Single-cell and repertoire profiling reveals immune remodelling in paediatric upper airway: insights from adenoid hypertrophy

<h4>Objectives</h4>To characterise the immune cellular landscape and paired B-cell and T-cell receptor repertoires of hypertrophic adenoids in children with obstructive sleep apnoea.<h4>Methods</h4>We performed 10x Genomics 5' single-cell RNA sequencing with paired V(D)J profiling on adenoid tissues from children (AH, <i>n</i> = 4; control, <i>n</i> = 4) and analysed 72 076 high-quality cells.<h4>Results</h4>Compared with controls, AH adenoids exhibited an expanded B-cell compartment (62.26% vs 51.94%, <i>P</i> = 0.029) and a modest increase in plasmacytoid dendritic cells (0.37% vs 0.15%, <i>P</i> = 0.029), accompanied by reduced T-cell representation (34.19% vs 44.54%, <i>P</i> = 0.029). Within the B-cell compartment, GC B cell populations were expanded in AH, particularly Cycling B cells (15.07% vs 2.86%, <i>P</i> = 0.029), whereas memory B cells were reduced (21.48% vs 32.18%, <i>P</i> = 0.029). B-cell receptor analysis demonstrated reduced somatic hypermutation frequencies across multiple mature B-cell subsets in AH, accompanied by an isotype distribution skewed towards IgM with reduced class-switched fractions. Although CD8⁺ tissue-resident memory T-cell (TRM) frequencies were similar between groups, CD8⁺ TRM in AH adenoids displayed interferon-polarised and antigen-processing signatures, and T-cell clonal expansion occurred predominantly within this subset.<h4>Conclusion</h4>These findings suggest that AH is not merely an anatomic cause of upper airway obstruction but also an immunologically active mucosal state associated with ongoing immune remodelling and antiviral defence.