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. Author manuscript; available in PMC: 2021 Jan 26.
Published in final edited form as: Immunity. 2020 Dec 22;54(2):235–246.e5. doi: 10.1016/j.immuni.2020.12.001

Figure 1. cDC-dependent but TCR-independent control over IgM responses to influenza hemagglutinin (HA), a model TD antigen.

Figure 1.

(A) Serum IgM versus IgG responses against HA that was injected intravenously along with lipid A adjuvant (n = 5 animals per group). The responses were elicited in the following groups: splenectomized versus sham control, Tcra−/− versus WT, Zbtb46-DTR chimeras receiving versus not receiving DT, and chimeras containing 50% Zbtb46-DTR:50% MHC class II-deficient (homozygous H2dlAb1-Ea) receiving versus not receiving DT. The dilution curves (mean ± SD) were quantified by endpoint dilution; **p < 0.02, ***p < 0.001, Student’s t test.

(B) These data provide functional evidence of a cDC-dependent but T cell-independent mechanism modulating humoral output (red arrow).

(C) Recapitulation of the IgM (and IgG) response deficits to HA via genetic ablation of IL-6 and IRF5 but not IL-12 (n = 5 animals per group). Antibody response deficits could be rescued by addition of recombinant murine IL-6. The dilution curves were quantified by endpoint dilution; **p < 0.005, *p < 0.05, ANOVA with Tukey’s test. See Figure S1 for chimera methodology, orthogonal demonstration using non-HA antigens, and antibody responses in Ifnar1−/− mice.