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The Development of CD4 super(+) T Effector Cells During the Type 2 Immune Response
by
Ekkens, M
, Nguyen, D
, Urban, J F
, Finkelman, F D
, Liu, Q
, Mitro, V
, Greenwald, R J
, Gause, W C
1999
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The Development of CD4 super(+) T Effector Cells During the Type 2 Immune Response
by
Ekkens, M
, Nguyen, D
, Urban, J F
, Finkelman, F D
, Liu, Q
, Mitro, V
, Greenwald, R J
, Gause, W C
1999
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The Development of CD4 super(+) T Effector Cells During the Type 2 Immune Response
Journal Article
The Development of CD4 super(+) T Effector Cells During the Type 2 Immune Response
1999
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Overview
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, antigen-presenting cell-(APC) derived stimuli produced following pattern recognition receptor binding during the innate response promotes the development of interferon- gamma (IFN- gamma ) producing cells and the associated type 1 immune response. In many cases, the balance between increased signaling strength and the innate response may determine whether the type 2 response develops. T cell receptor (TCR), CD4, and costimulatory molecule interactions may 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 development 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-deficient 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 type 2 immune response. The roles of CD28 and CTLA-4 during the type 2 response remain unclear. The type 2 response to infectious pathogens is pronounced in CD28 super(-/-) mice, suggesting that other costimulatory molecule interactions can substitute for CD28 for the development of IL-4 producing T cells and the associated type 2 immune response.
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