Prevention of superantigen-induced tolerance in vivo by interleukin-2 treatment. 1996 Submitted

Forskningsoutput: TidskriftsbidragArtikel i vetenskaplig tidskrift

Abstract

Injection of the superantigen staphylococcal enterotoxin A (SEA) activates both CD4+ and CD8+ T cells expressing certain families of T cell receptor (TCR) variable-region beta (V beta) chain. T cells respond with profound cytokine production and induction of cytotoxicity. Repeated injections, however, cause deletion and anergy of both CD4+ and CD8+ T cells, resulting in reduced frequency of SEA-responsive cells TCR-V beta11+ as well as reduced cytokine levels in serum upon challenge with SEA. Exogenous interleukin-2 (IL-2) in vivo rescued SEA-responsive CD4+ and CD8+ cells from SEA-induced deletion and/or increase expansion of SEA-primed cells as well as preventing downregulation of endogenous IL-2 production in vivo. Combined treatment with SEA and IL-2 also superinduced production of important cytokines for the cytotoxic function of T cells, tumour necrosis factor alpha, interferon gamma and IL-6, on a cellular level. These studies show that continuous stimulation with IL-2 in vivo could be useful for superantigen-based immunotherapy by induction of excessive T cell activation and by prevention of the development of T cell deletion and anergy.

Detaljer

Författare
  • Hans Belfrage
  • M Dohlsten
  • G Hedlund
  • T Kalland
Enheter & grupper
Forskningsområden

Ämnesklassifikation (UKÄ) – OBLIGATORISK

  • Cancer och onkologi
Originalspråkengelska
Sidor (från-till)77-82
TidskriftCancer Immunology and Immunotherapy
Volym44
Utgivningsnummer2
StatusPublished - 1997
PublikationskategoriForskning
Peer review utfördJa

Relaterad forskningsoutput

Belfrage, H., 1996, Department of Cell and Molecular Biology, Lund University. 58 s.

Forskningsoutput: AvhandlingDoktorsavhandling (sammanläggning)

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