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Age‐related defects in T‐cell metabolism
Author(s) -
Faulkner Matthew Floyd,
Lewis Virginia,
Durdik Jeannine M
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.2_supplement.361
Subject(s) - mitochondrion , microbiology and biotechnology , apoptosis , immune system , transporter , glucose transporter , metabolism , chemistry , biology , programmed cell death , function (biology) , carbohydrate metabolism , biochemistry , endocrinology , immunology , gene , insulin
Aging at the cellular and molecular level has been shown to involve declines in immune function. We are characterizing the responses of naïve T‐cells to activation. Activated T‐cells of aged mice initiate proliferation as well as their young counterparts, but have increased apoptotic rates. However, the mechanisms behind this post‐ activation death are not completely understood. Here we will show alterations in metabolic activities in T‐cells of aged mice through differences in the expression of glucose transporter (Glut 1), glucose uptake and lactate production. Additionally, we will correlate these findings with confocal studies of autophagocytic vesicle formation by analyzing microtubule‐associated protein ‐1 light chain 3 (LC3) as well as comparing relative amounts of active mitochondria versus total mitochondria using ratios of membrane potential dependant and independent dyes.