Interleukin (IL)-23 is a heterodimeric cytokine composed of a unique p19 subunit, and a common p40 subunit shared with IL-12. IL-12 is important for the development of T helper (Th)1 cells that are essential for host defense and tumor suppression. In contrast, IL-23 does not promote the development of interferon-γ–producing Th1 cells, but is one of the essential factors required for the expansion of a pathogenic CD4+ T cell population, which is characterized by the production of IL-17, IL-17F, IL-6, and tumor necrosis factor. Gene expression analysis of IL-23–driven autoreactive T cells identified a unique expression pattern of proinflammatory cytokines and other novel factors, distinguishing them from IL-12–driven T cells. Using passive transfer studies, we confirm that these IL-23–dependent CD4+ T cells are highly pathogenic and essential for the establishment of organ-specific inflammation associated with central nervous system autoimmunity.

Interleukin (IL) 23 is a heterodimeric cytokine composed of a p19 subunit and the p40 subunit of IL-12. IL-23 affects memory T cell and inflammatory macrophage function through engagement of a novel receptor (IL-23R) on these cells. Recent analysis of the contribution of IL-12 and IL-23 to central nervous system autoimmune inflammation demonstrated that IL-23 rather than IL-12 was the essential cytokine. Using gene-targeted mice lacking only IL-12 (p35−/−) or IL-23 (p19−/−), we show that the specific absence of IL-23 is protective, whereas loss of IL-12 exacerbates collagen-induced arthritis. IL-23 gene-targeted mice did not develop clinical signs of disease and were completely resistant to the development of joint and bone pathology. Resistance correlated with an absence of IL-17–producing CD4+ T cells despite normal induction of collagen-specific, interferon-γ–producing T helper 1 cells. In contrast, IL-12–deficient p35−/− mice developed more IL-17–producing CD4+ T cells, as well as elevated mRNA expression of proinflammatory tumor necrosis factor, IL-1β, IL-6, and IL-17 in affected tissues of diseased mice. The data presented here indicate that IL-23 is an essential promoter of end-stage joint autoimmune inflammation, whereas IL-12 paradoxically mediates protection from autoimmune inflammation.

Hypertensive disorders of pregnancy (HDP) are a group of medical complications in pregnancy and also a risk factor for severe pregnancy outcomes, but it lacks a large-scale epidemiological investigation in recent years. This survey represents a multicenter cross-sectional retrospective study to estimate the prevalence and analyze the risk factors for HDP among the pregnant women who had referred for delivery between January 1st 2011 and December 31st 2011 in China Mainland. A total of 112,386 pregnant women were investigated from 38 secondary and tertiary specialized or general hospitals randomly selected across the country, of which 5,869 had HDP, accounting for 5.22% of all pregnancies. There were significant differences in the prevalence of HDP between geographical regions, in which the North China showed the highest (7.44%) and Central China showed the lowest (1.23%). Of six subtypes of HDP, severe preeclampsia accounted for 39.96%, gestational hypertension for 31.40%, mild preeclampsia for 15.13%, chronic hypertension in pregnancy for 6.00%, preeclampsia superimposed on chronic hypertension for 3.68% and eclampsia for 0.89%. A number of risk factors for HDP were identified, including twin pregnancy, age of >35 years, overweight and obesity, primipara, history of hypertension as well as family history of hypertension and diabetes. The prevalence of pre-term birth, placental abruption and postpartum hemorrhage were significantly higher in women with HDP than those without HDP. The possible risk factors confirmed in this study may be useful for the development of early diagnosis and appropriate treatment of HDP.

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