ARPC1B-containing complexes) in immune cells and if variant-specific interactors (e.g., ARPC1B-WASP) are the key to functional specificity, how tissue microenvironments (e.g., lymph node stromal factors) buffer Arp2/3 dysfunction (e.g., DC migration discrepancies between in vitro and in vivo), and whether subtype-specific Arp2/3 defects drive distinct diseases (e.g., ARPC5 for immunodeficiency, ARPC1B for autoimmunity) and what the molecular link between variants and disease subtypes is. This evidence concerns the gene WAS and immune system disorder.