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Springer Seminars in Immunopathology : Volume 39

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T-cell signaling and immunopathologies

Regulatory T cells: roles of T cell receptor for their development and function

ZAP70: a master regulator of adaptive immunity

Lymphoproliferative disorders involving T helper effector cells with defective LAT signalosomes

Lymphoid tyrosine phosphatase and autoimmunity: human genetics rediscovers tyrosine phosphatases

Cbl-b in T-cell activation

Foxp3 positive regulatory T cells: a functional regulation by the E3 ubiquitin ligase Itch

SLAM family receptors and the SLAM-associated protein (SAP) modulate T cell functions

Immunopathologies linked to integrin signalling

Signals that influence T follicular helper cell differentiation and function

Exploring the roles of CD8+ T lymphocytes in the pathogenesis of autoimmune demyelination

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Exploring the roles of CD8+ T lymphocytes in the pathogenesis of autoimmune demyelination

Content Provider	Springer Nature Link
Author	Johnson, Trina A. Jirik, Frank R. Fournier, Sylvie
Copyright Year	2010
Abstract	Multiple sclerosis (MS) is an autoimmune disease characterized by mononuclear cell infiltrates, focal demyelination, and the development of sclerotic plaques within the central nervous system. Although CD8+ T lymphocytes are more abundant than CD4+ T lymphocytes in MS lesions, the latter cell type has been most commonly implicated in the genesis of this disease. Recent evidence, however, suggests that both T cell populations and their various subsets are able to contribute to disease initiation and progression. To gain insight into disease mechanisms of potential relevance to MS, a variety of animal models have been developed. Foremost among these has been experimental autoimmune encephalomyelitis (EAE), a rodent model of MS induced by the immunization of genetically susceptible animals with peptides derived from myelin-associated proteins. While EAE has contributed greatly to our understanding of mechanisms involved in autoimmune demyelination, this model has been of limited use as far as shedding light on the possible contributions of CD8+ T lymphocytes to disease pathogenesis. Herein, we review evidence supporting a role for CD8+ T lymphocytes in both MS and EAE and also highlight several novel murine systems designed for investigating the role(s) of CD8+ T cells in autoimmune demyelination.
Starting Page	197
Ending Page	209
Page Count	13
File Format	PDF
ISSN	18632297
Journal	Springer Seminars in Immunopathology
Volume Number	32
Issue Number	2
e-ISSN	18632300
Language	English
Publisher	Springer-Verlag
Publisher Date	2010-03-18
Publisher Place	Berlin, Heidelberg
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Multiple sclerosis Experimental autoimmune encephalomyelitis Demyelination CD8+ T lymphocyte CD4+ T lymphocyte Cytotoxic T lymphocyte Myelin oligodendrocyte glycoprotein Myelin basic protein Oligodendrocyte Transgenic mice Central nervous system Internal Medicine Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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HLA class II transgenic mice authenticate restriction of myelin oligodendrocyte glycoprotein‐specific immune response implicated in multiple sclerosis pathogenesis

The role of CD8(+) T cells in a model of multiple sclerosis induced with recombinant myelin oligodendrocyte glycoprotein.

A transgenic model of central nervous system autoimmunity mediated by CD4+ and CD8+ T and B cells.

Swift entry of myelin-specific T lymphocytes into the central nervous system in spontaneous autoimmune encephalomyelitis.

Tyrosine kinase 2 plays critical roles in the pathogenic CD4 T cell responses for the development of experimental autoimmune encephalomyelitis.

Notch signaling regulates T cell accumulation and function in the central nervous system during experimental autoimmune encephalomyelitis.

Chondroitin 6-O-sulfate ameliorates experimental autoimmune encephalomyelitis

The myelin-associated oligodendrocytic basic protein (MOBP) as a relevant primary target autoantigen in multiple sclerosis.

The influence of T cell Ig mucin-3 signaling on central nervous system autoimmune disease is determined by the effector function of the pathogenic T cells.

Exploring the roles of CD8+ T lymphocytes in the pathogenesis of autoimmune demyelination

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HLA class II transgenic mice authenticate restriction of myelin oligodendrocyte glycoprotein‐specific immune response implicated in multiple sclerosis pathogenesis

The role of CD8(+) T cells in a model of multiple sclerosis induced with recombinant myelin oligodendrocyte glycoprotein.

A transgenic model of central nervous system autoimmunity mediated by CD4+ and CD8+ T and B cells.

Swift entry of myelin-specific T lymphocytes into the central nervous system in spontaneous autoimmune encephalomyelitis.

Tyrosine kinase 2 plays critical roles in the pathogenic CD4 T cell responses for the development of experimental autoimmune encephalomyelitis.

Notch signaling regulates T cell accumulation and function in the central nervous system during experimental autoimmune encephalomyelitis.

Chondroitin 6-O-sulfate ameliorates experimental autoimmune encephalomyelitis

The myelin-associated oligodendrocytic basic protein (MOBP) as a relevant primary target autoantigen in multiple sclerosis.

The influence of T cell Ig mucin-3 signaling on central nervous system autoimmune disease is determined by the effector function of the pathogenic T cells.

Exploring the roles of CD8+ T lymphocytes in the pathogenesis of autoimmune demyelination