XXXX and Mortality in a Male Lewis @entity35 of Experimental Autoimmune @entity1651 .

@entity6220 @entity39 @entity19 @entity840 @entity1711 @entity409 @entity1710 @entity1651 @entity35 @entity99 @entity15 @entity528
BACKGROUND AND OBJECTIVES: @entity15 is an @entity6220 . This is due to migration of peripherally activated lymphocytes to central nervous system leading to inflammatory lesions. However, liver has an anti-inflammatory microenvironment. Myelin expression in the liver of @entity19 suppresses inflammatory lesions within central nervous system. Considering the notion that the inflammatory events originate from periphery, we investigated if the liver was affected in an animal model for @entity15 . METHODS: Experimental autoimmune @entity1651 was induced in male Lewis @entity35 using @entity840 spinal cord and complete Freund's adjuvant. Weight, clinical score, and survival rate were evaluated for 14 days post immunization. Liver sections were taken and stained with @entity1710 and @entity1711 and examined with an Olympus microscope. RESULTS: Mortality was accompanied by @entity409 . Sinusoidal congestion, pycnotic nuclei within hepatocytes, hepatocyte @entity39 , and severe widespread congestion along with fat accumulation within hepatocytes ( @entity528 ) were observed in liver tissue sections. CONCLUSION: @entity409 occurs in experimental autoimmune @entity1651 . The perpetuation of self antigen leading to continuous migration of extrahepatically activated T cells makes an inflammatory milieu in the liver. It follows migration and development of more inflammatory cells and may paralyses tolerance inducing mechanisms. Apart from @entity6220 , @entity99 may act as synergistic factor for debilitation and mortality.
