Impaired autoreactive T cell-induced T cell-T cell interaction in aged mice

Venkatachalam Udhayakumar, Bondada Subbarao, Aruna Seth, Mitzi Nagarkatti, Prakash S. Nagarkatti

Research output: Contribution to journalArticlepeer-review

10 Scopus citations

Abstract

Self-Ia-reactive (autoreactive) L3T4+ T cell clones have been shown earlier to stimulate the proliferation of syngeneic naive L3T4+ T cells and initiate a T cell-T cell (T-T) interaction leading to the generation of immunoregulatory circuits. Since aging has been shown to be associated with a decline of the immune responsiveness, age-related alterations in the T-T interaction was investigated in the present study. Using several I-Ed-specific autoreactive T cell clones isolated from 2- to 3-month-old (young) DBA/2 mice as stimulators, it was observed that L3T4+ T cells from 22- to 24-month-old (aged) DBA/2 mice, failed to demonstrate a significant response to the autoreactive T cells. In contrast, L3T4+ T cells from young mice responded strongly to the autoreactive T cell clones. The deficient T-T cell interaction in aged mice correlated with an impaired syngeneic mixed lymphocyte reaction in these mice, thereby suggesting that aging induces a defect both in the autoreactive T cells and in T cells which react with the autoreactive T cells. When exogenous recombinant interleukin 2 (rIL-2), recombinant interleukin 4 (rIL-4), or a combination of these was added to the interaction, it was observed that rIL-4 but not rIL-2 enhanced the T-T interaction in young mice. However, rIL-4 or a combination of rIL-2 and rIL-4 failed to correct the defective T-T interaction in aged mice. Since the T cell network is believed to play an important role in the maintenance of normal immune system homeostasis, the present study suggests that age-related alterations in T and B cell functions and increased susceptibility to autoimmune diseases with age may result from a defect in the T cell network regulation.

Original languageEnglish
Pages (from-to)299-307
Number of pages9
JournalCellular Immunology
Volume116
Issue number2
DOIs
StatePublished - Oct 15 1988

Bibliographical note

Funding Information:
’ The work at Virginia Polytechnic Institute and State University was supported by National Institute of Health Grants CA 45009 and CA 45010 and a BRSG grant awarded to P.S.N. and M.N. and the work at University of Kentucky was supported by National Institute of Health Grants AI 2 1490 and AG 0573 1, awarded to B.S. * Supported in part by PSP funds from the University of Kentucky.

ASJC Scopus subject areas

  • Immunology

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