Fig. 1: Viral-specific humoral responses are primarily compartmentalized within the liver in strictly hepatotropic viral infection.
From: iHALT unlocks liver functionality as a surrogate secondary lymphoid organ
a, Quantification of IgG-secreting ASCs during RHV infection in PBMCs, spleen, bone marrow and liver by ELISpot. Connecting line represents mean values. b,c, Correlations between bone marrow ASCs and splenic (b) or intrahepatic (c). Two-tailed nonparametric Spearman correlations with Pearson’s r. d, Serum IgG and intrahepatic ASCs after RHV infection. e,f, Total (e) and E2-specific (f) ASCs at 4 weeks post-RHV infection from n = 2 independent experiments. LN, lymph node. g, Representative ELISpot images of total and E2-specific ASCs in PBMCs and intrahepatic lymphocytes from mice at four weeks post-RHV infection (top) and chronically HCV-infected humans (bottom). h–k, Quantification of total (h,i) and E2-specific (j,k) ASCs from RHV-infected mice (h,j) and HCV-infected humans (i,k), with individual-matched paired comparisons shown between PBMCs and intrahepatic lymphocytes. Data from n = 15 mice from n = 2 independent experiments (j) and n = 9 individuals (k). Two-tailed, paired t-test; P = 0.0082 (i); P = 0.0019 (k). a–h,j, Mouse data are representative or pooled values from at least two independent experiments with at least three mice per group. g,i,k, Human data include nine individuals chronically infected with HCV. d–f, Data are mean ± s.e.m. *P < 0.05, **P ≤ 0.01, ***P ≤ 0.001, ****P ≤ 0.0001. NS, not significant (P < 0.05).
