Figure 6
Figure 6. Triggering of TLR4 and TRIF in B lymphocytes is required for the induction of TI anti-Aβ IgG responses. (A) Anti-Aβ IgG antibodies in the sera of WT mice receiving liposomes containing both MPLA (19 μg of MPLA per dose) and Aβ1-15 (94 μg of PalmAβ1-15 per dose) or a 1:1 mixture of MPLA-containing liposomes and Aβ1-15–containing liposomes (as indicated by arrows). The 2 liposome formulations were mixed before injection. Results are expressed as mean ± SD (n = 10 per group). (B) Schematic representation of the generation of mice expressing or lacking TLR4 on B lymphocytes. Splenocytes from WT, TLR4−/−, or TRIF−/− mice were transferred into B cell–deficient μMT mice. (C) Analysis of anti-Aβ IgG responses in B cell–deficient μMT mice receiving splenocytes from WT, TLR4−/−, or TRIF−/− mice followed by immunization with Aβ-peptide liposomes. Results are expressed as mean + SD (n = 3 per group).

Triggering of TLR4 and TRIF in B lymphocytes is required for the induction of TI anti-Aβ IgG responses. (A) Anti-Aβ IgG antibodies in the sera of WT mice receiving liposomes containing both MPLA (19 μg of MPLA per dose) and Aβ1-15 (94 μg of PalmAβ1-15 per dose) or a 1:1 mixture of MPLA-containing liposomes and Aβ1-15–containing liposomes (as indicated by arrows). The 2 liposome formulations were mixed before injection. Results are expressed as mean ± SD (n = 10 per group). (B) Schematic representation of the generation of mice expressing or lacking TLR4 on B lymphocytes. Splenocytes from WT, TLR4−/−, or TRIF−/− mice were transferred into B cell–deficient μMT mice. (C) Analysis of anti-Aβ IgG responses in B cell–deficient μMT mice receiving splenocytes from WT, TLR4−/−, or TRIF−/− mice followed by immunization with Aβ-peptide liposomes. Results are expressed as mean + SD (n = 3 per group).

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