Troublemaker T cells target ribosomal protein

Shipman, Lydia

doi:10.1038/nri3772

Research Highlight
Published: 14 November 2014

Autoimmunity

Troublemaker T cells target ribosomal protein

Lydia Shipman

Nature Reviews Immunology volume 14, page 776 (2014)Cite this article

1906 Accesses
2 Citations
10 Altmetric
Metrics details

Subjects

Access through your institution

Buy or subscribe

The authors cloned single T cell receptors (TCRs) from arthritogenic CD4⁺ effector T cells that were isolated from SKG mice; these mice spontaneously develop a disease that resembles human rheumatoid arthritis as a result of a genetic mutation that reduces the stringency of thymic negative selection. The ability of the cloned TCRs to cause disease was investigated in mice engineered to express the TCRs in developing T cells. The authors then sought to identify the epitope recognized by the TCR that caused the highest incidence of spontaneous rheumatoid arthritis-like disease, the so-called 7-39 TCR.

The serum from mice expressing the 7-39 TCR was found to react with an 18 kDa protein that was identified as the 60S ribosomal protein L23A (RPL23A) by mass spectrometry. Recombinant RPL23A protein induced dose-dependent interleukin-2 production by a 7-39 TCR-expressing T cell hybridoma, and also stimulated inflammatory cytokine production by CD4⁺ T cells from the draining lymph nodes of the arthritic joints of 7-39 TCR-expressing mice.

This is a preview of subscription content, access via your institution

Access options

Access through your institution

Buy this article

Purchase on SpringerLink
Instant access to the full article PDF.

USD 39.95

Prices may be subject to local taxes which are calculated during checkout

References

Ito, Y. et al. Detection of T cell responses to a ubiquitous cellular protein in autoimmune disease. Science 346, 363–368 (2014)
Article CAS PubMed PubMed Central Google Scholar

Download references

Authors