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T cell receptor V beta usage in murine experimental autoimmune thyroiditis.

Abstract：

:Mouse thyroglobulin (MTg)-sensitized spleen cells activated in vitro with MTg induced experimental autoimmune thyroiditis (EAT) in which the thyroid infiltrate consists primarily of mononuclear cells (MNC) (lymphocytic EAT). MTg-sensitized spleen cells cultured with MTg together with anti-IL2R antibody induce a granulomatous form of EAT in which the thyroid is infiltrated by MNC in addition to PMNs, histiocytes, and multinucleated giant cells. CD4+ T cells are the primary effector cells for both forms of EAT. The presence of specific T cell receptor (TCR) V beta families in the thyroid infiltrate was examined by flow cytometry and reverse transcription-polymerase chain reaction (RT-PCR) amplification of mRNA. At the time of maximal disease severity, cells infiltrating the thyroid expressed primarily V beta 8, V beta 4, V beta 11, and V beta 14 as determined by flow cytometry. RT-PCR confirmed these findings and also detected several additional V beta gene families, including V beta 1, V beta 2, V beta 6, V beta 13, and V beta 15; V beta 3, V beta 10, and V beta 12 were also detected in some, but not all, experiments. There were no differences in the V beta T cell repertoires in thyroids of mice with lymphocytic vs granulomatous EAT. RT-PCR analysis of intrathyroidal MNC 11 days after cell transfer showed TCR V beta mRNA transcripts to be primarily restricted to V beta 4, V beta 11, and V beta 14, whereas the predominant thyroid-infiltrating T cell 21 days after cell transfer was V beta 8+. Depletion of V beta 8+ T cells in recipient mice did not reduce EAT severity. TCR V beta usage shifted predominantly to V beta 4+, V beta 11+, or V beta 14+ T cells of both CD4+ and CD8+ T cell subsets. These results indicate that multiple V beta TCR are expressed in thyroids of mice with EAT.

journal_name

Cell Immunol

journal_title

Cellular immunology

authors

McMurray RW,Hoffman RW,Tang H,Braley-Mullen H

doi

10.1006/cimm.1996.0208

subject

Has Abstract

pub_date

1996-08-25 00:00:00

pages

1-9

issue

1

eissn

0008-8749

issn

1090-2163

pii

S0008-8749(96)90208-7

journal_volume

172

pub_type

杂志文章

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