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Related Experiment Videos

Inflammation activates self hsp60-specific T cells

S M Anderton1, R van der Zee, J A Goodacre

  • 1Department of Medicine (Rheumatology), University of Newcastle upon Tyne, GB.

European Journal of Immunology
|January 1, 1993
PubMed
Summary

Inflammation can activate T cells against self heat shock protein 60 (hsp60), even without bacterial hsp65 exposure. This finding may explain T cell responses in arthritis patients and the protective effects of hsp65 pre-immunization.

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Area of Science:

  • Immunology
  • Molecular Biology
  • Autoimmunity

Background:

  • Injection of incomplete Freund's adjuvant (IFA) in mice induces acute inflammation.
  • Popliteal lymph nodes exhibit major histocompatibility complex (MHC) class II-restricted proliferation upon challenge with Mycobacterium bovis 65-kDa heat shock protein (hsp65).

Purpose of the Study:

  • To investigate T cell activation against self heat shock protein 60 (hsp60) during inflammation.
  • To explore the cross-reactivity between bacterial hsp65 and self hsp60 epitopes.

Main Methods:

  • Generation of alpha beta T cell receptor-positive, CD4+, hsp65-specific T cell lines and clones from inflamed lymph nodes.
  • In vitro proliferation assays using recombinant hsp65, beta-galactosidase fusion proteins of human hsp60, and synthetic peptides of mouse hsp60.

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Main Results:

  • 87% of hsp65-specific T cell clones responded to human hsp60 fusion protein.
  • 70% of hsp60-responsive clones recognized a synthetic peptide from mouse hsp60.
  • This peptide induced significant T cell responses in IFA-primed, but not naive, mice.

Conclusions:

  • T cells specific for self hsp60 epitopes are activated during inflammatory responses.
  • This activation occurs independently of exogenous bacterial hsp65.
  • Findings may elucidate T cell responses in arthritis and the role of hsp65 in experimental arthritis models.