PDF下载 ( 195 KB)
Research progress of interleukin-32
-
摘要:
<正>白介素-32（IL-32）是新近发现的一种促炎细胞因子,研究发现:无论在抗病原微生物还是在自身免疫性疾病的炎症反应中,IL-32都发挥着重要作用。本文就其生物学特性、功能及其与临床的关系做一综述。
-
[1]Kim SH, Han SY, Azam TA, et al.Interleukin-32:a cytokine and inducer of TNF-α[J].Immunity, 2005, 22 (1) ∶131-142. [2]Dahl CA, Schall RP, He HL, et al.Identification of a novel gene expressed in activated natural killer cells and T cells[J].Immunol, 1992, 148 (2) ∶597-603. [3]Tanaka G, Kanaji S, Hirano A, et al.Induction and activation of the aryl Hydrocarbon receptor by interleukin-4in B cells[J].Int lm-munol, 2005, 17 (6) ∶797-805. [4]Goda C, Kanaji T, Kanaji S, et al.Involvement of IL-32in activation-induced cell death in T cells[J].Int lmmunol, 2006, 18 (2) ∶233-240. [5]Hirofumi S, Keishi F, Yumi Y, et al.Interactions between IL-32and tumor necrosis factor a1pha contribute to the exacerbation of immune-inflammatory diseases[J].Arthritis Res Ther, 2006, 8 (6) ∶1-13. [6]Dinarello CA, Kim SH.IL-32, a novel cytokine with a possible role in disease[J].Ann Rheum Dis, 2006, 65 (3) ∶1161-1164. [7]Netea MG, Azam T, Ferwerda G, et al.IL-32synergizes with nucleo-tide oligomerization domain (NOD) land (NOD) 2ligands for IL-1βand IL-6production through a caspase1-dependent mechanism[J].Proc Natl Acad Sci USA, 2005, 102 (45) ∶16309-16314. [8]Joosten LA, Netea MG, Kim SH, et al.IL-32, a proinflammatory cy-tokine in rheumatoid arthritis[J].Proc Natl Acad Sci USA, 2006, 103 (9) ∶3298-3303. [9]Nold F, Nold-Petry CA, Pott GB, et al.Endogenous IL-32con-trols cytokine and HIV-1production[J].Immnol, 2008, 181 (1) ∶557-565 [10]Marcondes AM, Andrew J, Derek LM, et al.Dysregulation of IL-32in myelodysplastic syndrome and chronic myelomonocytic leukemia modulates apoptosis and impairs NK function[J].Cellbiology, 2008, 105 (8) ∶2865-2870. [11]Conti P, Youinou P, Theoharides TC.Modulation of automunity by the latest interleukins (with special emphasis on IL-32) [J].Auto immune Rev, 2007, 6 (3) ∶131-137 [12]Netea MG, Lewis EC, Azam T, et al.Interleukin-32induces the differentiation of monocytes into macrophage-like cells[J].Proc Natl Acad Sci USA, 2008, 105 (9) ∶3515-20. [13]Kundu M, Basu J.IL-32:an emerging player in the immune re-sponse network against tuberculosis-[J].Plos Med, 2006, 3 (8) ∶e274. [14]Podolsky DK.Inflammatory bowel disease[J].N Engl J Med, 2002, 347 (6) ∶417-429. [15]Hibi T, Ogata H.Novel pathophysiological concepts of inflammatory bowel disease[J].Gastroenterol, 2006, 41 (1) ∶10-16. [16]Loftus EV Jr.Clinical epidemiology of inflammatory bowel disease:incidence, prevalence, and environmental influences[J].Gastroen-terology, 2004, 126 (6) ∶1504-1517. [17]Hugot JP, Chamaillard M, Zouali H, et al.Association of NOD2leucine-rich repeat variants with susceptibility to Crohn's disease[J].Nature, 2001, 411 (6837) ∶599-603. [18]Hugot JP.CARD15/NOD2mutations in Crohn's disease[J].Ann NY Acad Sci, 2006, 1072∶9-18. [19]Maeda S, Hsu LC, Liu H, et al.Nod2mutation in Crohn's disease potentiates NF-kappaB activity and IL-1beta processing[J].Sci-ence, 2005, 307 (5710) ∶734-738. [20]Shioya M, Nishida A, Yagi Y, et al.Epithelial overexpression of in-terleukin-32alpha in inflammatory bowel disease[J].Clin Exp Im-munol, 2007, 149 (3) ∶480-486. [21]Rasool ST, Tang H, Wu J, et al.Increased level of IL-32during human immunodeficiency virus infection suppresses HIV replication[J].Immunol lett[J].2008, 117 (2) ∶161-167. -
本文二维码
计量
- 文章访问数: 2924
- HTML全文浏览量: 3
- PDF下载量: 1110
- 被引次数: 0
下载:
