Spontaneous development in vitro of a myelin basic protein-specific suppressor T cell line

Shau Ku Huang, Subramaniam Sriram

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

T cell lines to myelin basic protein (MBP) developed following in vitro culture cause experimental allergic encephalomyelitis (EAE) upon transfer into naive recipient mice. We have, however, repeatedly observed that MBP-specific T cell lines lose their ability to transfer EAE after 40 days in culture. Analyses of such cell lines failed to show any differences in their proliferative responses to antigen, or in the secretion of interleukin-2 (IL-2) and/or IL-4 when compared to their encephalitogenic counterparts. In contrast, examinations of T cell receptor (TCR) β-chain gene rearrangement patterns showed sequential changes in the clonal population of cells concomitant with the loss of encephalitogenic function. Furthermore, transfer of a non-encephalitogenic, genotypically altered cell line after long-term in vitro culture into mice challenged with MBP suppressed the development of EAE. These findings suggest that the development of such putative regulatory cells in vivo may be involved in the recovery in EAE.

Original languageEnglish
Pages (from-to)177-183
Number of pages7
JournalJournal of Neuroimmunology
Volume25
Issue number2-3
DOIs
Publication statusPublished - Jan 1 1989
Externally publishedYes

Fingerprint

Myelin Basic Protein
Autoimmune Experimental Encephalomyelitis
T-Lymphocytes
Cell Line
T-Cell Receptor Genes
Gene Rearrangement
Interleukin-4
Interleukin-2
Antigens
In Vitro Techniques
Population

Keywords

  • Experimental allergic encephalomyelitis, suppression
  • T cell receptor

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy
  • Clinical Neurology
  • Neurology

Cite this

Spontaneous development in vitro of a myelin basic protein-specific suppressor T cell line. / Huang, Shau Ku; Sriram, Subramaniam.

In: Journal of Neuroimmunology, Vol. 25, No. 2-3, 01.01.1989, p. 177-183.

Research output: Contribution to journalArticle

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