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Injection of T‐cell receptor peptide reduces immunosenescence in aged C57BL/6 mice
Author(s) -
Bailin Liang,
Zezhong Zhang,
Paula Inserra,
Shuguang Jiang,
J Lee,
Andrea Garza,
John J. Marchalonis,
Ronald R. Watson
Publication year - 1998
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.1365-2567.1998.00470.x
Subject(s) - immunosenescence , t cell receptor , endocrinology , splenocyte , immune system , medicine , biology , cytokine , t cell , receptor , immunology , tumor necrosis factor alpha , interleukin 2 , spleen , microbiology and biotechnology
Previous studies established that retrovirally infected young mice produced large amounts of autoantibodies to certain T‐cell receptor (TCR) peptides whose administration diminished retrovirus‐induced immune abnormalities. C57BL/6 young (4 weeks) and old (16 months) female mice were injected with these same synthetic human TCR Vβ8.1 or 5.2 peptides. Administration of these autoantigenic peptides to old mice prevent immunosenesence, such as age‐related reduction in splenocyte proliferation and interleukin‐2 (IL‐2) secretion. TCR Vβ peptide injection into young mice had no effect on T‐ or B‐cell mitogenesis and IL‐4 production while modifying tumour necrosis factor‐α (TNF‐α), IL‐6, and interferon‐γ (IFN‐γ) secreted by mitogen‐stimulated spleen cells. TCR Vβ injection also retarded the excessive production of IL‐4, IL‐6 and TNF‐α induced by ageing. These data suggest that immune dysfunction and abnormal cytokine production, induced by the ageing process, were largely prevented by injection of selected TCR Vβ CDR1 peptides.

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