期刊
JOURNAL OF IMMUNOLOGY
卷 195, 期 2, 页码 507-518出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1500027
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资金
- National Institutes of Health [RO1AI048541, R21HD060089]
- National Institute of General Medical Sciences Training Grant [5T32GM008396-22]
Neonatal immunity exhibits weak Th1 but excessive Th2 responses, and the underlying mechanisms remain elusive. In this article, we show that neonatal basophils readily produce IL-4, a cytokine that proved to be pivotal in shaping the programs of both lymphocyte subsets. Besides promoting Th2 programs, IL-4 is captured by the IL-4 heteroreceptor (IL-4R alpha/IL-13R alpha 1) expressed on dendritic cells and instigates IL-12 downregulation. Under these circumstances, differentiating Th1 cells upregulate IL-13R alpha 1, leading to an unusual expression of the heteroreceptor, which will serve as a death marker for these Th1 cells during rechallenge with Ag. The resulting Th1/Th2 imbalance impacts childhood immunity culminating in sensitivity to allergic reactions, susceptibility to microbial infection and perhaps poor efficacy of pediatric vaccines.
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