Alterations of T-cell functions during Friend leukemia complex infection: Defective signal transduction?

E. Soldaini, D. Matteucci, M. R. Capobianchi, F. Baldinotti, A. Giovannetti, F. Dianzani, M. Bendinelli

Research output: Contribution to journalArticlepeer-review

Abstract

Proliferative and interleukin responses to T-cell mitogens such as concanavalin A (Con A) were rapidly and progressively reduced in BALB/c mice infected with the Friend leukemia complex (FLC) or its helper, Friend murine leukemia virus (F-MuLV). In contrast, a combination of the protein kinase C activator phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA) and the Ca++ ionophore A23187 elicited a normal lymphoproliferative response up to 8 days postinfection (p.i.) and normal interleukin-2 (IL-2) and interferon-γ responses up to day 14 p.i. Exogenous IL-2 failed to restore the lymphoproliferative response of infected cells regardless of the stimulation used. These results showed that the T-cell deficits may be at least partly attributable to a derangement of the signal transduction pathway leading to activation. Spleen cells passed through nylon wool columns reacquired a normal responsiveness to Con A ± TPA up to 14 days p.i. The latter finding suggests that the alterations in signal transduction are not caused by primary defect of the responder-T cells but may result from an extrinsic suppressive mechanism.

Original languageEnglish
Pages (from-to)139-149
Number of pages11
JournalViral Immunology
Volume4
Issue number3
Publication statusPublished - 1991

ASJC Scopus subject areas

  • Immunology
  • Virology

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