A reply to “TCR+/BCR+ dual-expressing cells and their associated public BCR clonotype are not enriched in type 1 diabetes”

Rizwan Ahmed, Zahra Omidian, Adebola Giwa, Thomas Donner, Chunfa Jie, Abdel Rahim A. Hamad

Research output: Contribution to journalArticlepeer-review

Abstract

We have recently identified a novel lymphocyte that is a dual expresser (DE) of TCRαβ and BCR. DEs in T1D patients are predominated by a public BCR clonotype (clone-x) that encodes a potent autoantigen that cross-activates insulin-reactive T cells. Betts and colleagues were able to detect DEs but alleged to not detect high DE frequency, clone-x, or similar clones in T1D patients. Unfortunately, the authors did not follow our methods and when they did, their flow cytometric data at two sites were conflicting. Moreover, contrary to their claim, we identified clones similar to clone-x in their data along with clones bearing the core motif (DTAMVYYFDYW). Additionally, their report of no increased usage of clone-x VH/DH genes by bulk B cells confirms rather than challenges our results. Finally, the authors failed to provide data verifying purity of their sorted DEs, making it difficult to draw reliable conclusion of their repertoire analysis. This Matters Arising Response paper addresses the Japp et al. (2021) Matters Arising paper, published concurrently in Cell.

Original languageEnglish (US)
Pages (from-to)840-843
Number of pages4
JournalCell
Volume184
Issue number3
DOIs
StatePublished - Feb 4 2021

Keywords

  • DE cells
  • TCR
  • X cells
  • autoimmunity
  • dual expresser cells
  • insulin-mimotope
  • public BCR clonotype
  • type 1 diabetes
  • x-autoantigen

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

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