IL10 and Epstein-Barr virus infection: LMP1 mimics CD40 signalling to activate multiple B-cell growth and survival pathways, particularly NF-κB.34 In parallel, LMP2A mimics the B-cell receptor (BCR) signalling cascade by bypassing the BCR and signalling directly through Syk/RAS/PI3K, Bruton’s tyrosine kinase (BTK) and STAT3, leading to increased IL10 production.35 IL10 then promotes B-cell proliferation and survival via autocrine mechanisms.35,36 In addition, EBV infection also induces CD40 ligand expression that can provide co-stimulatory activity.37