Interleukin-32 in Inflammatory Autoimmune Diseases
2
조회
0
다운로드
6
인용
0
참고문헌
키워드
초록
Interleukin-32 (IL-32) is a cytokine inducing crucial inflammatory cytokines such as tumor necrosis factor-α (TNFα) and IL-6 and its expression is elevated in various inflammatory autoimmune diseases, certain cancers, as well as viral infections. IL-32 gene was first cloned from activated T cells, however IL-32 expression was also found in other immune cells and non-immune cells. IL-32 gene was identified in most mammals except rodents. It is transcribed as multiple-spliced variants in the absence of a specific activity of each isoform. IL-32 has been studied mostly in clinical fields such as infection, autoimmune, cancer, vascular disease, and pulmonary diseases. It is difficult to investigate the precise role of IL-32 in vivo due to the absence of IL-32 gene in mouse. The lack of mouse IL-32 gene restricts in vivo studies and restrains further development of IL-32 research in clinical applications although IL-32 new cytokine getting a spotlight as an immune regulatory molecule processing important roles in autoimmune, infection, and cancer. In this review, we discuss the regulation and function of IL-32 in inflammatory bowel diseases and rheumatoid arthritis.
Abstract
Interleukin-32 (IL-32) is a cytokine inducing crucial inflammatory cytokines such as tumor necrosis factor-α (TNFα) and IL-6 and its expression is elevated in various inflammatory autoimmune diseases, certain cancers, as well as viral infections. IL-32 gene was first cloned from activated T cells, however IL-32 expression was also found in other immune cells and non-immune cells. IL-32 gene was identified in most mammals except rodents. It is transcribed as multiple-spliced variants in the absence of a specific activity of each isoform. IL-32 has been studied mostly in clinical fields such as infection, autoimmune, cancer, vascular disease, and pulmonary diseases. It is difficult to investigate the precise role of IL-32 in vivo due to the absence of IL-32 gene in mouse. The lack of mouse IL-32 gene restricts in vivo studies and restrains further development of IL-32 research in clinical applications although IL-32 new cytokine getting a spotlight as an immune regulatory molecule processing important roles in autoimmune, infection, and cancer. In this review, we discuss the regulation and function of IL-32 in inflammatory bowel diseases and rheumatoid arthritis.
참고문헌 (22)
- Netea, M. G., "IL-32 synergizes with nucleotide oligomerization domain (NOD) 1 and NOD2 ligands for IL-1beta and IL-6 production through a caspase 1-dependent mechanism", Proc. Natl. Acad. Sci. USA, 102, pp.16309~16314 (2005)
- Imaeda, H., "A new isoform of interleukin-32 suppresses IL-8 mRNA expression in the intestinal epithelial cell line HT-29", Mol. Med. Rep, 4, pp.483~487 (2011)
- Shioya, M., "Epithelial overexpression of interleukin- 32alpha in inflammatory bowel disease", Clin. Exp. Immunol, 149, pp.480~486 (2007)
- Ciccia, F., "Increased expression of interleukin-32 in the inflamed ileum of ankylosing spondylitis patients", Rheumatology (Oxford), 51, pp.1966~1972 (2012)
- Andoh, A., "Mucosal cytokine network in inflammatory bowel disease", World J. Gastroenterol, 14, pp.5154~5161 (2008)
- Fantini, M. C., "New players in the cytokine orchestra of inflammatory bowel disease", Inflamm. Bowel Dis, 13, pp.1419~1423 (2007)
- Felaco, P., "IL-32: a newly-discovered proinflammatory cytokine", J. Biol. Regul. Homeost. Agents, 23, pp.141~147 (2009)
- Choi, J., "Paradoxical effects of constitutive human IL-32{gamma} in transgenic mice during experimental colitis", Proc. Natl. Acad. Sci. USA, 107, pp.21082~21086 (2010)
- Netea, M. G., "Interleukin- 32 induces the differentiation of monocytes into macrophage-like cells", Proc. Natl. Acad. Sci. USA, 105, pp.3515~3520 (2008)
- Choi, J. D., "Identification of the most active interleukin-32 isoform", Immunology, 126, pp.535~542 (2009)
- Kim, Y. G., "Effect of interleukin-32gamma on differentiation of osteoclasts from CD14＋ monocytes", Arthritis Rheum, 62, pp.515~523 (2010)
- Moon, Y. M., "IL-32 and IL-17 interact and have the potential to aggravate osteoclastogenesis in rheumatoid arthritis", Arthritis Res. Ther, 14, pp.R246~ (2012)
- Xu, W. D, "IL-32 with potential insights into rheumatoid arthritis", Clin. Immunol, 147, pp.89~94 (2013)
- Joosten, L. A., "IL-32, a proinflammatory cytokine in rheumatoid arthritis", Proc. Natl. Acad Sci. USA, 103, pp.3298~3303 (2006)
- Gui, M., "Clinical significance of interleukin-32 expression in patients with rheumatoid arthritis", Asian Pac. J. Allergy Immunol, 31, pp.73~78 (2013)
- Jeong, H. J, "Inhibition of IL-32 and TSLP production through the attenuation of caspase-1 activation in an animal model of allergic rhinitis by Naju Jjok (Polygonum tinctorium)", Int. J. Mol. Med, 33, pp.142~150 (2014)
- Cagnard, N, "Interleukin-32, CCL2, PF4F1 and GFD10 are the only cytokine", chemokine genes differentially expressed by in vitro cultured rheumatoid and osteoarthritis fibroblast-like synoviocytes, 2005, pp.16, 289~292
- Zivojinovic, S. M, "Tumor necrosis factor blockade differentially affects innate inflammatory and Th17 cytokines in rheumatoid arthritis", J. Rheumatol, 39, pp.18~21 (2012)
- Heinhuis, B., "Tumour necrosis factor alpha-driven IL-32 expression in rheumatoid arthritis synovial tissue amplifies an inflammatory cascade", Ann. Rheum. Dis, 70, pp.660~667 (2011)
- Heinhuis, B., "Inflammation-dependent secretion and splicing of IL-32{gamma} in rheumatoid arthritis", Proc. Natl. Acad. Sci. USA, 108, pp.4962~4967 (2011)
- Alsaleh, G., "Innate immunity triggers IL-32 expression by fibroblast-like synoviocytes in rheumatoid arthritis", Arthritis Res. Ther, 12, pp.R135~ (2010)
- Kim, S. H, "Interleukin-32: a cytokine and inducer of TNFalpha", Immunity, 22, pp.131~142 (2005)