Figure 5.

TLR2–NF‐KB/JNK signaling pathways mediate TSLP production to prevent apoptosis of basophils and DCs. (A) OVA‐immunized mice received TSLP or anti‐TSLP were subjected to flow cytometry for determination of apoptosis in basophils and DCs in the lung. (B) Lung cell suspensions of OVA‐immunized mice were stimulated with TSLP or anti‐TSLP in vitro and were subsequently subjected to flow cytometry for the analysis of apoptosis in basophils and DCs. (C) Expression level of anti‐apoptosis protein Bcl‐XL in bone marrow‐derived basophils (BMBas) and BMDCs after TSLP treatment at different time points. (D) Analysis of p‐p65, p‐JNK, and p‐p38 in BEAS‐2B cells after OVA, HDM, and fungi stimulation in BEAS‐2B cells by western blot. (E) Expression level of TSLP mRNA in BEAS‐2B cells treated with inhibitors of NF‐κB, JNK, and p38 followed by OVA, HDM, and fungi stimulation by RT‐PCR. (F) Analysis of NF‐κB and p‐JNK in OxPAPC‐pretreated BEAS‐2B cells with OVA, HDM, and fungi stimulation by western blot. (G) Analysis of NF‐κB and JNK signals in OVA‐stimulated pBECs from WT or TLR2^−/− mice by western blot. For statistical analysis of apoptosis, data are pooled from three independent experiments with five mice each. For RT‐PCR and western blot, data are pooled from five independent experiments. One representative western blot of five independent experiments is shown. Values are shown as mean ± SD and statistical analysis employed unpaired two‐tailed Student's t‐test. *p < 0.05, **p < 0.01, and ***p < 0.001.