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. Author manuscript; available in PMC: 2015 May 27.
Published in final edited form as: Immunity. 2014 Jan 16;40(1):78–90. doi: 10.1016/j.immuni.2013.10.023

Figure 3. Impaired CD4+ T cells response in MyD88T-KO mice is caused by defective IL-1 signaling.

Figure 3

(A, B) Expression of the receptors for IL-1 (A) and IL-18 (B) in CD4+ T cells in the draining lymph nodes of immunized MyD88T-KO and wild-type control mice as measured by qPCR. The expression levels were normalized to the level of naïve CD4+ T cells. A representative experiment using the pooled samples from 5–10 mice per genotype is shown. (C, D) CD4+ T cell response of Rag2-deficient mice reconstituted with a 3:1 mix of bone marrow from TCRβ-deficient mice and IL1RKO, IL18KO, or TLR2KO; TLR4KO mice, respectively. CD4+ T cells were restimulated with OVA in the presence of irradiated splenocytes 7 days after the immunzation of the bone marrow chimeras in the feet with OVA + LPS in IFA. The proliferation was measured 3 days later by 3H-thymidine incorporation (C) and the secretion of IFNγ and IL-17 of the restimulated CD4+ T cells was measured by ELISA (D). A epresentative experiment is shown. (E, F). CD4+ T cell response of mixed bone marrow chimeras harboring bone marrow of IL1RKO, IL18KO, or wild-type mice mixed with bone marrow of TCRβKO mice in a ratio of 1:3 after footpad immunization with OVA + LPS in IFA. A representative experiment is shown.