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 Immunodeficiency.