Human interferons signal through three receptor classes: the Type I IFN receptor (IFNAR1/IFNAR2), the Type II IFN receptor (IFNGR1/IFNGR2), and the Type III IFN receptor (IFNLR1/IL10RB). PBL's monoclonal antibodies cover all three classes. Neutralizing clones block receptor signaling, enabling assessment of whether a given effect is receptor-dependent; binding clones detect or confirm receptor presence without disrupting signaling.
Type I IFN Receptor: IFNAR1 and IFNAR2
IFNAR1 and IFNAR2 form the receptor for IFN-alpha and IFN-beta. IFNAR2 carries most of the ligand-binding affinity; IFNAR1 is required for signal transduction once IFN is bound. Engagement of both chains activates JAK1 and TYK2, leading to STAT1/STAT2 phosphorylation and formation of the ISGF3 complex that drives interferon-stimulated gene expression.
Type II IFN Receptor: IFNGR2
IFN-gamma signals through IFNGR1 and IFNGR2. IFNGR1 does most of the ligand binding; IFNGR2 recruits JAK2 and is required for STAT1 activation downstream.
Type III IFN Receptor: IFNLR1
IFNLR1 pairs with IL10RB to form the receptor for IFN-lambda. Unlike the broadly expressed Type I receptor, IFNLR1 is largely restricted to epithelial cells at mucosal surfaces, which is what makes IFN-lambda signaling separable from Type I IFN in mucosal antiviral research.