Fig. 3: T cell responses to ancestral and Omicron BA.1 SARS-CoV-2 after vaccination.

a,b, IFNγ T cell response to SARS-CoV-2 spike measured by Oxford Immunotec assay presented as the proportion of individuals with or without an anti-SARS-CoV-2 spike T cell response (a) and the magnitude of IFNγ T cell response in disease groups (n = 645) and healthy controls (n = 189) (b). a,b, The statistical comparison presented is disease group compared to healthy controls (HC) in all participants in group 1. c,d, IFNγ T cell response to ancestral and Omicron BA.1 spike or pools of peptides covering regions mutated in BA.1 and their ancestral equivalents, measured by in-house IFNγ ELISpot at post-V2 timepoint (n = 59 participants selected from liver, rheumatic and inflammatory disease cohorts). e–h, Selected examples of the correlation of anti-SARS-CoV-2 RBD binding total Ig with IFNγ T cell response to ancestral SARS-CoV-2 spike at pre-V2 (e,g) and post-V2 (f,h) timepoints in group 1 (all disease groups) (e,f) and ANCA-associated vasculitis on rituximab patients (g,h). Unpaired statistical comparisons (b,c,d) were assessed with a Kruskal–Wallis test with post hoc Dunn’s testing (adjusted alpha = 0.003). Paired statistical tests were performed with two-sided Wilcoxon’s rank-sum test with Bonferroni correction (adjusted alpha = 0.0125). a–c, * indicates statistically significant by Bonferroni-adjusted alpha. ***adjusted P < 0.001, ****adjusted P < 0.0001. e–h, Correlations are Spearman’s rank-sum correlation, and fitted line is presented. b, Boxes represent median and IQR; whiskers represent ±1.5× IQR. AAV, ANCA-associated vasculitis; CD, Crohn’s disease; CLD, chronic liver disease; HD, hemodialysis; HD on IS, hemodialysis on immunosuppression; HM, hematological malignancy; IA, inflammatory arthritis; L-AI, autoimmune hepatitis; L-Cir, liver cirrhosis; L-Tr, liver transplant; Nucleocapsid negative, N-ve; Nucleocapsid positive, N+ve; NS, not significant; RC, rheumatic conditions; SC, solid cancer; UC, ulcerative colitis.