Showing papers by "Arthur A. Vandenbark published in 2017"
01 Jan 2017
TL;DR: It is demonstrated that blocking MIF signaling either by targeting MIF or CD74 could prove very beneficial in inhibiting disease progression, and partial MHC class II constructs, that include the HLA-DRα1 domain, could bind to CD74 and block MIF binding and signaling.
Abstract: Macrophage migration inhibitory factor (MIF) and its receptor, CD74, are pivotal regulators of the immune system. In this chapter we review the roles of MIF and CD74 in multiple sclerosis (MS) and its mouse model, experimental autoimmune encephalomyelitis (EAE). MIF is produced by a number of cells that are involved in MS pathology, such as monocytes and T cells. MIF effects on MS and EAE have been attributed to disease progression, as it was shown to prolong and enhance the pro-inflammatory functions of these cells. In addition, CD74 was also shown to be involved in this process. We and others demonstrated that blocking MIF signaling either by targeting MIF or CD74 could prove very beneficial in inhibiting disease progression. As such, partial MHC class II constructs, that include the HLA-DRα1 domain, could bind to CD74 and block MIF binding and signaling. This results in reversal of clinical signs of EAE and promotion of neuroprotection, thus, pointing to the therapeutic potential of regulating MIF and CD74 in MS.