Assessment of PIR-B expression in the allergic lung. (A) Expression of PIR-B was assessed by gene chip analysis in saline-challenged, OVA-challenged, and Aspergillus fumigatus (Asp)–challenged mice; *P < .05 when comparing OVA- and Asp-treated mice with saline groups. (B) The cellular source for PIR-B expression was assessed in the BALF of OVA-challenged mice. Data are represented as percentage of cell population from total BALF cells plus or minus SD and was defined by flow cytometric analysis as follows: macrophages (Mac, FSC^high, Mac-3⁺, CCR3⁻), (Eos, SSC^high, CCR3⁺), neutrophils (Neut, SSC^intermediate, CCR3⁻, Gr-1⁺), T cells (FSC^low, SSC^low, B220⁻, CD3⁺), and B cells (FSC^low, SSC^low, B220⁺, CD3⁻). Values in parentheses indicate the mean fluorescent intensity (MFI) of PIR-A/B expression on the various cell population. (C) Analysis of the expression of PIR-A/B on various cell populations in the BALF of OVA-challenged mice. (D) The relative expression of PIR-B and PIR-A on eosinophils was assessed by FACS analysis by staining for PIR-A/B on wild-type (WT) or Pirb^−/− eosinophils. (E) Data shown are a representative histogram plot of n = 4. The lungs of Asp-challenged wild-type and Δdbl-GATA were assessed for PIR-B expression; *P < .05 when comparing Asp-treated wild-type and Asp-treated Δdbl-GATA mice. The average difference for the hybridization signal after saline and allergen challenge is depicted (n = 3 mice for saline groups, n = 2-4 mice for OVA and Aspergillus experimental groups). PIR-B expression was assessed on gated eosinophils. Error bars represent SD.