Cell state · L2
B.memory.pDC_imprint
877 cells in the full atlas (not the displayed sample).
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Marker genes
APBB1IP, CD1C, FCRL2, HCK, KLK1, LILRA4, PLAC8, PLD4, PPP1R14A, RNASEK, SYK
Annotation genes
CD1C, FCRL2, LILRA4, PLD4, SYK
Annotation rationales
The coexistence of LILRA4/PLD4/CD1C (pDC/cDC-skewed transcripts) with FCRL2/SYK (B-cell memory/BCR signaling) indicates type-I IFN imprinting rather than cellular contamination. Such programs are typically induced by TLR7/9 sensing of nucleic acids during viral exposure or autoimmune flares, transiently endowing B cells with heightened antiviral and endosomal processing features while preserving BCR competence. HCK/PLAC8 support innate-like phagosome and interferon circuitry; APBB1IP (RIAM) suggests integrin activation for immune-synapse dynamics under inflammatory conditions. This signature captures memory B cells adapted to interferon-rich milieus.
Functional implications
Functions as an innate-tuned memory module that integrates pDC-like antiviral readiness into the adaptive B-cell compartment. These cells are primed for vigorous TLR7/9 responses, produce inflammatory cues that shape Tfh and dendritic-cell help, and can present antigen efficiently while retaining the capacity to differentiate into antibody-secreting cells. In infection, they bolster early antiviral control and accelerate class-switched recall; in autoimmunity, the same circuitry may amplify nucleic-acid–driven responses, contributing to disease unless restrained by regulatory networks.
Marker and functional descriptions are atlas annotations. Explore gene expression, trait associations and regulatory elements in the interactive browsers; see the browser guide.