Deletion of a coordinate regulator of type 2 cytokine expression in mice
Markus Mohrs1, 2, Catherine M. Blankespoor3, Zhi-En Wang1, Gaby G. Loots3, Veena Afzal3, Husein Hadeiba2, Kanade Shinkai2, Edward M. Rubin3
& Richard M. Locksley1, 2
1
Howard Hughes Medical Institute, University of California San Francisco, San Francisco, CA 94143, USA.
2
Departments of Medicine and Microbiology-Immunology, University of California San Francisco, San Francisco, CA 94143, USA.
3
Genome Sciences Department, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA.
Mechanisms that underlie the patterning of cytokine expression in T helper (TH) cell subsets remain incompletely defined. An evolutionarily conserved 400-bp noncoding sequence in the intergenic region between the genes Il4 and Il13, designated conserved noncoding sequence 1 (CNS-1), was deleted in mice. The capacity to develop TH2 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. A T cell−specific element critical for the optimal expression of type 2 cytokines may represent the evolution of a regulatory sequence exploited by adaptive immunity.
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400-bp noncoding sequence in the intergenic region between the genes Il4 and Il13, designated conserved noncoding sequence 1 (CNS-1), was deleted in mice. The capacity to develop TH2 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. A T cell−specific element critical for the optimal expression of type 2 cytokines may represent the evolution of a regulatory sequence exploited by adaptive immunity.
