By Irun R. Cohen, Ariel Miller
Simply because autoimmune problems can wreak havoc in either people and animals, those issues are actually the gadgets of excessive and targeted study. This ebook information particular animal versions for a number of autoimmune issues. The members are famous gurus who care for the panoply of experimentally prompted autoimmune issues, together with encephalomyelitis, allergic neuritis, uveoretinitis, myocarditis, and hepatitis. additionally incorporated are discussions of spontaneously showing illnesses comparable to autoimmune thyroiditis and systemic lupus erythematosus. Many different issues also are lined during this complete advisor. guaranteed to be an relief within the making plans of person experiments and broader learn courses, this booklet can be a invaluable addition to the library of all practising immunologists drawn to immune procedure functionality and disorder.
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Additional info for Autoimmune Disease Models. A Guidebook
Virology 176, 244-254. D a l C a n t o , M . C . ( 1 9 9 0 ) . In " H a n d b o o k o f M u l t i p l e S c l e r o s i s " (S. D . C o o k , E d . ) , p p . 6 3 - 1 0 0 . M a r c e l Dekker, N e w York/Basel. D a l C a n t o , M . C , and L i p t o n , H . L. ( 1 9 7 5 ) . Lab. Invest. 3 3 , 6 2 6 - 6 3 7 . D a l C a n t o , M . C , and L i p t o n , H . L. ( 1 9 8 2 ) . Am. J. Pathol. 106, 2 0 - 2 9 . Dal C a n t o , M . C , and R a b i n o w i t z , S. G . ( 1 9 8 2 ) . Ann. Neurol. 11, 1 0 9 - 1 2 7 .
Two to 3 weeks after infection, mice develop a spastic paresis o f the hind limbs, which, in SJL^J mice, has a chronic course resulting in severe paralysis (Lipton, 1975). In contrast, infection o f SJL^J mice with the tissue culture-adapted BeAn 8386 strain does not produce clinical evidence o f a first phase o f polio-like disease. Clinical signs develop slowly with no major changes in gait from day to day. Mice begin to show signs o f clinical disease 3 5 - 4 0 days postinfection and develop a chronic, progressive paralysis with no recovery or remitting episodes.
1993b). Autoimmune T-cell reactivity against the major myelin proteins, myelin basic protein (MBP) and proteolipid protein (PLP) does not appear to be involved in the induction o f the demyelination process following T M E V in fection. Demyelination cannot be transferred from TMEV-infected donors to 3. Theiler's Virus-Induced Demyelinating Disease 35 normal, non-TMEV-infected recipients with either serum or lymphoid cells (Barbano and Dal Canto, 1984). , 1987). , 1990). The lack o f neuroantigen reactivity in TMEV-infected mice, as measured by functional T-cell analyses, is paralleled by the absence of significant amino acid homology between the T M E V capsid proteins (VP1, VP2, or VP3) and M B P or PLP (Miller et al, 1987).
Autoimmune Disease Models. A Guidebook by Irun R. Cohen, Ariel Miller