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J Biol Chem, Vol. 273, Issue 14, 8119-8129, April 3, 1998
From the Department of Immunology and the Division of Rheumatology,
Department of Medicine, Mayo Clinic Foundation, Rochester, Minnesota
55905
Changes in T cell populations and concomitant
perturbation of T cell effector functions have been postulated to
account for many aging-related immune dysfunctions. Here, we report
that high frequencies of CD28null CD4+ T cells were
found in elderly individuals. Because deviations in the function of
these unusual CD4+ T cells might be directly related to CD28
deficiency, we examined the molecular basis for the loss of CD28
expression in CD4+ T cells. In reporter gene bioassays, the minimal
promoter of the CD28 gene was mapped to the proximal 400 base pairs (bp) of the 5' untranslated region. CD28 deficiency was
associated with the loss of two noncompeting binding activities within
a 67-bp segment of the minimal promoter. These binding activities were
not competed by consensus Ets, Elk, or
AP3 motifs that were found within the sequence stretch. The DNA-protein complexes were also not recognized by antibodies to Ets-related transcription factors. Furthermore, introduction of mutations into the 67-bp segment at positions corresponding to the two
DNA-protein interaction sites, i.e. nucleotides spanning 
206 to 179 and 171 to 148, resulted in the loss of specific nuclear factor binding activities and the abrogation of promoter activity. These observations implicate at least two regulatory motifs
in the constitutive expression of CD28. The loss of binding activity of
trans-acting factors specific for these sequences may
contribute to the accumulation CD4+CD28null T cells during
aging.
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