CD4+ T cells and APC populations during autoimmune diseases, such as multiple sclerosis, and he has a particular interest in neuroimmunology. His primary research focus is to determine the cellular and molecular mechanisms underlying the differential effect of structurally modified forms of anti-CD80 monoclonal antibody (mAb) in the CD4+ Th1 cell mediated disease model of PLP139-151-induced EAE. His current findings suggest that stimulation of CD80 on a CD4+ T cell activated in Th1-promoting conditions induces an increase in the amount of IFN-¿ produced per cell and increases Th1 cell survival within the CNS. These findings suggesting a mechanism by which anti-CD80 mAb treatment of PLP139-151-primed mice exacerbates disease, while treatment with anti-CD80 Fab fragments decrease disease severity. In line with his research studying the role of CD80 expression and reverse signaling to the cell expressing CD80, he has also been studying the role of B7-H4 in CD4+ T cell function. B7-H4 is a recently discovered B7-family member molecule hypothesized to inhibit effector CD4+ T cell responses. Since current approaches for regulation of human autoimmune diseases are largely broad-based immunosuppressive strategies necessitating the physical deletion/inhibition of entire subsets of T cells or non-specific inhibition of antigen presentation or pro-inflammatory cytokine production which could compromise the host’s ability to combat opportunistic pathogens and/or increase risk of neoplasia, therefore we are currently investing the ability of short-term therapy with B7-H4 Ig may prove to be clinically viable.