Role of IL-32 Gamma on Bone Metabolism in Autoimmune Arthritis
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초록
IL-32 acts as a pro-inflammatory cytokine by inducing the synthesis of inflammatory molecules as well as promoting the morphological changes involved in the transformation of monocytes into osteoclasts (OCs). Evaluation of the functions of IL-32 has mainly focused on its inflammatory properties, such as involvement in the pathogenesis of various autoimmune diseases. Recently, IL-32 was shown to be involved in bone metabolism, in which it promotes the differentiation and activation of OCs and plays a key role in bone resorption in inflammatory conditions. IL-32γ also regulates bone formation in conditions such as ankylosing spondylitis and osteoporosis. In this review, we summarize the results of recent studies on the role of IL-32γ in bone metabolism in inflammatory arthritis.
Abstract
IL-32 acts as a pro-inflammatory cytokine by inducing the synthesis of inflammatory molecules as well as promoting the morphological changes involved in the transformation of monocytes into osteoclasts (OCs). Evaluation of the functions of IL-32 has mainly focused on its inflammatory properties, such as involvement in the pathogenesis of various autoimmune diseases. Recently, IL-32 was shown to be involved in bone metabolism, in which it promotes the differentiation and activation of OCs and plays a key role in bone resorption in inflammatory conditions. IL-32γ also regulates bone formation in conditions such as ankylosing spondylitis and osteoporosis. In this review, we summarize the results of recent studies on the role of IL-32γ in bone metabolism in inflammatory arthritis.
참고문헌 (60)
- Jung SM, "Cytokine-mediated bone destruction in rheumatoid arthritis", J Immunol Res, 2014, pp.263625~ (2014)
- Lories R, "The balance of tissue repair and remodeling in chronic arthritis", Nat Rev Rheumatol, 7, pp.700~707 (2011)[DOI]
- Khawar B, "A panoramic spectrum of complex interplay between the immune system and IL-32 during pathogenesis of various systemic infections and inflammation", Eur J Med Res, 20, pp.7~ (2015)[DOI]
- Dinarello CA, "IL-32, a novel cytokine with a possible role in disease", Ann Rheum Dis, 65(Suppl 3), pp.iii61~iii64 (2006)
- Khawar MB, "Il-32: a novel pluripotent inflammatory interleukin, towards gastric inflammation, gastric cancer, and chronic rhino sinusitis", Mediators Inflamm, 2016, pp.8413768~ (2016)
- 김수현, "Interleukin-32 in Inflammatory Autoimmune Diseases", Immune Network, 14(3), pp.123~127 (2014), 대한면역학회
- Xu WD, "IL-32 with potential insights into rheumatoid arthritis", Clin Immunol, 147, pp.89~94 (2013)[DOI]
- Kim SH, "Interleukin-32: a cytokine and inducer of <TEX>$TNF{\alpha}$<", TEX>, 2005, pp.22, 131~142
- Calabrese F, "IL-32, a novel proinflammatory cytokine in chronic obstructive pulmonary disease", Am J Respir Crit Care Med, 178, pp.894~901 (2008)[DOI]
- Shoda H, "Interactions between IL-32 and tumor necrosis factor alpha contribute to the exacerbation of immune-inflammatory diseases", Arthritis Res Ther, 8, pp.R166~ (2006)[DOI]
- Zhou Y, "Important role of the IL-32 inflammatory network in the host response against viral infection", Viruses, 7, pp.3116~3129 (2015)[DOI]
- 김선종, "Interleukin-32γ Transgenic Mice Resist LPS-Mediated Septic Shock", Journal of Microbiology and Biotechnology, 24(8), pp.1133~1142 (2014), 한국미생물·생명공학회[DOI]
- 서은희, "Detection of Expressed IL-32 in Human Stomach Cancer Using ELISA and Immunostaining", Journal of Microbiology and Biotechnology, 18(9), pp.1606~1612 (2008), 한국미생물·생명공학회
- Sorrentino C, "Expression of IL-32 in human lung cancer is related to the histotype and metastatic phenotype", Am J Respir Crit Care Med, 180, pp.769~779 (2009)[DOI]
- Nishida A, "Interleukin-32 expression in the pancreas", J Biol Chem, 284, pp.17868~17876 (2009)[DOI]
- Kang YH, "Dysregulation of overexpressed IL-<TEX>$32{\alpha}$<", TEX> in hepatocellular carcinoma suppresses cell growth and induces apoptosis through inactivation of <TEX>$NF-{\kappa}B$<, Cancer Lett, pp.2012, 318[DOI]
- Kang JW, "Interaction network mapping among IL-32 isoforms", Biochimie, 101, pp.248~251 (2014)[DOI]
- Choi JD, "Identification of the most active interleukin-32 isoform", Immunology, 126, pp.535~542 (2009)[DOI]
- El-Far M, "Proinflammatory isoforms of IL-32 as novel and robust biomarkers for control failure in HIV-infected slow progressors", Sci Rep, 6, pp.22902~ (2016)[DOI]
- Heinhuis B, "Interleukin-32: a predominantly intracellular proinflammatory mediator that controls cell activation and cell death", Cytokine, 60, pp.321~327 (2012)[DOI]
- Lee EJ, "Interleukin-32 gamma stimulates bone formation by increasing mir-29a in osteoblastic cells and prevents the development of osteoporosis", Sci Rep, 7, pp.40240~ (2017)[DOI]
- Lee EJ, "High level of interleukin-32 gamma in the joint of ankylosing spondylitis is associated with osteoblast differentiation", Arthritis Res Ther, 17, pp.350~ (2015)[DOI]
- Kim YG, "Effect of interleukin-<TEX>$32{\gamma}$<", TEX> on differentiation of osteoclasts from CD14+ monocytes, 2010, pp.62, 515~523
- Bae S, "Elevated interleukin-32 expression in granulomatosis with polyangiitis", Rheumatology (Oxford), 51, pp.1979~1988 (2012)[DOI]
- Gasiuniene E, "Levels of il-32 in serum, induced sputum supernatant, and bronchial lavage fluid of patients with chronic obstructive pulmonary disease", COPD, 13, pp.569~575 (2016)[DOI]
- Novick D, "Proteinase 3 is an IL-32 binding protein", Proc Natl Acad Sci U S A, 103, pp.3316~3321 (2006)[DOI]
- Koutsokera A, "Pulmonary biomarkers in COPD exacerbations: a systematic review", Respir Res, 14, pp.111~ (2013)[DOI]
- Barnes PJ, "Immunology of asthma and chronic obstructive pulmonary disease", Nat Rev Immunol, 8, pp.183~192 (2008)[DOI]
- Damen MS, "Interleukin-32 in chronic inflammatory conditions is associated with a higher risk of cardiovascular diseases", Atherosclerosis, 264, pp.83~91 (2017)[DOI]
- Netea MG, "IL-32 synergizes with nucleotide oligomerization domain (NOD) 1 and NOD2 ligands for IL-<TEX>$1{\beta}$<", TEX> and IL-6 production through a caspase 1-dependent mechanism, 2005, pp.102, 16309~16314
- Peyrin-Biroulet L, "NODs in defence: from vulnerable antimicrobial peptides to chronic inflammation", Trends Microbiol, 14, pp.432~438 (2006)[DOI]
- 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)
- Choi J, "Paradoxical effects of constitutive human IL-<TEX>$32{\gamma}$<", TEX> in transgenic mice during experimental colitis, 2010, pp.107, 21082~21086
- Kang JW, "A proinflammatory cytokine interleukin-<TEX>$32{\beta}$<", TEX> promotes the production of an anti-inflammatory cytokine interleukin-10, 2009, pp.128, e532~e540
- Zhang M, "Serum levels of cytokines in systemic lupus erythematosus: association study in a Chinese population", Z Rheumatol, 73, pp.277~280 (2014)[DOI]
- Inoue M, "Three cases of lupus nephritis patients with serum interleukin-<TEX>$32{\gamma}$<", TEX> detection, 2014, pp.23, 1187~1191
- Meyer N, "IL-32 is expressed by human primary keratinocytes and modulates keratinocyte apoptosis in atopic dermatitis", J Allergy Clin Immunol, 125, pp.858~865 (2010)[DOI]
- Heinhuis B, "Inflammation-dependent secretion and splicing of IL-<TEX>$32{\gamma}$<", TEX> in rheumatoid arthritis, 2011, pp.108, 4962~4967
- Joosten LA, "IL-32, a proinflammatory cytokine in rheumatoid arthritis", Proc Natl Acad Sci U S A, 103, pp.3298~3303 (2006)[DOI]
- Nakayama M, "Enhanced susceptibility to lipopolysaccharide-induced arthritis and endotoxin shock in interleukin-32 alpha transgenic mice through induction of tumor necrosis factor alpha", Arthritis Res Ther, 14, pp.R120~ (2012)[DOI]
- 이은진, "Interleukin-32 Gamma as a New Face in Inflammatory Bone Diseases", 대한류마티스학회지, 24(1), pp.14~20 (2017), 대한류마티스학회[DOI]
- McInnes IB, "Cytokines in the pathogenesis of rheumatoid arthritis", Nat Rev Immunol, 7, pp.429~442 (2007)[DOI]
- Takayanagi H, "Osteoimmunology: shared mechanisms and crosstalk between the immune and bone systems", Nat Rev Immunol, 7, pp.292~304 (2007)[DOI]
- Gravallese EM, "Synovial tissue in rheumatoid arthritis is a source of osteoclast differentiation factor", Arthritis Rheum, 43, pp.250~258 (2000)[DOI]
- Komine M, "Tumor necrosis factor-<TEX>${\alpha}$<", TEX> cooperates with receptor activator of nuclear factor <TEX>${\kappa}B$<, Bone, pp.2001, 28[DOI]
- Kitaura H, "M-CSF mediates TNF-induced inflammatory osteolysis", J Clin Invest, 115, pp.3418~3427 (2005)[DOI]
- Azuma Y, "Tumor necrosis factor-<TEX>${\alpha}$<", TEX> induces differentiation of and bone resorption by osteoclasts, 2000, pp.275, 4858~4864
- Lubberts E, "IL-17 promotes bone erosion in murine collagen-induced arthritis through loss of the receptor activator of <TEX>$NF-{\kappa}B$<", TEX> ligand, J Immunol, pp.2003, 170[DOI]
- Yago T, "IL-17 induces osteoclastogenesis from human monocytes alone in the absence of osteoblasts, which is potently inhibited by anti-TNF-<TEX>${\alpha}$<", TEX> antibody: a novel mechanism of osteoclastogenesis by IL-17, 2009, pp.108, 947~955
- Mun SH, "Tumor necrosis factor <TEX>${\alpha}$<", TEX>-induced interleukin-32 is positively regulated via the Syk, JNK$<, pp.TEX> pathway in rheumatoid synovial fibroblasts, Arthritis Rheum[DOI]
- Mabilleau G, "Interleukin-32 promotes osteoclast differentiation but not osteoclast activation", PLoS One, 4, pp.e4173~ (2009)[DOI]
- Boyle WJ, "Osteoclast differentiation and activation", Nature, 423, pp.337~342 (2003)[DOI]
- Kim YG, "The influence of interleukin-<TEX>$32{\gamma}$<", TEX> on osteoclastogenesis with a focus on fusion-related genes, 2012, pp.32, 201~206
- Sieper J, "Critical appraisal of assessment of structural damage in ankylosing spondylitis: implications for treatment outcomes", Arthritis Rheum, 58, pp.649~656 (2008)[DOI]
- Schett G, "Can we stop progression of ankylosing spondylitis?", Best Pract Res Clin Rheumatol, 24, pp.363~371 (2010)[DOI]
- Matsuo K, "Osteoclast-osteoblast communication", Arch Biochem Biophys, 473, pp.201~209 (2008)[DOI]
- Moon YM, "IL-32 and IL-17 interact and have the potential to aggravate osteoclastogenesis in rheumatoid arthritis", Arthritis Res Ther, 14, pp.R246~ (2012)[DOI]
- Kundu M, "IL-32: an emerging player in the immune response network against tuberculosis?", PLoS Med, 3, pp.e274~ (2006)[DOI]
- Yucong Z, "Serum functional dickkopf-1 levels are inversely correlated with radiographic severity of ankylosing spondylitis", Clin Lab, 60, pp.1527~1531 (2014)
- Uderhardt S, "Blockade of dickkopf (DKK)-1 induces fusion of sacroiliac joints", Ann Rheum Dis, 69, pp.592~597 (2010)[DOI]
