Tα1-induced Treg cells inhibit alloreactivity. (A) Murine CD4+ T lymphocytes from TLNs of mice that received transplants were stimulated with irradiated allogeneic splenocytes, autologous splenic DCs stimulated with conidia, or concanavalin A. T-cell proliferation was assessed in a 5-day MLR assay and measured by H3-thymidine incorporation over the last 8 hours. *P < .05, recipient versus donor mice. **P < .05, T-cell– and/or DC-treated mice versus untreated mice. ***P < .05, Tα1-treated DCs versus untreated DCs. (B-C) Proliferative activity and IFN-γ production by purified CD4+CD25– T cells from recipient mice against autologous splenic DCs pulsed with Aspergillus conidia (B) or allogeneic (BALB/c) splenic DCs (C) in the presence of TLN CD4+CD25+ T cells from recipient mice receiving FL-DCs (a) or Tα1–GM-DCs (b). The data shown are representative results from 1 of 3 independent experiments. *P < .05, Aspergillus- or alloantigen-specific reactivity versus unstimulated cells. **P < .05, Tα1-treated versus untreated DCs. (D) Peritoneal neutrophils (PMNs) were exposed to resting conidia in the presence of lung CD4+CD25+ T cells from FL-DC–treated (a) or Tα1-GM-DC–treated mice (b) for 60 minutes for oxidant production (expressed as nanomoles O2–/106 cells) or 24 hours for cytokine production (pg/mL by ELISA). *P < .05, conidia-exposed versus unexposed PMNs. **P < .05, unexposed versus Treg–exposed PMNs. ***P < .05, CD25+ (a) versus CD25+ (b) Treg.
