Chapter 17

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辅助性T细胞17/白介素17在动脉粥样硬化发生与发展中的作用

<正>炎症反应贯穿于动脉粥样硬化发生、斑块形成、易损斑块破裂到血栓形成的全过程,与急性冠状动脉综合征(acute coronary syndrome,ACS)的病理生理过程密不可分。大量研究表明,免疫细胞是动脉粥样硬化的直接参与者[1],T细胞在动脉粥样硬化病变进展中起到了关键性的作用,根据所产     

17 alpha-hydroxylation deficiency

Cases of sexual immaturity and male pseudohermaphroditism due to disorders such as androgen resistance, 5 alpha-reductase deficiency, cholesterol desmolase deficiency, 3 beta-hydroxysteroid dehydrogenase deficiency, and testicular and ovary dysgenesis can easily be distinguished from 17 alpha-OHD. None of these disturbances result in hypertension. In the only other form of juvenile hypertension due to congenital adrenal hyperplasia, 11 beta-OHD, androgen excess leads to female pseudohermaphroditism and precocious puberty in the male patient. Patients with dexamethasone-suppressible hyperaldosteronism present with no sexual abnormalities. A diagnosis of 17 alpha-OHD can be readily assumed in the female patient with primary amenorrhea, hypertension, and hypokalemia. The absence of aldosterone, a measurement that is readily available, establishes this diagnosis even without the measurement of DOC.     

Interleukin-17 and the interleukin-17 family member network.

Interleukin-17 (now known as IL-17A), is a homodimer of two 155 amino acid chains secreted by CD4+ activated memory T cells (CD45+ RO+) and is available as a glycosylated 20- to 30-kDa homodimeric peptide. Human IL-17 shows amino acid sequence identity of 62.5 and 58% to the mouse and rat sequences, respectively. IL-17 can regulate the function of a variety of cell types, plays an important role in the maturation of hematopoietic progenitor cells, and induces production of proinflammatory mediators. Here, for the first time, we summarize the biological effects of IL-17 and its family members as important players of T cell-mediated immune responses and underline the important implications of this cytokine in inflammation and degenerative diseases.     

A novel pro-lymphangiogenic function for Th17/IL-17

Th17 cells, in addition to their proinflammatory functions, have been recognized as potent inducers of angiogenesis in autoimmune diseases and malignancies. In the present study, we demonstrate distinct mechanisms by which IL-17 induces lymphangiogenesis. Using the mouse cornea micropocket and cell culture assays, our data demonstrate that IL-17 directly promotes growth of lymphatic vessels by inducing increased expression of prolymphangiogenic VEGF-D and proliferation of lymphatic endothelial cells. However, IL-17-induced growth of blood vessels is primarily mediated through IL-1β secretion by IL-17-responsive cells. Furthermore, in vivo blockade of IL-17 in a preclinical model of Th17-dominant autoimmune ocular disease demonstrates a significant reduction in the corneal lymphangiogenesis and in the progression of clinical disease. Taken together, our findings demonstrate a novel prolymphangiogenic function for Th17/IL-17, indicating that IL-17 can promote the progression and amplification of immunity in part through its induction of lymphangiogenesis.     

17-Ketosteroid and 17-hydroxycorticosteroid excretion in patients with duodenal ulceration

The 24-hour excretion of 17-ketosteroids and 17-hydroxycorticosteroids has been estimated in a series of male duodenal ulcer subjects and compared with that of 56 normal male controls. It has been found that both 17-ketosteroid and 17-hydroxycorticosteroid excretion is less in ulcer subjects than in the control group; these differences are not large but in the case of 17-hydroxycorticosteroids they are statistically significant. For active ulcers (107 men) 17-hydroxycorticosteroid excretion is approximately 78% of normal and 17-ketosteroid excretion 93% of normal; in the quiescent phase (50 men) the differences are rather larger, being respectively 71% and 86% of normal. This reduced excretion persists after operation in both the short term, six months after operation (53 men), and the long term, 10 years and more after gastric resection (39 men).