Research progress of interleukin-17 and interleukin-35 in autoimmune diseases

ZHANG Xiaodan; XU Yanyan; MA Tiankui; ZHU Yonghong; FAN Qiuling

doi:10.7619/jcmp.20220266

Journal of Clinical Medicine in Practice > 2022 > 26(10): 125-129. > DOI: 10.7619/jcmp.20220266

ZHANG Xiaodan, XU Yanyan, MA Tiankui, ZHU Yonghong, FAN Qiuling. Research progress of interleukin-17 and interleukin-35 in autoimmune diseases[J]. Journal of Clinical Medicine in Practice, 2022, 26(10): 125-129. DOI: 10.7619/jcmp.20220266

Citation:

PDF (573 KB)

Research progress of interleukin-17 and interleukin-35 in autoimmune diseases

1.
Department of Nephrology, the First Affiliated Hospital of China Medical University, Shenyang, Liaoning, 110000
2.
Department of Nephrology, the Fourth Affiliated Hospital of China Medical University, Shenyang, Liaoning, 110000

More Information

Received Date: January 18, 2022
Available Online: May 24, 2022

Graphical Abstract

Abstract

Abstract

Autoimmune diseases are the outcomes of a breakdown of immune tolerance that eventually leads to tissue damage, but the etiology of which has not been elucidated. Helper T cells (Th17), regulatory T cells (Treg), Treg/Th17 imbalance and related cytokines are closely related to the occurrence and development of autoimmune diseases. Interleukin (IL) -17 mainly secreted by Th17, has a pro-inflammatory effect and is involved in the occurrence and development of various autoimmune diseases. IL-35 as an important cytokine related to Th17/Treg is a novel cytokine in the IL-12 family, is mainly produced by Treg and has a negative immunomodulatory effect. This article reviewed the function, mechanism and role of IL-17 and IL-35 in autoimmune diseases, in order to provide theoretical basis for the treatment of these diseases.
- interleukin-35,
- interleukin-17,
- cytokines,
- autoimmune diseases

FullText(HTML)

References (48)

References

[1]	FASCHING P, STRADNER M, GRANINGER W, et al. Therapeutic potential of targeting the Th17/treg axis in autoimmune disorders[J]. Molecules, 2017, 22(1): 134. doi: 10.3390/molecules22010134
[2]	GUO K L, ZHANG X M. Cytokines that modulate the differentiation of Th17 cells in autoimmune uveitis[J]. J Immunol Res, 2021, 2021: 6693542.
[3]	WANG D, LEI L. Interleukin-35 regulates the balance of Th17 and Treg responses during the pathogenesis of connective tissue diseases[J]. Int J Rheum Dis, 2021, 24(1): 21-27. doi: 10.1111/1756-185X.13962
[4]	ZHANG J F, ZHANG Y S, WANG Q P, et al. Interleukin-35 in immune-related diseases: protection or destruction[J]. Immunology, 2019, 157(1): 13-20. doi: 10.1111/imm.13044
[5]	GOUDA M M, BHANDARY Y P. Acute lung injury: IL-17A-mediated inflammatory pathway and its regulation by curcumin[J]. Inflammation, 2019, 42(4): 1160-1169. doi: 10.1007/s10753-019-01010-4
[6]	CHEN F D, CAO A, YAO S X, et al. mTOR mediates IL-23 induction of neutrophil IL-17 and IL-22 production[J]. J Immunol, 2016, 196(10): 4390-4399. doi: 10.4049/jimmunol.1501541
[7]	TAMASSIA N, ARRUDA-SILVA F, CALZETTI F, et al. A reappraisal on the potential ability of human neutrophils to express and produce IL-17 family members in vitro: failure to reproducibly detect it[J]. Front Immunol, 2018, 9: 795. doi: 10.3389/fimmu.2018.00795
[8]	LI X X, BECHARA R, ZHAO J J, et al. IL-17 receptor-based signaling and implications for disease[J]. Nat Immunol, 2019, 20(12): 1594-1602. doi: 10.1038/s41590-019-0514-y
[9]	HERJAN T, HONG L Z, BUBENIK J, et al. IL-17-receptor-associated adaptor Act1 directly stabilizes mRNAs to mediate IL-17 inflammatory signaling[J]. Nat Immunol, 2018, 19(4): 354-365. doi: 10.1038/s41590-018-0071-9
[10]	LI N, WANG J C, LIANG T H, et al. Pathologic finding of increased expression of interleukin-17 in the synovial tissue of rheumatoid arthritis patients[J]. Int J Clin Exp Pathol, 2013, 6(7): 1375-1379.
[11]	ZHANG X, YUAN Y P, PAN Z P, et al. Elevated circulating IL-17 level is associated with inflammatory arthritis and disease activity: a meta-analysis[J]. Clin Chim Acta, 2019, 496: 76-83. doi: 10.1016/j.cca.2019.06.026
[12]	KE D S, FU X M, XUE Y, et al. IL-17A regulates the autophagic activity of osteoclast precursors through RANKL-JNK₁ signaling during osteoclastogenesis in vitro[J]. Biochem Biophys Res Commun, 2018, 497(3): 890-896. doi: 10.1016/j.bbrc.2018.02.164
[13]	SLOWIKOWSKI K, NGUYEN H N, NOSS E H, et al. CUX1 and IκBζ (NFKBIZ) mediate the synergistic inflammatory response to TNF and IL-17A in stromal fibroblasts[J]. Proc Natl Acad Sci USA, 2020, 117(10): 5532-5541. doi: 10.1073/pnas.1912702117
[14]	CHANG L, FENG X, GAO W. Proliferation of rheumatoid arthritis fibroblast-like synoviocytes is enhanced by IL-17-mediated autophagy through STAT3 activation[J]. Connect Tissue Res, 2019, 60(4): 358-366. doi: 10.1080/03008207.2018.1552266
[15]	KIM E K, KWON J E, LEE S Y, et al. IL-17-mediated mitochondrial dysfunction impairs apoptosis in rheumatoid arthritis synovial fibroblasts through activation of autophagy[J]. Cell Death Dis, 2017, 8(1): e2565.
[16]	PARK J S, KIM N R, LIM M A, et al. Deficiency of IL-1 receptor antagonist suppresses IL-10-producing B cells in autoimmune arthritis in an IL-17/Th17-dependent manner[J]. Immunol Lett, 2018, 199: 44-52. doi: 10.1016/j.imlet.2018.05.003
[17]	ROELEVELD D M, KOENDERS M I. The role of the Th17 cytokines IL-17 and IL-22 in Rheumatoid Arthritis pathogenesis and developments in cytokine immunotherapy[J]. Cytokine, 2015, 74(1): 101-107. doi: 10.1016/j.cyto.2014.10.006
[18]	LI Z H, NIU H Q, YAO H T, et al. IL-17A upregulates P-glycoprotein expression in peripheral blood lymphocytes of patients with rheumatoid arthritis through TAK1[J]. Clin Exp Rheumatol, 2020, 38(2): 299-305.
[19]	MOULTON V R, TSOKOS G C. T cell signaling abnormalities contribute to aberrant immune cell function and autoimmunity[J]. J Clin Invest, 2015, 125(6): 2220-2227. doi: 10.1172/JCI78087
[20]	ROZO C, CHINENOV Y, MAHARAJ R K, et al. Targeting the RhoA-ROCK pathway to reverse T-cell dysfunction in SLE[J]. Ann Rheum Dis, 2017, 76(4): 740-747. doi: 10.1136/annrheumdis-2016-209850
[21]	MA K Y, DU W H, XIAO F, et al. IL-17 sustains the plasma cell response via p38-mediated Bcl-xL RNA stability in lupus pathogenesis[J]. Cell Mol Immunol, 2021, 18(7): 1739-1750. doi: 10.1038/s41423-020-00540-4
[22]	SATOH Y, NAKANO K, YOSHINARI H, et al. A case of refractory lupus nephritis complicated by psoriasis vulgaris that was controlled with secukinumab[J]. Lupus, 2018, 27(7): 1202-1206. doi: 10.1177/0961203318762598
[23]	LIU Y L, YAN W M, YUAN W, et al. Treg/Th17 imbalance is associated with poor autoimmune hepatitis prognosis[J]. Clin Immunol, 2019, 198: 79-88. doi: 10.1016/j.clim.2018.11.003
[24]	BERINGER A, MIOSSEC P. IL-17 and IL-17-producing cells and liver diseases, with focus on autoimmune liver diseases[J]. Autoimmun Rev, 2018, 17(12): 1176-1185. doi: 10.1016/j.autrev.2018.06.008
[25]	AN J H. Expression and significance of Th17 cells and related factors in patients with autoimmune hepatitis[J]. Comb Chem High Throughput Screen, 2019, 22(4): 232-237. doi: 10.2174/1386207322666190402160455
[26]	GUTKOWSKI K, GUTKOWSKA D, KISZKA J, et al. Serum IL-17 level predicts inflammatory activity in patients with autoimmune hepatitis[J]. Pol Arch Intern Med, 2018: 128(3): 150-156.
[27]	KIMURA N, YAMAGIWA S, SUGANO T, et al. Possible involvement of chemokine C-C receptor 7-programmed cell death-1 + follicular helper T-cell subset in the pathogenesis of autoimmune hepatitis[J]. J Gastroenterol Hepatol, 2018, 33(1): 298-306. doi: 10.1111/jgh.13844
[28]	MA L, ZHANG L W, ZHUANG Y, et al. The imbalance between Foxp3 + tregs and Th1/Th17/Th22 cells in patients with newly diagnosed autoimmune hepatitis[J]. J Immunol Res, 2018, 2018: 3753081.
[29]	STEIN S, HENZE L, POCH T, et al. IL-17A/F enable cholangiocytes to restrict T cell-driven experimental cholangitis by upregulating PD-L1 expression[J]. J Hepatol, 2021, 74(4): 919-930. doi: 10.1016/j.jhep.2020.10.035
[30]	MANN H, KRYŠTFKOVO, ZÁMECNÍK J, et al. Interleukin-35 in idiopathic inflammatory myopathies[J]. Cytokine, 2021, 137: 155350. doi: 10.1016/j.cyto.2020.155350
[31]	MA N, FANG Y, XU R N, et al. Ebi3 promotes T-and B-cell division and differentiation via STAT3[J]. Mol Immunol, 2019, 107: 61-70. doi: 10.1016/j.molimm.2019.01.009
[32]	DAMBUZA I M, HE C, CHOI J K, et al. IL-12p35 induces expansion of IL-10 and IL-35-expressing regulatory B cells and ameliorates autoimmune disease[J]. Nat Commun, 2017, 8(1): 719. doi: 10.1038/s41467-017-00838-4
[33]	LI X Y, FANG P, YANG W Y, et al. IL-35, as a newly proposed homeostasis-associated molecular pattern, plays three major functions including anti-inflammatory initiator, effector, and blocker in cardiovascular diseases[J]. Cytokine, 2019, 122: 154076. doi: 10.1016/j.cyto.2017.06.003
[34]	WU S Q, LI Y X, LI Y X, et al. Interleukin-35 attenuates collagen-induced arthritis through suppression of vascular endothelial growth factor and its receptors[J]. Int Immunopharmacol, 2016, 34: 71-77. doi: 10.1016/j.intimp.2016.02.018
[35]	LI Y X, WU S Q, LI Y X, et al. Interleukin-35 (IL-35) inhibits proliferation and promotes apoptosis of fibroblast-like synoviocytes isolated from mice with collagen-induced arthritis[J]. Mol Biol Rep, 2016, 43(9): 947-956. doi: 10.1007/s11033-016-4034-7
[36]	LIU S Y, LI Y X, XIA L P, et al. IL-35 prevent bone loss through promotion of bone formation and angiogenesis in rheumatoid arthritis[J]. Clin Exp Rheumatol, 2019, 37(5): 820-825.
[37]	LI Y X, YUAN L, JIANG S Y, et al. Interleukin-35 stimulates tumor necrosis factor-α activated osteoblasts differentiation through Wnt/β-catenin signaling pathway in rheumatoid arthritis[J]. Int Immunopharmacol, 2019, 75: 105810. doi: 10.1016/j.intimp.2019.105810
[38]	KAMIYA Y, KIKUCHI T, GOTO H, et al. IL-35 and RANKL synergistically induce osteoclastogenesis in RAW264 mouse monocytic cells[J]. Int J Mol Sci, 2020, 21(6): 2069. doi: 10.3390/ijms21062069
[39]	JING L, KIM S, SUN L, et al. IL-37-and IL-35/IL-37-producing plasma cells in chronic periodontitis[J]. J Dent Res, 2019, 98(7): 813-821. doi: 10.1177/0022034519847443
[40]	YAGO T, NANKE Y, KAWAMOTO M, et al. IL-35 inhibits human osteoclastogenesis from monocytes induced by receptor-activator of NF-κB ligand[J]. Cent Eur J Immunol, 2018, 43(2): 148-154. doi: 10.5114/ceji.2018.77384
[41]	IRANSHAHI N, ASSAR S, AMIRI S M, et al. Decreased gene expression of Epstein-Barr virus-induced gene 3 (EBI-3) may contribute to the pathogenesis of rheumatoid arthritis[J]. Immunol Invest, 2019, 48(4): 367-377. doi: 10.1080/08820139.2018.1549066
[42]	ŠENOLT L, ŠUMOVÁB, JANDOVÁR, et al. Interleukin 35 synovial fluid levels are associated with disease activity of rheumatoid arthritis[J]. PLoS One, 2015, 10(7): e0132674. doi: 10.1371/journal.pone.0132674
[43]	LI Y X, YAO L T, LIU S Y, et al. Elevated serum IL-35 levels in rheumatoid arthritis are associated with disease activity[J]. J Investig Med, 2019, 67(3): 707-710. doi: 10.1136/jim-2018-000814
[44]	HE D, LIU M, LIU B. Interleukin-35 as a new biomarker of renal involvement in lupus nephritis patients[J]. Tohoku J Exp Med, 2018, 244(4): 263-270. doi: 10.1620/tjem.244.263
[45]	YE Z, JIANG Y F, SUN D J, et al. The plasma interleukin (IL)-35 level and frequency of circulating IL-35 + regulatory B cells are decreased in a cohort of Chinese patients with new-onset systemic lupus erythematosus[J]. Sci Rep, 2019, 9(1): 13210. doi: 10.1038/s41598-019-49748-z
[46]	LU D, PENG Q, CHEN D D, et al. Expression imbalance of IL-17/IL-35 in peripheral blood and placental tissue of pregnant women in preeclampsia[J]. Taiwan J Obstet Gynecol, 2020, 59(3): 409-414. doi: 10.1016/j.tjog.2020.03.013
[47]	JIANG S H, SHAN F L, ZHANG Y W, et al. Increased serum IL-17 and decreased serum IL-10 and IL-35 levels correlate with the progression of COPD[J]. Int J Chron Obstruct Pulmon Dis, 2018, 13: 2483-2494. doi: 10.2147/COPD.S167192
[48]	CORREALE J, MARRODAN M, CARNERO CONTENTTI E. Interleukin-35 is a critical regulator of immunity during helminth infections associated with multiple sclerosis[J]. Immunology, 2021, 164(3): 569-586. doi: 10.1111/imm.13389

Cited By

Cited by

Periodical cited type(2)

1.	李燕，罗欢，王丹. 宫颈鳞状上皮内病变和宫颈癌Th17、HIF-1α水平变化与HPV感染的关系. 中国性科学. 2024(04): 92-95 .
2.	李艳，莫馨霈，熊秋霞. 自身免疫性疾病的重要治疗靶点白细胞介素-17的研究进展. 中国医药导报. 2024(20): 36-41 .

Other cited types(1)

Get Citation

PDF

XML

Article views (243) PDF downloads (15) Cited by(3)

Turn off MathJax

Article Contents

Abstract

References

Research progress of interleukin-17 and interleukin-35 in autoimmune diseases

Abstract

References

Cited by

Periodical cited type(2)

Other cited types(1)

Catalog

Export File

Citation

Format

Content