Role and progress of innate immunity in pathogenesis of osteoarthritis_Chinese Journal of Reparative and Reconstructive Surgery

Authors：

XIE Jinwei , HUANG Zeyu ,  PEI Fuxing

Department of Orthopaedics, West China Hospital, Sichuan University, Chengdu Sichuan, 610041, P.R.China;

Corresponding author：

PEI Fuxing, Email: peifuxing@vip.163.com

Keywords：

Osteoarthritis; innate immunity; inflammation; macrophage

DOI：

10.7507/1002-1892.201810068

Video：

Export PDF Favorites Scan Get Citation

Abstract Full text Figures/Tables Video References Cited by

Objective To review and summarize the role and progress of innate immunity in the pathogenesis of osteoarthritis (OA).Methods The domestic and foreign literature in recent years was reviewed. The role of innate immune-mediated inflammation, macrophages, T cells, and complement systems in the pathogenesis of OA, potential therapeutic targets, and the latest research progress were summarized.Results With the deepening of research, OA is gradually considered as a low-grade inflammation, in which innate immunity plays an important role. The polarization of synovial macrophage subpopulation in OA has been studied extensively. Current data shows that the failure of transformation from M1 subtype to M2 subtype is a key link in the progression of OA. T cells and complement system are also involved in the pathological process of OA.Conclusion At present, the role of innate immunity in the progress of OA has been played in the spotlight, whereas the specific mechanism has not been clear. The macrophage subtype polarization is a potential therapeutic target for early prevention and treatment of OA.

Citation： XIE Jinwei, HUANG Zeyu, PEI Fuxing. Role and progress of innate immunity in pathogenesis of osteoarthritis. Chinese Journal of Reparative and Reconstructive Surgery, 2019, 33(3): 370-376. doi: 10.7507/1002-1892.201810068 Copy

1.	Glyn-Jones S, Palmer AJ, Agricola R, et al. Osteoarthritis. Lancet, 2015, 386(9991): 376-387.
2.	薛庆云, 王坤正, 裴福兴, 等. 中国 40 岁以上人群原发性骨关节炎患病状况调查. 中华骨科杂志, 2015, 35(12): 1206-1212.
3.	郭保逢, 秦泗河, 黄野. 膝关节骨关节炎的保膝治疗进展. 中国修复重建外科杂志, 2018, 32(10): 1292-1296.
4.	贾笛, 李彦林, 王坤, 等. 非编码 RNA 调控骨关节炎的分子生物学研究进展. 中国修复重建外科杂志, 2017, 31(3): 374-378.
5.	丁烨, 任静宜, 于洪强, 等. 病原相关分子模式和损伤相关分子模式在免疫炎症反应中的作用. 国际口腔医学杂志, 2016, 43(2): 172-176.
6.	Anderson P. Intrinsic mRNA stability helps compose the inflammatory symphony. Nat Immunol, 2009, 10(3): 233-234.
7.	Hao S, Baltimore D. The stability of mRNA influences the temporal order of the induction of genes encoding inflammatory molecules. Nat Immunol, 2009, 10(3): 281-288.
8.	Huang Z, Kraus VB. Does lipopolysaccharide-mediated inflammation have a role in OA? Nat Rev Rheumatol, 2016, 12(2): 123-129.
9.	Yu L, Wang L, Chen S. Endogenous toll-like receptor ligands and their biological significance. J Cell Mol Med, 2010, 14(11): 2592-2603.
10.	Mosser DM, Edwards JP. Exploring the full spectrum of macrophage activation. Nat Rev Immunol, 2008, 8(12): 958-969.
11.	Spite M, Clària J, Serhan CN. Resolvins, specialized proresolving lipid mediators, and their potential roles in metabolic diseases. Cell Metab, 2014, 19(1): 21-36.
12.	Furman BD, Kimmerling KA, Zura RD, et al. Articular ankle fracture results in increased synovitis, synovial macrophage infiltration, and synovial fluid concentrations of inflammatory cytokines and chemokines. Arthritis Rheumatol, 2015, 67(5): 1234-1239.
13.	Rafferty JL, Siepmann JI, Schure MR. The effects of chain length, embedded polar groups, pressure, and pore shape on structure and retention in reversed-phase liquid chromatography: molecular-level insights from Monte Carlo simulations. J Chromatogr A, 2009, 1216(12): 2320-2331.
14.	Honsawek S, Yuktanandana P, Tanavalee A, et al. Plasma and synovial fluid connective tissue growth factor levels are correlated with disease severity in patients with knee osteoarthritis. Biomarkers, 2012, 17(4): 303-308.
15.	Ayral X, Pickering EH, Woodworth TG, et al. Synovitis: a potential predictive factor of structural progression of medial tibiofemoral knee osteoarthritis—results of a 1 year longitudinal arthroscopic study in 422 patients. Osteoarthritis Cartilage, 2005, 13(5): 361-367.
16.	Daghestani HN, Pieper CF, Kraus VB. Soluble macrophage biomarkers indicate inflammatory phenotypes in patients with knee osteoarthritis. Arthritis Rheumatol, 2015, 67(4): 956-965.
17.	Roemer FW, Guermazi A, Felson DT, et al. Presence of MRI-detected joint effusion and synovitis increases the risk of cartilage loss in knees without osteoarthritis at 30-month follow-up: the MOST study. Ann Rheum Dis, 2011, 70(10): 1804-1809.
18.	Lopez-Castejon G, Brough D. Understanding the mechanism of IL-1β secretion. Cytokine Growth Factor Rev, 2011, 22(4): 189-195.
19.	Kim JH, Jeon J, Shin M, et al. Regulation of the catabolic cascade in osteoarthritis by the zinc-ZIP8-MTF1 axis. Cell, 2014, 156(4): 730-743.
20.	Okamura Y, Watari M, Jerud ES, et al. The extra domain A of fibronectin activates Toll-like receptor 4. J Biol Chem, 2001, 276(13): 10229-10233.
21.	Scheibner KA, Lutz MA, Boodoo S, et al. Hyaluronan fragments act as an endogenous danger signal by engaging TLR2. J Immunol, 2006, 177(2): 1272-1281.
22.	Taylor KR, Yamasaki K, Radek KA, et al. Recognition of hyaluronan released in sterile injury involves a unique receptor complex dependent on Toll-like receptor 4, CD44, and MD-2. J Biol Chem, 2007, 282(25): 18265-18275.
23.	Lees S, Golub SB, Last K, et al. Bioactivity in an Aggrecan 32-mer fragment is mediated via Toll-like receptor 2. Arthritis Rheumatol, 2015, 67(5): 1240-1249.
24.	Liu-Bryan R. Synovium and the innate inflammatory network in osteoarthritis progression. Curr Rheumatol Rep, 2013, 15(5): 323.
25.	Kraus VB. Osteoarthritis: The zinc link. Nature, 2014, 507(7493): 441-442.
26.	Lewis JS Jr, Furman BD, Zeitler E, et al. Genetic and cellular evidence of decreased inflammation associated with reduced incidence of posttraumatic arthritis in MRL/MpJ mice. Arthritis Rheum, 2013, 65(3): 660-670.
27.	Olson SA, Furman BD, Kraus VB, et al. Therapeutic opportunities to prevent post-traumatic arthritis: Lessons from the natural history of arthritis after articular fracture. J Orthop Res, 2015, 33(9): 1266-1277.
28.	Happonen KE, Saxne T, Aspberg A, et al. Regulation of complement by cartilage oligomeric matrix protein allows for a novel molecular diagnostic principle in rheumatoid arthritis. Arthritis Rheum, 2010, 62(12): 3574-3583.
29.	Kalchishkova N, Fürst CM, Heinegård D, et al. NC4 Domain of cartilage-specific collagen IX inhibits complement directly due to attenuation of membrane attack formation and indirectly through binding and enhancing activity of complement inhibitors C4B-binding protein and factor H. J Biol Chem, 2011, 286(32): 27915-27926.
30.	Yamasaki K, Muto J, Taylor KR, et al. NLRP3/cryopyrin is necessary for interleukin-1beta (IL-1beta) release in response to hyaluronan, an endogenous trigger of inflammation in response to injury. J Biol Chem, 2009, 284(19): 12762-12771.
31.	Kim HA, Cho ML, Choi HY, et al. The catabolic pathway mediated by Toll-like receptors in human osteoarthritic chondrocytes. Arthritis Rheum, 2006, 54(7): 2152-2163.
32.	Radstake TR, Roelofs MF, Jenniskens YM, et al. Expression of toll-like receptors 2 and 4 in rheumatoid synovial tissue and regulation by proinflammatory cytokines interleukin-12 and interleukin-18 via interferon-gamma. Arthritis Rheum, 2004, 50(12): 3856-3865.
33.	Orlowsky EW, Kraus VB. The role of innate immunity in osteoarthritis: when our first line of defense goes on the offensive. J Rheumatol, 2015, 42(3): 363-371.
34.	Schroder K, Tschopp J. The inflammasomes. Cell, 2010, 140(6): 821-832.
35.	Mosser DM, Edwards JP. Exploring the full spectrum of macrophage activation. Nat Rev Immunol, 2008, 8(12): 958-969.
36.	Munitz A, Brandt EB, Mingler M, et al. Distinct roles for IL-13 and IL-4 via IL-13 receptor alpha1 and the type Ⅱ IL-4 receptor in asthma pathogenesis. Proc Natl Acad Sci U S A, 2008, 105(20): 7240-7245.
37.	Piscaer TM, Müller C, Mindt TL, et al. Imaging of activated macrophages in experimental osteoarthritis using folate-targeted animal single-photon-emission computed tomography/computed tomography. Arthritis Rheum, 2011, 63(7): 1898-1907.
38.	de Visser HM, Korthagen NM, Müller C, et al. Imaging of Folate receptor expressing macrophages in the rat groove model of osteoarthritis: using a new DOTA-Folate conjugate. Cartilage, 2018, 9(2): 183-191.
39.	Wu CL, McNeill J, Goon K, et al. Conditional macrophage depletion increases inflammation and does not inhibit the development of osteoarthritis in obese macrophage Fas-induced apoptosis-transgenic mice. Arthritis Rheumatol, 2017, 69(9): 1772-1783.
40.	Zhang H, Lin C, Zeng C, et al. Synovial macrophage M1 polarisation exacerbates experimental osteoarthritis partially through R-spondin-2. Ann Rheum Dis, 2018, 77(10): 1524-1534.
41.	Bondeson J, Wainwright SD, Lauder S, et al. The role of synovial macrophages and macrophage-produced cytokines in driving aggrecanases, matrix metalloproteinases, and other destructive and inflammatory responses in osteoarthritis. Arthritis Res Ther, 2006, 8(6): R187.
42.	Blom AB, van Lent PL, Libregts S, et al. Crucial role of macrophages in matrix metalloproteinase-mediated cartilage destruction during experimental osteoarthritis: involvement of matrix metalloproteinase 3. Arthritis Rheum, 2007, 56(1): 147-157.
43.	Blom AB, van Lent PL, Holthuysen AE, et al. Synovial lining macrophages mediate osteophyte formation during experimental osteoarthritis. Osteoarthritis Cartilage, 2004, 12(8): 627-635.
44.	Samavedi S, Diaz-Rodriguez P, Erndt-Marino JD, et al. A three-dimensional chondrocyte-macrophage coculture system to probe inflammation in experimental osteoarthritis. Tissue Eng Part A, 2017, 23(3-4): 101-114.
45.	Zhang H, Lin C, Zeng C, et al. Synovial macrophage M1 polarisation exacerbates experimental osteoarthritis partially through R-spondin-2. Ann Rheum Dis, 2018, 77(10): 1524-1534.
46.	Utomo L, Bastiaansen-Jenniskens YM, Verhaar JA, et al. Cartilage inflammation and degeneration is enhanced by pro-inflammatory (M1) macrophages in vitro, but not inhibited directly by anti-inflammatory (M2) macrophages. Osteoarthritis Cartilage, 2016, 24(12): 2162-2170.
47.	Dai M, Sui B, Xue Y, et al. Cartilage repair in degenerative osteoarthritis mediated by squid type Ⅱ collagen via immunomodulating activation of M2 macrophages, inhibiting apoptosis and hypertrophy of chondrocytes. Biomaterials, 2018, 180: 91-103.
48.	Zhang X, Morrison DC. Lipopolysaccharide structure-function relationship in activation versus reprogramming of mouse peritoneal macrophages. J Leukoc Biol, 1993, 54(5): 444-450.
49.	Malyshev I, Malyshev Y. Current concept and update of the macrophage plasticity concept: intracellular mechanisms of reprogramming and M3 macrophage "Switch" phenotype. Biomed Res Int, 2015, 2015: 341308.
50.	Topoluk N, Steckbeck K, Siatkowski S, et al. Amniotic mesenchymal stem cells mitigate osteoarthritis progression in a synovial macrophage-mediated in vitro explant coculture model. J Tissue Eng Regen Med, 2018, 12(4): 1097-1110.
51.	Manferdini C, Paolella F, Gabusi E, et al. Adipose stromal cells mediated switching of the pro-inflammatory profile of M1-like macrophages is facilitated by PGE2: in vitro evaluation. Ostemooarthritis Cartilage, 2017, 25(7): 1161-1171.
52.	de Lange-Brokaar BJ, Ioan-Facsinay A, van Osch GJ, et al. Synovial inflammation, immune cells and their cytokines in osteoarthritis: a review. Osteoarthritis Cartilage, 2012, 20(12): 1484-1499.
53.	Pessler F, Chen LX, Dai L, et al. A histomorphometric analysis of synovial biopsies from individuals with Gulf War Veterans’ Illness and joint pain compared to normal and osteoarthritis synovium. Clin Rheumatol, 2008, 27(9): 1127-1134.
54.	Symons JA, McCulloch JF, Wood NC, et al. Soluble CD4 in patients with rheumatoid arthritis and osteoarthritis. Clin Immunol Immunopathol, 1991, 60(1): 72-82.
55.	Hussein MR, Fathi NA, El-Din AM, et al. Alterations of the CD4(+), CD8(+) T cell subsets, interleukins-1beta, IL-10, IL-17, tumor necrosis factor-alpha and soluble intercellular adhesion molecule-1 in rheumatoid arthritis and osteoarthritis: preliminary observations. Pathol Oncol Res, 2008, 14(3): 321-328.
56.	Kriegova E, Manukyan G, Mikulkova Z, et al. Gender-related differences observed among immune cells in synovial fluid in knee osteoarthritis. Osteoarthritis Cartilage, 2018, 26(9): 1247-1256.
57.	de Jong H, Berlo SE, Hombrink P, et al. Cartilage proteoglycan aggrecan epitopes induce proinflammatory autoreactive T-cell responses in rheumatoid arthritis and osteoarthritis. Ann Rheum Dis, 2010, 69(1): 255-262.
58.	Penatti A, Facciotti F, De Matteis R, et al. Differences in serum and synovial CD4+ T cells and cytokine profiles to stratify patients with inflammatory osteoarthritis and rheumatoid arthritis. Arthritis Res Ther, 2017, 19(1): 103.
59.	Rosshirt N, Hagmann S, Tripel E, et al. A predominant Th1 polarization is present in synovial fluid of end-stage osteoarthritic knee joints-analysis of peripheral blood, synovial fluid & synovial membrane. Clin Exp Immunol, 2018.[Epub ahead of print].
60.	Sae-Jung T, Sengprasert P, Apinun J, et al. Functional and T cell receptor repertoire analyses of peripheral blood and infrapatellar fat pad T cells in knee osteoarthritis. J Rheumatol, 2018.[Epub ahead of print].
61.	Li YS, Luo W, Zhu SA, et al. T cells in osteoarthritis: alterations and beyond. Front Immunol, 2017, 8: 356.
62.	Sturfelt G, Truedsson L. Complement in the immunopathogenesis of rheumatic disease. Nat Rev Rheumatol, 2012, 8(8): 458-468.
63.	Corvetta A, Pomponio G, Rinaldi N, et al. Terminal complement complex in synovial tissue from patients affected by rheumatoid arthritis, osteoarthritis and acute joint trauma. Clin Exp Rheumatol, 1992, 10(5): 433-438.
64.	Struglics A, Okroj M, Swård P, et al. The complement system is activated in synovial fluid from subjects with knee injury and from patients with osteoarthritis. Arthritis Res Ther, 2016, 18(1): 223.
65.	Wang Q, Rozelle AL, Lepus CM, et al. Identification of a central role for complement in osteoarthritis. Nat Med, 2011, 17(12): 1674-1679.

1. Glyn-Jones S, Palmer AJ, Agricola R, et al. Osteoarthritis. Lancet, 2015, 386(9991): 376-387.
2. 薛庆云, 王坤正, 裴福兴, 等. 中国 40 岁以上人群原发性骨关节炎患病状况调查. 中华骨科杂志, 2015, 35(12): 1206-1212.
3. 郭保逢, 秦泗河, 黄野. 膝关节骨关节炎的保膝治疗进展. 中国修复重建外科杂志, 2018, 32(10): 1292-1296.
4. 贾笛, 李彦林, 王坤, 等. 非编码 RNA 调控骨关节炎的分子生物学研究进展. 中国修复重建外科杂志, 2017, 31(3): 374-378.
5. 丁烨, 任静宜, 于洪强, 等. 病原相关分子模式和损伤相关分子模式在免疫炎症反应中的作用. 国际口腔医学杂志, 2016, 43(2): 172-176.
6. Anderson P. Intrinsic mRNA stability helps compose the inflammatory symphony. Nat Immunol, 2009, 10(3): 233-234.
7. Hao S, Baltimore D. The stability of mRNA influences the temporal order of the induction of genes encoding inflammatory molecules. Nat Immunol, 2009, 10(3): 281-288.
8. Huang Z, Kraus VB. Does lipopolysaccharide-mediated inflammation have a role in OA? Nat Rev Rheumatol, 2016, 12(2): 123-129.
9. Yu L, Wang L, Chen S. Endogenous toll-like receptor ligands and their biological significance. J Cell Mol Med, 2010, 14(11): 2592-2603.
10. Mosser DM, Edwards JP. Exploring the full spectrum of macrophage activation. Nat Rev Immunol, 2008, 8(12): 958-969.
11. Spite M, Clària J, Serhan CN. Resolvins, specialized proresolving lipid mediators, and their potential roles in metabolic diseases. Cell Metab, 2014, 19(1): 21-36.
12. Furman BD, Kimmerling KA, Zura RD, et al. Articular ankle fracture results in increased synovitis, synovial macrophage infiltration, and synovial fluid concentrations of inflammatory cytokines and chemokines. Arthritis Rheumatol, 2015, 67(5): 1234-1239.
13. Rafferty JL, Siepmann JI, Schure MR. The effects of chain length, embedded polar groups, pressure, and pore shape on structure and retention in reversed-phase liquid chromatography: molecular-level insights from Monte Carlo simulations. J Chromatogr A, 2009, 1216(12): 2320-2331.
14. Honsawek S, Yuktanandana P, Tanavalee A, et al. Plasma and synovial fluid connective tissue growth factor levels are correlated with disease severity in patients with knee osteoarthritis. Biomarkers, 2012, 17(4): 303-308.
15. Ayral X, Pickering EH, Woodworth TG, et al. Synovitis: a potential predictive factor of structural progression of medial tibiofemoral knee osteoarthritis—results of a 1 year longitudinal arthroscopic study in 422 patients. Osteoarthritis Cartilage, 2005, 13(5): 361-367.
16. Daghestani HN, Pieper CF, Kraus VB. Soluble macrophage biomarkers indicate inflammatory phenotypes in patients with knee osteoarthritis. Arthritis Rheumatol, 2015, 67(4): 956-965.
17. Roemer FW, Guermazi A, Felson DT, et al. Presence of MRI-detected joint effusion and synovitis increases the risk of cartilage loss in knees without osteoarthritis at 30-month follow-up: the MOST study. Ann Rheum Dis, 2011, 70(10): 1804-1809.
18. Lopez-Castejon G, Brough D. Understanding the mechanism of IL-1β secretion. Cytokine Growth Factor Rev, 2011, 22(4): 189-195.
19. Kim JH, Jeon J, Shin M, et al. Regulation of the catabolic cascade in osteoarthritis by the zinc-ZIP8-MTF1 axis. Cell, 2014, 156(4): 730-743.
20. Okamura Y, Watari M, Jerud ES, et al. The extra domain A of fibronectin activates Toll-like receptor 4. J Biol Chem, 2001, 276(13): 10229-10233.
21. Scheibner KA, Lutz MA, Boodoo S, et al. Hyaluronan fragments act as an endogenous danger signal by engaging TLR2. J Immunol, 2006, 177(2): 1272-1281.
22. Taylor KR, Yamasaki K, Radek KA, et al. Recognition of hyaluronan released in sterile injury involves a unique receptor complex dependent on Toll-like receptor 4, CD44, and MD-2. J Biol Chem, 2007, 282(25): 18265-18275.
23. Lees S, Golub SB, Last K, et al. Bioactivity in an Aggrecan 32-mer fragment is mediated via Toll-like receptor 2. Arthritis Rheumatol, 2015, 67(5): 1240-1249.
24. Liu-Bryan R. Synovium and the innate inflammatory network in osteoarthritis progression. Curr Rheumatol Rep, 2013, 15(5): 323.
25. Kraus VB. Osteoarthritis: The zinc link. Nature, 2014, 507(7493): 441-442.
26. Lewis JS Jr, Furman BD, Zeitler E, et al. Genetic and cellular evidence of decreased inflammation associated with reduced incidence of posttraumatic arthritis in MRL/MpJ mice. Arthritis Rheum, 2013, 65(3): 660-670.
27. Olson SA, Furman BD, Kraus VB, et al. Therapeutic opportunities to prevent post-traumatic arthritis: Lessons from the natural history of arthritis after articular fracture. J Orthop Res, 2015, 33(9): 1266-1277.
28. Happonen KE, Saxne T, Aspberg A, et al. Regulation of complement by cartilage oligomeric matrix protein allows for a novel molecular diagnostic principle in rheumatoid arthritis. Arthritis Rheum, 2010, 62(12): 3574-3583.
29. Kalchishkova N, Fürst CM, Heinegård D, et al. NC4 Domain of cartilage-specific collagen IX inhibits complement directly due to attenuation of membrane attack formation and indirectly through binding and enhancing activity of complement inhibitors C4B-binding protein and factor H. J Biol Chem, 2011, 286(32): 27915-27926.
30. Yamasaki K, Muto J, Taylor KR, et al. NLRP3/cryopyrin is necessary for interleukin-1beta (IL-1beta) release in response to hyaluronan, an endogenous trigger of inflammation in response to injury. J Biol Chem, 2009, 284(19): 12762-12771.
31. Kim HA, Cho ML, Choi HY, et al. The catabolic pathway mediated by Toll-like receptors in human osteoarthritic chondrocytes. Arthritis Rheum, 2006, 54(7): 2152-2163.
32. Radstake TR, Roelofs MF, Jenniskens YM, et al. Expression of toll-like receptors 2 and 4 in rheumatoid synovial tissue and regulation by proinflammatory cytokines interleukin-12 and interleukin-18 via interferon-gamma. Arthritis Rheum, 2004, 50(12): 3856-3865.
33. Orlowsky EW, Kraus VB. The role of innate immunity in osteoarthritis: when our first line of defense goes on the offensive. J Rheumatol, 2015, 42(3): 363-371.
34. Schroder K, Tschopp J. The inflammasomes. Cell, 2010, 140(6): 821-832.
35. Mosser DM, Edwards JP. Exploring the full spectrum of macrophage activation. Nat Rev Immunol, 2008, 8(12): 958-969.
36. Munitz A, Brandt EB, Mingler M, et al. Distinct roles for IL-13 and IL-4 via IL-13 receptor alpha1 and the type Ⅱ IL-4 receptor in asthma pathogenesis. Proc Natl Acad Sci U S A, 2008, 105(20): 7240-7245.
37. Piscaer TM, Müller C, Mindt TL, et al. Imaging of activated macrophages in experimental osteoarthritis using folate-targeted animal single-photon-emission computed tomography/computed tomography. Arthritis Rheum, 2011, 63(7): 1898-1907.
38. de Visser HM, Korthagen NM, Müller C, et al. Imaging of Folate receptor expressing macrophages in the rat groove model of osteoarthritis: using a new DOTA-Folate conjugate. Cartilage, 2018, 9(2): 183-191.
39. Wu CL, McNeill J, Goon K, et al. Conditional macrophage depletion increases inflammation and does not inhibit the development of osteoarthritis in obese macrophage Fas-induced apoptosis-transgenic mice. Arthritis Rheumatol, 2017, 69(9): 1772-1783.
40. Zhang H, Lin C, Zeng C, et al. Synovial macrophage M1 polarisation exacerbates experimental osteoarthritis partially through R-spondin-2. Ann Rheum Dis, 2018, 77(10): 1524-1534.
41. Bondeson J, Wainwright SD, Lauder S, et al. The role of synovial macrophages and macrophage-produced cytokines in driving aggrecanases, matrix metalloproteinases, and other destructive and inflammatory responses in osteoarthritis. Arthritis Res Ther, 2006, 8(6): R187.
42. Blom AB, van Lent PL, Libregts S, et al. Crucial role of macrophages in matrix metalloproteinase-mediated cartilage destruction during experimental osteoarthritis: involvement of matrix metalloproteinase 3. Arthritis Rheum, 2007, 56(1): 147-157.
43. Blom AB, van Lent PL, Holthuysen AE, et al. Synovial lining macrophages mediate osteophyte formation during experimental osteoarthritis. Osteoarthritis Cartilage, 2004, 12(8): 627-635.
44. Samavedi S, Diaz-Rodriguez P, Erndt-Marino JD, et al. A three-dimensional chondrocyte-macrophage coculture system to probe inflammation in experimental osteoarthritis. Tissue Eng Part A, 2017, 23(3-4): 101-114.
45. Zhang H, Lin C, Zeng C, et al. Synovial macrophage M1 polarisation exacerbates experimental osteoarthritis partially through R-spondin-2. Ann Rheum Dis, 2018, 77(10): 1524-1534.
46. Utomo L, Bastiaansen-Jenniskens YM, Verhaar JA, et al. Cartilage inflammation and degeneration is enhanced by pro-inflammatory (M1) macrophages in vitro, but not inhibited directly by anti-inflammatory (M2) macrophages. Osteoarthritis Cartilage, 2016, 24(12): 2162-2170.
47. Dai M, Sui B, Xue Y, et al. Cartilage repair in degenerative osteoarthritis mediated by squid type Ⅱ collagen via immunomodulating activation of M2 macrophages, inhibiting apoptosis and hypertrophy of chondrocytes. Biomaterials, 2018, 180: 91-103.
48. Zhang X, Morrison DC. Lipopolysaccharide structure-function relationship in activation versus reprogramming of mouse peritoneal macrophages. J Leukoc Biol, 1993, 54(5): 444-450.
49. Malyshev I, Malyshev Y. Current concept and update of the macrophage plasticity concept: intracellular mechanisms of reprogramming and M3 macrophage "Switch" phenotype. Biomed Res Int, 2015, 2015: 341308.
50. Topoluk N, Steckbeck K, Siatkowski S, et al. Amniotic mesenchymal stem cells mitigate osteoarthritis progression in a synovial macrophage-mediated in vitro explant coculture model. J Tissue Eng Regen Med, 2018, 12(4): 1097-1110.
51. Manferdini C, Paolella F, Gabusi E, et al. Adipose stromal cells mediated switching of the pro-inflammatory profile of M1-like macrophages is facilitated by PGE2: in vitro evaluation. Ostemooarthritis Cartilage, 2017, 25(7): 1161-1171.
52. de Lange-Brokaar BJ, Ioan-Facsinay A, van Osch GJ, et al. Synovial inflammation, immune cells and their cytokines in osteoarthritis: a review. Osteoarthritis Cartilage, 2012, 20(12): 1484-1499.
53. Pessler F, Chen LX, Dai L, et al. A histomorphometric analysis of synovial biopsies from individuals with Gulf War Veterans’ Illness and joint pain compared to normal and osteoarthritis synovium. Clin Rheumatol, 2008, 27(9): 1127-1134.
54. Symons JA, McCulloch JF, Wood NC, et al. Soluble CD4 in patients with rheumatoid arthritis and osteoarthritis. Clin Immunol Immunopathol, 1991, 60(1): 72-82.
55. Hussein MR, Fathi NA, El-Din AM, et al. Alterations of the CD4(+), CD8(+) T cell subsets, interleukins-1beta, IL-10, IL-17, tumor necrosis factor-alpha and soluble intercellular adhesion molecule-1 in rheumatoid arthritis and osteoarthritis: preliminary observations. Pathol Oncol Res, 2008, 14(3): 321-328.
56. Kriegova E, Manukyan G, Mikulkova Z, et al. Gender-related differences observed among immune cells in synovial fluid in knee osteoarthritis. Osteoarthritis Cartilage, 2018, 26(9): 1247-1256.
57. de Jong H, Berlo SE, Hombrink P, et al. Cartilage proteoglycan aggrecan epitopes induce proinflammatory autoreactive T-cell responses in rheumatoid arthritis and osteoarthritis. Ann Rheum Dis, 2010, 69(1): 255-262.
58. Penatti A, Facciotti F, De Matteis R, et al. Differences in serum and synovial CD4+ T cells and cytokine profiles to stratify patients with inflammatory osteoarthritis and rheumatoid arthritis. Arthritis Res Ther, 2017, 19(1): 103.
59. Rosshirt N, Hagmann S, Tripel E, et al. A predominant Th1 polarization is present in synovial fluid of end-stage osteoarthritic knee joints-analysis of peripheral blood, synovial fluid & synovial membrane. Clin Exp Immunol, 2018.[Epub ahead of print].
60. Sae-Jung T, Sengprasert P, Apinun J, et al. Functional and T cell receptor repertoire analyses of peripheral blood and infrapatellar fat pad T cells in knee osteoarthritis. J Rheumatol, 2018.[Epub ahead of print].
61. Li YS, Luo W, Zhu SA, et al. T cells in osteoarthritis: alterations and beyond. Front Immunol, 2017, 8: 356.
62. Sturfelt G, Truedsson L. Complement in the immunopathogenesis of rheumatic disease. Nat Rev Rheumatol, 2012, 8(8): 458-468.
63. Corvetta A, Pomponio G, Rinaldi N, et al. Terminal complement complex in synovial tissue from patients affected by rheumatoid arthritis, osteoarthritis and acute joint trauma. Clin Exp Rheumatol, 1992, 10(5): 433-438.
64. Struglics A, Okroj M, Swård P, et al. The complement system is activated in synovial fluid from subjects with knee injury and from patients with osteoarthritis. Arthritis Res Ther, 2016, 18(1): 223.
65. Wang Q, Rozelle AL, Lepus CM, et al. Identification of a central role for complement in osteoarthritis. Nat Med, 2011, 17(12): 1674-1679.

Chinese Journal of Reparative and Reconstructive Surgery

Role and progress of innate immunity in pathogenesis of osteoarthritis

Abstract Full text Figures/Tables Video References Cited by

Previous Article

Next Article

Format

Content