Follicular T cells are clonally and transcriptionally distinct in B cell-driven mouse autoimmune disease

Elliot H. Akama-Garren, Theo Broek, Lea Simoni, Carlos Castrillon, Cees E. Poel and Michael C. Carroll ()
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Elliot H. Akama-Garren: Harvard Medical School
Theo Broek: Harvard Medical School
Lea Simoni: Harvard Medical School
Carlos Castrillon: Harvard Medical School
Cees E. Poel: Harvard Medical School
Michael C. Carroll: Harvard Medical School

Nature Communications, 2021, vol. 12, issue 1, 1-19

Abstract: Abstract Pathogenic autoantibodies contribute to tissue damage and clinical decline in autoimmune disease. Follicular T cells are central regulators of germinal centers, although their contribution to autoantibody-mediated disease remains unclear. Here we perform single cell RNA and T cell receptor (TCR) sequencing of follicular T cells in a mouse model of autoantibody-mediated disease, allowing for analyses of paired transcriptomes and unbiased TCRαβ repertoires at single cell resolution. A minority of clonotypes are preferentially shared amongst autoimmune follicular T cells and clonotypic expansion is associated with differential gene signatures in autoimmune disease. Antigen prediction using algorithmic and machine learning approaches indicates convergence towards shared specificities between non-autoimmune and autoimmune follicular T cells. However, differential autoimmune transcriptional signatures are preserved even amongst follicular T cells with shared predicted specificities. These results demonstrate that follicular T cells are phenotypically distinct in B cell-driven autoimmune disease, providing potential therapeutic targets to modulate autoantibody development.

Date: 2021
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DOI: 10.1038/s41467-021-27035-8

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