Deletion of a coordinate regulator of type 2 cytokine expression in mice
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作者:
Mohrs, M
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机构:Univ Calif San Francisco, Howard Hughes Med Inst, San Francisco, CA 94143 USA
Mohrs, M
Blankespoor, CM
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机构:Univ Calif San Francisco, Howard Hughes Med Inst, San Francisco, CA 94143 USA
Blankespoor, CM
Wang, ZE
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机构:Univ Calif San Francisco, Howard Hughes Med Inst, San Francisco, CA 94143 USA
Wang, ZE
Loots, GG
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机构:Univ Calif San Francisco, Howard Hughes Med Inst, San Francisco, CA 94143 USA
Loots, GG
Afzal, V
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机构:Univ Calif San Francisco, Howard Hughes Med Inst, San Francisco, CA 94143 USA
Afzal, V
Hadeiba, H
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机构:Univ Calif San Francisco, Howard Hughes Med Inst, San Francisco, CA 94143 USA
Hadeiba, H
Shinkai, K
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机构:Univ Calif San Francisco, Howard Hughes Med Inst, San Francisco, CA 94143 USA
Shinkai, K
Rubin, EM
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机构:Univ Calif San Francisco, Howard Hughes Med Inst, San Francisco, CA 94143 USA
Rubin, EM
Locksley, RM
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Univ Calif San Francisco, Howard Hughes Med Inst, San Francisco, CA 94143 USAUniv Calif San Francisco, Howard Hughes Med Inst, San Francisco, CA 94143 USA
Locksley, RM
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机构:
[1] Univ Calif San Francisco, Howard Hughes Med Inst, San Francisco, CA 94143 USA
[2] Univ Calif San Francisco, Dept Med, San Francisco, CA 94143 USA
[3] Univ Calif San Francisco, Dept Microbiol Immunol, San Francisco, CA 94143 USA
[4] Univ Calif Berkeley, Lawrence Berkeley Lab, Genome Sci Dept, Berkeley, CA 94720 USA
Mechanisms that underlie the patterning of cytokine expression in T helper (T-H) cell subsets remain incompletely defined. An evolutionarily conserved similar to 400.bp noncoding sequence in the intergenic region between the genes Il4 and III3, designated conserved noncoding sequence I (CNS-1), was deleted in mice. The capacity to develop T(H)2 cells was compromised in vitro and in vivo in the absence of CNS-1. Despite the profound effect in T cells, mast cells from CNS-1(-/-) mice maintained their capacity to produce interleukin 4. AT cell-specific element critical for the optimal expression of type 2 cytokines may represent the evolution of a regulatory sequence exploited by adaptive immunity.