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Review
. 2007:79:43-72.
doi: 10.1016/S0074-7742(07)79003-7.

The role of CD4 T cells in the pathogenesis of multiple sclerosis

Tanuja Chitnis  1
Affiliations
Review

The role of CD4 T cells in the pathogenesis of multiple sclerosis

Tanuja Chitnis. Int Rev Neurobiol. 2007.

Abstract

T lymphocytes play a central role in the pathogenesis of multiple sclerosis (MS) (Zhang et al., 1992). Both CD4+ and CD8+ T cells have been demonstrated in MS lesions, with CD4+ T cells predominating in acute lesions and CD8+ T cells being observed more frequently in chronic lesions (Raine, 1994). Additionally, T cells are found in all four of the described histopathologic subtypes of MS (Lucchinetti et al., 2000). Activated myelin-reactive CD4+ T cells are present in the blood and cerebrospinal fluid (CSF) of MS patients; in contrast, only nonactivated myelin-reactive T cells are present in the blood of controls (Zhang et al., 1994). The success of several T-cell-targeted therapies in MS reinforces the importance of the role of the T cell in MS pathogenesis. Here, we outline basic concepts in CD4+ T-cell immunology and summarize the current understanding of the role of CD4+ T cells in the pathogenesis of MS.

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Figures

Fig. 1
Fig. 1
Factors that influence T helper cell differentiation.
See this image and copyright information in PMC

References

    1. Achiron A., Lavie G., Kishner I., Stern Y., Sarova‐Pinhas I., Ben‐Aharon T., Barak Y., Raz H., Lavie M., Barliya T., Faibel M., Cohen I.R., Mandel M. T cell vaccination in multiple sclerosis relapsing‐remitting nonresponders patients. Clin. Immunol. 2004;113:155–160. - PubMed
    1. Aggarwal S., Ghilardi N., Xie M.H., de Sauvage F.J., Gurney A.L. Interleukin‐23 promotes a distinct CD4 T cell activation state characterized by the production of interleukin‐17. J. Biol. Chem. 2003;278:1910–1914. - PubMed
    1. Aharoni R., Teitelbaum D., Arnon R., Sela M. Copolymer 1 acts against the immunodominant epitope 82–100 of myelin basic protein by T cell receptor antagonism in addition to major histocompatibility complex blocking. Proc. Natl. Acad. Sci. USA. 1999;96:634–639. - PMC - PubMed
    1. Aharoni R., Teitelbaum D., Leitner O., Meshorer A., Sela M., Arnon R. Specific Th2 cells accumulate in the central nervous system of mice protected against experimental autoimmune encephalomyelitis by copolymer 1. Proc. Natl. Acad. Sci. USA. 2000;97:11472–11477. - PMC - PubMed
    1. Aharoni R., Meshorer A., Sela M., Arnon R. Oral treatment of mice with copolymer 1 (glatiramer acetate) results in the accumulation of specific Th2 cells in the central nervous system. J. Neuroimmunol. 2002;126:58–68. - PubMed

Further Reading

    1. Cannella B., Raine C.S. The adhesion molecule and cytokine profile of multiple sclerosis lesions. Ann. Neurol. 1995;37:424–435. - PubMed
    1. Lucchinetti C., Bruck W., Parisi J., Scheithauer B., Rodriguez M., Lassmann H. Heterogeneity of multiple sclerosis lesions: Implications for the pathogenesis of demyelination. Ann. Neurol. 2000;47:707–717. - PubMed

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