Abstract
Abstract Auto-aggressive T cells are responsible for the onset and perpetuation of autoimmune diseases, including Type 1 Diabetes (T1D) and Multiple Sclerosis (MS). A subset of CD4 T cells, CD4+CD40+ cells, have an expansive role in the Non-Obese Diabetic (NOD) mouse model of T1D. Not only do CD4+CD40+ cells increase in number with the onset of disease, but they are necessary and sufficient in transferring T1D from NOD to NOD.scid mice. Because CD4+CD40+ cells have an imperative role in the development of disease in T1D, we considered that these cells might also be involved in Experimental Autoimmune Encephalomyelitis (EAE), a neurological disease which mimics human MS. When given myelin oligodendrocyte glycoprotein (MOG) and pertussis toxin (PT), C57Bl/6 mice develop neurological symptoms and impaired motor functions similar to those in human MS patients. Data shows an increase, not only in CD4 T cells, but also in CD4+CD40+ cells in mice receiving induction of EAE. This does not occur in their control counterparts. Further, purified splenic CD4+CD40+ cells from asymptomatic disease induced C57Bl/6 mice rapidly transfer EAE to C57Bl/6.scid recipients with only 1.2x106 cells, demonstrating that CD4+CD40+ cells alone can induce EAE. Also, we show cerebral infiltrates of immune cells in localized regions of the brain of the CD4+CD40+ recipient mice, suggesting that these lesions are similar to the lesions found in human MS patients.
Published Version
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