Early defect T_H2 expansion and RELM-β expression in TFF2^−/− mice is responsible for delayed immunity against N. brasiliensis infection. (A) IL4 and IL13 mRNA transcripts in naive WT and TFF2^−/− mice or 3 d after N. brasiliensis infection. Means ± SE of five to six mice/group are shown. (B) Representative dot plot showing IL-13–positive CD4⁺ lymphocytes within the LN of naive WT and TFF2^−/− mice or 3 d after N. brasiliensis infection. Four individual mice/group were analyzed for infected samples, whereas naive LNs were pooled from two to three mice. (C) Mean percentage (±SE) of IL-13–positive CD4⁺ lymphocytes from the experiment described in B. (D) Serum IL-4 abundance, as determined by in vivo cytokine capture assay at 0, 7, and 12 d after infection. Means ± SE of five to six mice/group are shown. (E) Intestinal RELM-β mRNA transcript levels at 0, 7, and 12 d after infection. Means ± SE of five to six mice/group are shown. (F) N. brasiliensis intestinal worms recovered from intestinal lumen on day 8 from WT versus TFF2^−/− mice that were injected with vehicle or rIL-4/anti–IL-4 complexes (IL-4C) at days 0 and 4. Means ± SE of five to six mice/group are shown. n.d., not detected. (G) Immunofluorescence staining for RELM-β within the jejunum of mice from the experiment described in F. Cell nuclei stained with DAPI. Bars, 50 µm. Data are representative of three to four independent experiments (*, P < 0.05; **, P < 0.01).