Absence of AD and attenuation of associated humoral and lung inflammatory response in CX₃CR1-deficient mice. AD was induced on abdominal skin in CX₃CR1^+/+ and CX₃CR1^gfp/gfp mice by epicutaneous LACK sensitization for three 1-wk periods, with a 2-wk interval between applications. At day 49, sera were collected and animals were challenged by LACK nebulization. At day 50, AHR to increasing concentrations of methacholine was measured by invasive plethysmography. Then, mice were sacrificed and BALF was collected and analyzed on cytospin preparations. Skin samples were collected at the site of sensitization. (A) May-Grünwald Giemsa staining of skin sections. Black arrows indicate mast cells and, in the inset, eosinophils. (B) Epidermal thickness. (C) Eosinophil, mast cell, MHC II⁺, and CD4⁺ T cell numbers in dermis. (D) Ig concentrations in serum. Total IgE (left), LACK-specific IgG₁ (middle), and LACK-specific IgG_2a (right) concentrations are shown. Horizontal bars indicate mean. (E) AHR to increasing methacholine concentrations. Resistance was evaluated by invasive plethysmography. (F) Lung inflammatory response: total number of cells, macrophages, neutrophils, lymphocytes, and eosinophils in BALF. Data are expressed as mean ± SEM (n = 6–10 animals per group). One out of two independent experiments is shown for each panel. *, P < 0.05; ** P < 0.01.