The development of CD4(+) T effector cells during the type 2 immune response

Multiple pathways may be involved in the development of interleukin 4 (IL-4 ) producing T helper (Th) cells and the associated type 2 immune response. Increasing evidence suggests that the strength of signals delivered to the T cell may favor the development of the type 2 response. In contrast, antig en-presenting cell- (APC) derived stimuli produced following pattern recogn ition receptor binding during the innate response promotes the development of interferon-gamma (IFN-gamma) producing cells and the associated type 1 i mmune response. In many cases, the balance between increased signaling stre ngth and the innate response may determine whether the type 2 response deve lops. T cell receptor (TCR), CD4, and costimulatory molecule interactions m ay all contribute to signal strength, but the type 2 immune response may be particularly dependent on the availability of coreceptor and costimulatory molecule interactions. B7 ligand interactions are required for the develop ment of the type 2 immune response and interaction of CD28 with either B7-1 or B7-2 can provide sufficient signals for its initiation. In B7-2-deficie nt mice, the initial type 2 immune response is intact, but the response is not sustained, suggesting that B7-2 is important at later stages of the typ e 2 immune response. The roles of CD28 and CTLA-4 during the type 2 respons e remain unclear. The type 2 response to infectious pathogens is pronounced in CD28(-/-) mice, suggesting that. other costimulatory molecule interacti ons can substitute for CD28 for the development of IL-4 producing T cells a nd the associated type 2 immune response.