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A BACH2—STAT5 transcriptional module is identified that is essential for C3 expression in activated CD4+ T cells and redirects C3 output toward a short, intracellular proteoform with noncanonical complement activity.
A systematic catalog of eRNAs in human adaptive immune cells is defined and a distal transcribed enhancer is identified that fine-tunes KRAS signaling in Tfh cells to support effective vaccine responses, establishing eRNAs as noncoding regulators of T cell circuits controlling antibody production.
A previously unrecognized CPM-dependent mechanism that balances C5aR1 and C5aR2 signaling to limit pathological T cell activation is uncovered, revealing an intrinsic complement-driven checkpoint that constrains effector T cell immunity.
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