AICDA and infection: The Cda2-independent polyclonal Th2 cell response to gpr4Δgpr5Δ infection was also significantly lower than the responses to KN99α and rim101Δ infections (S7B Fig.), indicating the defect in antigen-specific Th2 cell accumulation to gpr4Δgpr5Δ infection was not due to differential expression of cda2 between the strains.