University of Exeter
Browse

Identifying the 'Achilles heel' of type 1 diabetes.

Download (624.4 kB)
journal contribution
posted on 2025-08-01, 13:48 authored by M Battaglia, JH Buckner, MK Levings, SJ Richardson, FS Wong, TI Tree
When Thetis dipped her son Achilles into the River Styx to make him immortal, she held him by the heel, which was not submerged, and thus created a weak spot that proved deadly for Achilles. Millennia later, Achilles heel is part of today's lexicon meaning an area of weakness or a vulnerable spot that causes failure. Also implied is that an Achilles heel is often missed, forgotten or under-appreciated until it is under attack, and then failure is fatal. Paris killed Achilles with an arrow 'guided by the Gods'. Understanding the pathogenesis of type 1 diabetes (T1D) in order to direct therapy for prevention and treatment is a major goal of research into T1D. At the International Congress of the Immunology of Diabetes Society, 2018, five leading experts were asked to present the case for a particular cell/element that could represent 'the Achilles heel of T1D'. These included neutrophils, B cells, CD8+ T cells, regulatory CD4+ T cells, and enteroviruses, all of which have been proposed to play an important role in the pathogenesis of type 1 diabetes. Did a single entity emerge as 'the' Achilles heel of T1D? The arguments are summarized here, to make this case.

History

Related Materials

Rights

© 2021 British Society for Immunology

Notes

This is the author accepted manuscript. The final version is available from Oxford University Press via the DOI in this record

Journal

Clinical and Experimental Immunology

Pagination

167-178

Publisher

Oxford University Press/British Society for Immunology

Place published

England

Version

  • Accepted Manuscript

Language

en

FCD date

2022-01-26T16:21:12Z

FOA date

2022-02-22T00:00:00Z

Citation

Vol. 204, No. 2, pp. 167-178

Department

  • Archive

Usage metrics

    University of Exeter

    Categories

    No categories selected

    Exports

    RefWorks
    BibTeX
    Ref. manager
    Endnote
    DataCite
    NLM
    DC