EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS IN THE ABSENCE OF A CLASSICAL DELAYED-TYPE HYPERSENSITIVITY REACTION Severe ParalyticDiseaseCorrelateswiththe Presenceof Interleukin2 Receptor-positiveCellsInfiltrating the CentralNervous System
msra(2003)
摘要
Experimental allergic encephalomyelitis (EAE),' is an autoimmune paralytic and inflammatory disease of the central nervous system (CNS) induced by the injection, in CFA, of heterologous myelin basic protein (MBP) or whole brain homogenate. It is one of the principal animal models for human CNS inflammatory and demyelinating disorders such as multiple sclerosis (MS) ; both diseases are characterized by considerable infiltration of leukocytes into the CNS, whose phenotypes have been extensively documented in the rat (1), mouse (2), guinea pig (3), and in brain tissue from MS patients (4). While there is now little doubt that EAE after MBP injection has a cellular pathogenesis and that its induction is dependent on the presence of functioning T cells of the helper/inducer (CD4+) lineage (5-8), it is not yet known how these cells induce disease. Moreover, the use of defined CD4' encephalitogenic T cell lines and clones in both mice (7) and rats (8), while greatly increasing our understanding of some aspects of this disease, in particular the means by which self antigen may be presented to such autoreactive cells, has not significantly furthered our understanding of the actual mechanisms of damage in the CNS. The accumulation of a considerable cellular infiltrate in the CNS of animals with EAE, whether induced with T cell lines (7, 8) or via conventional means after injection of MBP and adjuvant or transfer of cells from actively immunized animals (9, 10), has been taken as evidence that EAE may be the clinical manifestation of a delayed-type hypersensitivity (DTH) reaction in the CNS. All that can be said with confidence, however, is that appropriate MBP-specific CD4+ cells, when injected into recipient rats or mice, are sufficient to induce both clinical signs and classic histological evidence of EAE (i .e ., perivascular leukocyte infiltration reminiscent of a DTH reaction), but exactly which of the infiltrating J. Sedgwick is supported by a Postdoctoral Fellowship from the Multiple Sclerosis Society of Great Britain and Northern Ireland . S. Brostoff is supported in part by National Institute ofHealth research grant NS-11867 . 'Abbreviations used in this paper: CNS, central nervous system ; DTH, delayed-type hypersensitivity ; EAE, experimental allergic encephalomyelitis ; L-CA, leukocyte-common antigen ; MBP, myelin basic protein ; MS, multiple sclerosis .
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