In BriefSingle-nucleotide polymorphisms in ETS1 are associated with systemic lupus erythematosus (SLE). Kim et al. show that Ets1 deletion in T cells, but not B cells or DCs, result in SLE-like humoral autoimmunity, which was due to the expansion of GATA-3 + Bcl6 + Tfh2 cells and could be alleviated by neutralizing IL-4. Tfh2 frequencies in SLE patients correlate with disease parameters, suggesting therapeutic relevance for IL-4 blockade.

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