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Yamanouchi J Rainbow D Serra P Howlett S Hunter K Garner VE Gonzalez-Munoz A Clark J Veijola R Cubbon R Chen SL Rosa R Cumiskey AM Serreze DV Gregory S Rogers J Lyons PA Healy B Smink LJ Todd JA Peterson LB Wicker LS Santamaria P 《Nature genetics》2007,39(3):329-337
Autoimmune diseases are thought to result from imbalances in normal immune physiology and regulation. Here, we show that autoimmune disease susceptibility and resistance alleles on mouse chromosome 3 (Idd3) correlate with differential expression of the key immunoregulatory cytokine interleukin-2 (IL-2). In order to test directly that an approximately twofold reduction in IL-2 underpins the Idd3-linked destabilization of immune homeostasis, we show that engineered haplodeficiency of Il2 gene expression not only reduces T cell IL-2 production by twofold but also mimics the autoimmune dysregulatory effects of the naturally occurring susceptibility alleles of Il2. Reduced IL-2 production achieved by either genetic mechanism correlates with reduced function of CD4(+) CD25(+) regulatory T cells, which are critical for maintaining immune homeostasis. 相似文献
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