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

Belfrage, Hans LU ; Dohlsten, M ; Hedlund, G and Kalland, T (1997) In Cancer Immunology and Immunotherapy 44(2). p.77-82
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... (More)
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. (Less)
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author
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organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Cancer Immunology and Immunotherapy
volume
44
issue
2
pages
77 - 82
publisher
Springer
ISSN
1432-0851
language
English
LU publication?
yes
id
6062a663-1611-458a-ae4b-3bd3d5e09c0f (old id 32340)
date added to LUP
2016-04-01 15:33:44
date last changed
2018-11-21 20:35:08
@article{6062a663-1611-458a-ae4b-3bd3d5e09c0f,
  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.}},
  author       = {{Belfrage, Hans and Dohlsten, M and Hedlund, G and Kalland, T}},
  issn         = {{1432-0851}},
  language     = {{eng}},
  number       = {{2}},
  pages        = {{77--82}},
  publisher    = {{Springer}},
  series       = {{Cancer Immunology and Immunotherapy}},
  title        = {{Prevention of superantigen-induced tolerance in vivo by interleukin-2 treatment. 1996 Submitted}},
  volume       = {{44}},
  year         = {{1997}},
}