Given that SAT cells and ABCs also contribute to SLE pathophysiology in murine models (16, 23), these results raise the hypothesis that the aberrant interactions between Tph and Tfh cells, which correspond to SAT cells in humans, and ABCs within TLTs might be a common pathological mechanism for driving chronic inflammation across multiple diseases and conserved across species. Here, TPH1 is linked to systemic lupus erythematosus.