Dampness syndrome aggravates T helper 17/regulatory T imbalance to promote renal injury in rats with experimental membranous nephropathy

doi:10.19852/j.cnki.jtcm.2025.05.009

Journal of Traditional Chinese Medicine ›› 2025, Vol. 45 ›› Issue (5): 1028-1039.DOI: 10.19852/j.cnki.jtcm.2025.05.009

• Original Articles • Previous Articles Next Articles

Dampness syndrome aggravates T helper 17/regulatory T imbalance to promote renal injury in rats with experimental membranous nephropathy

SHAN Wenjun¹, GU Haowen¹, GUAN Haiyu¹, LI Ping²^,³^,⁴^,⁵, WANG Yi¹, HAN Miaoru¹, WANG Houchun¹, HUANG Xiaoyan²^,³^,⁴(), BAO Kun²^,³^,⁴^,⁵()

1 Guangzhou University of Chinese Medicine, Guangzhou 510145, China
2 State Key Laboratory of Dampness Syndrome of Chinese Medicine, the Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510006, China
3 Guangdong-Hong Kong-Macau Joint Lab on Chinese Medicine and Immune Disease Research, Guangzhou 510006, China
4 Nephrology Department, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou 510006, China
5 Guangdong Provincial Key Laboratory of Chinese Medicine for Prevention and Treatment of Refractory Chronic Disease, the Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510006, China

Received:2024-09-12 Accepted:2025-01-14 Online:2025-10-15 Published:2025-09-15
Contact: Prof. BAO Kun, State Key Laboratory of Dampness Syndrome of Chinese Medicine, the Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510006, China; Guangdong-Hong Kong-Macau Joint Lab on Chinese Medicine and Immune Disease Research, Guangzhou 510006, China; Nephrology Department, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou 510006, China; Guangdong Provincial Key Laboratory of Chinese Medicine for Prevention and Treatment of Refractory Chronic Disease, the Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510006, China. baokun@aliyun.com;
Prof. HUANG Xiaoyan, NState Key Laboratory of Dampness Syndrome of Chinese Medicine, the Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510006, China; Guangdong-Hong Kong-Macau Joint Lab on Chinese Medicine and Immune Disease Research, Guangzhou 510006, China; Nephrology Department, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou 510006, China. hxyan2013@126.com,Telephone: + 86-20-39318891
About author:SHAN Wenjun and GU Haowen are co-first authors and contributed equally to this work
Supported by:
Special Project of State Key Laboratory of Dampness Syndrome of Chinese Medicine: a Randomized Controlled Clinical Study of Sanqi Qushi Granules in the Treatment of Membranous Nephropathy(SZ2021ZZ36);a Cohort Study on the Pathogenesis and Evolution of Dampness Syndrome in Idiopathic Membranous Nephropathy and Its Material Basis(SZ2021ZZ09);the National Natural Science Foundation of China: Research on the Role of Damp Nephropathy based on the Metabolic Disorders-T helper 17/Regulatory T Imbalance Evil in the Progression of Membranous(81974565);the Guangzhou Science and Technology Plan Project: Exploring the Mechanism of Treating Membranous Nephropathy based on Dampness from the Perspective of Regulating Amino Acid Metabolism Disorders(2023A03J0746);Multi-omics Study to Explore the Material Basis of Dampness Syndrome in Membranous Nephropathy and the Intervention Mechanism of Sanqi Qushi Decoction(2024A03J0117);a Multimodal Machine Learning Prediction Model based on Pathological Images, Transcriptomics and Traditional Chinese Medicine Syndromes to Explore the Prognosis-related lncRNA Molecules of Membranous Nephropathy and the Intervention Mechanism of Sanqi Qushi Decoction(2025A03J4062);Research Project of Guangdong Provincial Hospital of Traditional Chinese Medicine: Construction of a Risk Management Prediction Model for Membranous Nephropathy Based on Artificial Intelligence Technology(YN2023HL03);Study on the Pathogenesis Evolution and Microbiological Mechanism of Membranous Nephropathy with Dampness Syndrome Based on the Changes of Tongue Coating Microecology(YN2023MB10);Post-doctoral Research Project of Guangdong Provincial Hospital of Chinese Medicine: Study on the Mechanism of Yinyang Shengmai Method in Regulating Myocardial Infarction in Diabetic Rats based on Ang/Vascular Endothelial Growth Factor-Mediated Angiogenesis(10814);Funding Project of Guangdong Provincial Administration of Traditional Chinese Medicine: Study on the Mechanism of "Dampness Stagnation in Blood Collaterals" inducing Vascular Aging Based on Oxidative Stress-inflammation Crosstalk and Intervention of Traditional Chinese Medicine(20233021);China Postdoctoral Science Foundation Funded Project: Study on the Mechanism of Shenmai Injection in Promoting Angiogenesis after Myocardial Infarction in Rats with Qi and Yin Deficiency Type Diabetic Nephropathy(2023M730810)

Abstract

Abstract:

OBJECTIVE: To examine the T helper 17 (Th17)/regulatory T (Treg) immune balance in passive Heymann nephritis (PHN) rats with dampness syndrome (DS).

METHODS: Rats were divided into four groups: normal control (NC), PHN model, PHN + DS model, and DS model. The DS model was created by administering lard, a 60% cold sucrose solution, and Chinese Baijiu viagavage. In contrast, PHN was induced in male Sprague-Dawley rats by injecting anti-Fx1A serum into the tail vein. The general condition of the rats was assessed, while the levels of urine protein, albumin, and serum creatinine were measured using commercially available kits. Pathological renal damage was evaluated using hematoxylin and eosin, periodic acid-schiff, and periodic acid-silver methenamine staining, while podocyte damage was assessed through immunohistochemistry. The proportions of Th17 cells and Treg cells in peripheral blood mononuclear cells were quantified by flow cytometry. Plasma cytokine levels of interleukin 17, transforming growth factor-β1, and interleukin 6 were determined by enzyme-linked immunosorbent assay.

RESULTS: This study demonstrated a significant increase in proteinuria and total cholesterol levels in PHN rats with DS, along with more severe histopathological kidney damage. DS exacerbated podocyte damage in PHN rats. Additionally, the number of Treg cells was significantly reduced, while the ratio of Th17/Treg cells was significantly elevated in PHN rats with DS.

CONCLUSION: In conclusion, the findings of our study indicate that the presence of DS exacerbates renal injury in PHN, a rat model used to simulate experimental membranous nephropathy. This observation may be closely linked to the exacerbation of the Th17/Treg imbalance and podocyte injury in PHN rats induced by DS.

Key words: glomerulonephritis, membranous, Th17 cells, T-lymphocytes, regulatory, dampness syndrome

SHAN Wenjun, GU Haowen, GUAN Haiyu, LI Ping, WANG Yi, HAN Miaoru, WANG Houchun, HUANG Xiaoyan, BAO Kun. Dampness syndrome aggravates T helper 17/regulatory T imbalance to promote renal injury in rats with experimental membranous nephropathy[J]. Journal of Traditional Chinese Medicine, 2025, 45(5): 1028-1039.

Figures/Tables 12

Figure 1 Comparison of the appearance of rats in each group A: appearance of rats in the NC group; B: appearance of rats in the PHN group; C: appearance of rats in the PHN + DS group; D: appearance of rats in the DS group. NC group: injected with saline (0.5 mL per 100 g body weight) into the tail vein once and gavaged with distilled water (1 mL per 100 g body weight) daily (n = 6); PHN group: injected with anti-Fx1A serum (0.5 mL per 100 g body weight) into the tail vein once and gavaged with lard (1 mL per 100 g body weight) every other day, a 60% cold sucrose solution (0.5 mL per 100 g body weight), and Chinese Baijiu with 56% purity (0.5 mL per 100 g body weight) every other day (n = 6); PHN+DS group: injected with anti-Fx1A serum (0.5 mL per 100 g body weight) into the tail vein once and gavaged with distilled water (1 mL per 100 g body weight) daily (n = 6); DS group: injected with saline (0.5 mL per 100 g body weight) into the tail vein once and gavaged with lard (1 mL per 100 g body weight) every other day, a 60% cold sucrose solution (0.5 mL per 100 g body weight), and Chinese Baijiu with 56% purity (0.5 mL per 100 g body weight) every other day (n = 6). NC: normal control; PHN: passive Heymann nephritis; DS: dampness syndrome.

Table 1 The average daily feed intake of rats in each group at different time points (g)

Group	Day 0	Day 6	Day 12	Day 18	Day 24	Day 30
NC	23.00	23.50	23.67	24.67	26.17	27.00
PHN	23.25	23.00	23.17	23.20	21.00	19.50
PHN+DS	22.80	19.50	21.00	20.17	18.83	18.17
DS	23.10	20.50	20.50	21.33	21.67	22.17

Table 2 The average daily water intake of rats in each group at different time points (mL)

Group	n	Day 0	Day 6	Day 12	Day 18	Day 24	Day 30
NC	6	43.00	42.83	42.83	43.67	44.17	45.17
PHN	6	42.00	43.00	43.00	43.58	41.25	41.30
PHN+DS	6	42.50	33.67	32.83	34.17	32.67	28.17
DS	6	40.56	33.50	33.42	33.50	33.25	31.17

Table 3 Comparison of the body weight of rats in each group at different time points (g, x - ± s)

Group	n	Day 0	Day 6	Day 12	Day 18	Day 24	Day 30
NC	6	217±13	244±17	279±32	323±30	367±20	395±25
PHN	6	219±7	255±9	280±16	320±18	351±29	322±19^b
PHN+DS	6	221±6	247±14	263±19	309±26	338±29	300±29^b
DS	6	220±10	240±16	260±18	302±16	331±19^a	355±23^bcd

Table 4 Comparison of the proteinuria levels of rats in each group at different time points (mg, x - ± s)

Group	n	Week 1	Week 2	Week 3
NC	6	6.46±1.76	9.01±1.46	6.66±1.15
PHN	6	12.73±9.62	42.36±9.89^c	55.70±13.95^c
PHN+DS	6	15.97±5.11^a	57.26±16.08^c	93.94±19.10^ce
DS	6	5.40±1.04^b	8.26±2.23^df	5.70±2.06^df

Table 5 Comparison of the ALB, TC, TG, SCr levels of rats in each group at different time points ( x - ± s)

Group	n	ALB (g/L)	TC (mmol/L)	TG (mmol/L)	SCr (μmol/L)
NC	6	22.50±1.01	1.05±0.26	0.42±0.08	20.61±1.49
PHN	6	19.72±1.51^a	5.59±1.11^a	3.08±0.35^a	34.03±5.07^a
PHN+DS	6	18.82±2.07^a	7.71±0.65^ac	3.88±0.69^a	39.72±6.64^a
DS	6	21.01±1.73^b	1.42±0.34^de	0.61±0.13^de	21.20±1.88^de

Figure 2 Comparison of the renal pathology of rats in each group (×400) A-D: HE staining of renal tissue from rats; E-H: PAS staining of renal tissue from rats; J-L: Masson staining of renal tissue from rats; M-P: PASM staining of renal tissue from rats; A, E, J, M: NC group; B, F, J, N: PHN group; C, G, K, O: PHN+DS group; D, H, L, P: DS group. NC group: injected with saline (0.5 mL per 100 g body weight) into the tail vein once and gavaged with distilled water (1 mL per 100 g body weight) daily (n = 6); PHN group: injected with anti-Fx1A serum (0.5 mL per 100 g body weight) into the tail vein once and gavaged with lard (1 mL per 100 g body weight) every other day, a 60% cold sucrose solution (0.5 mL per 100 g body weight), and Chinese Baijiu with 56% purity (0.5 mL per 100 g body weight) every other day (n = 6); PHN + DS group: injected with anti-Fx1A serum (0.5 mL per 100 g body weight) into the tail vein once and gavaged with distilled water (1 mL per 100 g body weight) daily (n = 6); DS group: injected with saline (0.5 mL per 100 g body weight) into the tail vein once and gavaged with lard (1 mL per 100 g body weight) every other day, a 60% cold sucrose solution (0.5 mL per 100 g body weight), and Chinese Baijiu with 56% purity (0.5 mL per 100 g body weight) every other day (n = 6). NC: normal control; PHN: passive Heymann nephritis; DS: dampness syndrome; HE: hematoxylin and eosin; PAS: periodic acid-schiff; PASM: periodic acid-silver methenamine.

Figure 3 Comparison of the podocyte injury of rats in each group (×400) A-D: nephrin expression in the renal tissue of rats; E-H: podocin expression in the renal tissue of rats; I-L: synaptopodin expression in the renal tissue of rats; A, E, I: NC group; B, F, J: PHN group; C, G, K: PHN+DS group; D, H, L: DS group. All pictures were stained by immunohistochemical method, with PBS used as the negative control. NC group: injected with saline (0.5 mL per 100 g body weight) into the tail vein once and gavaged with distilled water (1 mL per 100 g body weight) daily (n = 6); PHN group: injected with anti-Fx1A serum (0.5 mL per 100 g body weight) into the tail vein once and gavaged with lard (1 mL per 100 g body weight) every other day, a 60% cold sucrose solution (0.5 mL per 100 g body weight), and Chinese Baijiu with 56% purity (0.5 mL per 100 g body weight) every other day (n = 6); PHN + DS group: injected with anti-Fx1A serum (0.5 mL per 100 g body weight) into the tail vein once and gavaged with distilled water (1 mL per 100 g body weight) daily (n = 6); DS group: injected with saline (0.5 mL per 100 g body weight) into the tail vein once and gavaged with lard (1 mL per 100 g body weight) every other day, a 60% cold sucrose solution (0.5 mL per 100 g body weight), and Chinese Baijiu with 56% purity (0.5 mL per 100 g body weight) every other day (n = 6). NC: normal control; PHN: passive Heymann nephritis; DS: dampness syndrome; PBS: phosphate-buffered saline.

Table 6 Comparison of the average optical density of nephrin, podocin, and synaptopodin in kidneys of rats in each group ( x - ± s)

Group	n	Nephrin	Podocin	Synaptopodin
NC	6	0.233±0.017	0.221±0.014	0.243±0.010
PHN	6	0.202±0.013^a	0.189±0.010^a	0.202±0.025^a
PHN+DS	6	0.171±0.013^ab	0.165±0.018^ab	0.201±0.015^a
DS	6	0.226±0.013^bc	0.213±0.014^bc	0.234±0.014^bc

Figure 4 Comparison of the percentages of Th17, Treg in PBMCs of rats o in each group A-D: percentages of Th17 cells in PBMCs of rats; E-H: percentages of Treg cells in PBMCs of rats; A, E: NC group; B, F: PHN group; C, G: PHN + DS group; D, H: DS group. NC group: injected with saline (0.5 mL per 100 g body weight) into the tail vein once and gavaged with distilled water (1 mL per 100 g body weight) daily (n = 6); PHN group: injected with anti-Fx1A serum (0.5 mL per 100 g body weight) into the tail vein once and gavaged with lard (1 mL per 100 g body weight) every other day, a 60% cold sucrose solution (0.5 mL per 100 g body weight), and Chinese Baijiu with 56% purity (0.5 mL per 100 g body weight) every other day (n = 6); PHN + DS group: injected with anti-Fx1A serum (0.5 mL per 100 g body weight) into the tail vein once and gavaged with distilled water (1 mL per 100 g body weight) daily (n = 6); DS group: injected with saline (0.5 mL per 100 g body weight) into the tail vein once and gavaged with lard (1 mL per 100 g body weight) every other day, a 60% cold sucrose solution (0.5 mL per 100 g body weight), and Chinese Baijiu with 56% purity (0.5 mL per 100 g body weight) every other day (n = 6). NC: normal control; PHN: passive Heymann nephritis; DS: dampness syndrome; Th17: T helper 17; Treg: regulatory T; PBMCs: peripheral blood mononuclear cells.

Table 7 Comparison of the percentages of Th17, Treg and the ratio of Th17/Treg in PBMCs of rats in each group ( x - ± s)

Group	n	Th17	Treg	Th17/Treg
NC	6	0.508±0.093	8.867±1.746	0.060±0.155
PHN	6	0.752±0.227^a	8.553±1.144	0.090±0.029
PHN+DS	6	0.935±0.134^b	6.647±1.429^ac	0.152±0.042^bd
DS	6	0.800±0.183^b	6.808±1.332^ac	0.115±0.026^be

Table 8 Comparison of the IL-17, IL-6, TGF-β1 levels in serum of rats in each group (pg/mL, x - ± s)

Group	n	IL-17	IL-6	TGF-β1
NC	6	144±43	4±0	314±83
PHN	6	452±141^a	5±1	182±64^b
PHN+DS	6	787±189^bc	6±1^a	136±66^b
DS	6	146±39^cd	5±1	132±55^b

References 54.

1.	Ronco P, Beck L, Debiec H, et al. Membranous nephropathy. Nat Rev Dis Primers 2021; 7: 69. DOI PMID
2.	Claudio P. Primary membranous nephropathy: an endless story. J Nephrol 2023; 36: 563-74.
3.	Li LS, Liu ZH. Epidemiologic data of renal diseases from a single unit in China: analysis based on 13 519 renal biopsies. Kidney Int 2004; 66: 920-3.
4.	Couser WG. Primary membranous nephropathy. Clin J Am Soc Nephrol 2017; 12: 983-97.
5.	Lai WL, Yeh TH, Chen PM, et al. Membranous nephropathy: a review on the pathogenesis, diagnosis, and treatment. J Formos Med Assoc 2015; 114: 102-11.
6.	Zhu P, Zhou FD, Wang SX, Zhao MH, Wang HY. Increasing frequency of idiopathic membranous nephropathy in primary glomerular disease: a 10-year renal biopsy study from a single Chinese nephrology centre. Nephrology (Carlton) 2015; 20: 560-6.
7.	Xie J, Chen N. Primary glomerulonephritis in mainland China: an overview. Contrib Nephrol. 2013; 181: 1-11. DOI PMID
8.	Motavalli R, Etemadi J, Kahroba H, Mehdizadeh A, Yousefi M. Immune system-mediated cellular and molecular mechanisms in idiopathic membranous nephropathy pathogenesis and possible therapeutic targets. Life Sci 2019; 238: 116923.
9.	Paquissi FC, Abensur H. The Th17/IL-17 axis and kdney diseases, with focus on lupus nephritis. Front Med (Lausanne) 2021; 8: 654912.
10.	Zhu X, Li S, Zhang Q, et al. Correlation of increased Th17/Treg cell ratio with endoplasmic reticulum stress in chronic kidney disease. Medicine (Baltimore) 2018; 97: e10748.
11.	Motavalli R, Etemadi J, Soltani-Zangbar MS, et al. Altered Th17/Treg ratio as a possible mechanism in pathogenesis of idiopathic membranous nephropathy. Cytokine 2021; 141: 155452.
12.	Rosenzwajg M, Languille E, Debiec H, et al. B- and T-cell subpopulations in patients with severe idiopathic membranous nephropathy may predict an early response to rituximab. Kidney Int 2017; 92: 227-37. DOI PMID
13.	Chen Y, Sun BG, Zhang SJ, Chen ZX, Hardi CF, Xiang T. Observations of TCRVβ gene expression in rats with dampness syndrome. Evid Based Complement Alternat Med 2014; 2014: 373608.
14.	Hong X, Li C, Cai F, et al. Construction of questionnaire for damp type of membranous nephropathy and correlation between urine protein and damp syndrome. Guangzhou Zhong Yi Yao Da Xue Xue Bao 2021; 38: 2260-7.
15.	Zhang S, Chen Z, Lin Y. Effect of Chinese medicine for resolving dampness on activated and functional T lymphocyte subsets in chronic hepatitis B patients with dampness syndrome. Zhong Guo Zhong Xi Yi Jie He Za Zhi 2006; 26: 1078-81.
16.	Gong Y, Liu L, He X, et al. The th17/treg immune balance in ulcerative colitis patients with two different chinese syndromes: dampness-heat in large intestine and spleen and kidney Yang deficiency syndrome. Evid Based Complement Alternat Med 2015; 2015: 264317.
17.	Glassock RJ. The pathogenesis of idiopathic membranous nephropathy: a 50-year odyssey. Am J Kidney Dis 2010; 56: 157-67. DOI PMID
18.	Wang CS, Greenbaum LA. Nephrotic syndrome. Pediatr Clin North Am 2019; 66: 73-85.
19.	Tu DQ, Jin J, Hu X, Ren Y, Zhao L, He Q. Curcumin improves the renal autophagy in rat experimental membranous nephropathy via regulating the PI3K/AKT/mTOR and Nrf2/HO-1 signaling pathways. Biomed Res Int 2020; 2020: 7069052.
20.	Glassock RJ. Diagnosis and natural course of membranous nephropathy. Semin Nephrol 2003; 23: 324-32. DOI PMID
21.	Frazier KS, Obert LA. Drug-induced glomerulonephritis: the spectre of biotherapeutic and antisense oligonucleotide immune activation in the kidney. Toxicol Pathol 2018; 46: 904-17. DOI PMID
22.	Jefferson JA, Pippin JW, Shankland SJ. Experimental models of membranous nephropathy. Drug Discov Today Dis Models 2010; 7: 27-33.
23.	Kaysen GA, Paukert TT, Menke DJ, Couser WG, MH H. Plasma volume expansion is necessary for edema formation in the rate with Heymann nephritis. Am J Physiol 1985; 248: F247-253.
24.	Fau ZM, Druet P. Passive Heymann's nephritis as a model of immune glomerulonephritis mediated by antibodies to immunoglobulins. Clin Exp Immunol 1980; 41: 189-95.
25.	Wang XH, Yang YN, Liang Y, et al. Structural modulation of gut microbiota during alleviation of experimental passive Heymann nephritis in rats by a traditional Chinese herbal formula. Biomed Pharmacother. 2022; 145: 112475.
26.	Lu A, Jiang M, Zhang C, Chan K. An integrative approach of linking Traditional Chinese Medicine pattern classification and biomedicine diagnosis. J Ethnopharmacol 2012; 141: 549-56. DOI PMID
27.	Hao Y, Yuan X, Qian P, Bai G, Wang Y. The serum analysis of dampness syndrome in patients with coronary heart disease and chronic renal failure based on the theory of "Same Syndromes in Different Diseases". Biomed Res Int 2017; 2017: 3805806.
28.	Zhong J, He L, Ding X. Study on clinical syndrome classification and related biochemical indexes in 146 cases of chronic renal failure. J Tradit Chin Med 2006; 47: 374-77.
29.	Nagata M. Podocyte injury and its consequences. Kidney Int 2016; 89: 1221-30. DOI PMID
30.	Benzing T. Signaling at the slit diaphragm. J Am Soc Nephrol 2004; 15: 1382-91. DOI PMID
31.	Kestilä M, Lenkkeri U, Männikkö M, et al. Positionally cloned gene for a novel glomerular protein--nephrin--is mutated in congenital nephrotic syndrome. Mol Cell 1998; 1: 575-82. DOI PMID
32.	Holzman LB, St John PL, Kovari IA, Verma R, Holthofer H, DR A. Nephrin localizes to the slit pore of the glomerular epithelial cell. Kidney Int 1999; 56: 1481-91. PMID
33.	Putaala H, Soininen R, Kilpeläinen P, Wartiovaara J, Tryggvason K. The murine nephrin gene is specifically expressed in kidney, brain and pancreas: inactivation of the gene leads to massive proteinuria and neonatal death. Hum Mol Genet 2001; 10: 1-8. PMID
34.	Ruotsalainen V, Patrakka J, Tissari P, et al. Role of nephrin in cell junction formation in human nephrogenesis. Am J Pathol 2000; 157: 1905-16. PMID
35.	Jalanko H. Pathogenesis of proteinuria: lessons learned from nephrin and podocin. Pediatr Nephrol 2003; 18: 487-91. PMID
36.	Roselli S, Gribouval O, Boute N, et al. Podocin localizes in the kidney to the slit diaphragm area. Am J Pathol 2002; 160: 131-9. DOI PMID
37.	Huber TB, Simons M, Hartleben B, et al. Molecular basis of the functional podocin-nephrin complex: mutations in the NPHS2 gene disrupt nephrin targeting to lipid raft microdomains. Hum Mol Genet 2003; 12: 3397-405. PMID
38.	Kawachi H, Koike H, Kurihara H, Sakai T, Shimizu F. Cloning of rat homologue of podocin: expression in proteinuric states and in developing glomeruli. J Am Soc Nephrol 2003; 14: 46-56. PMID
39.	Yu H, Kistler A, Faridi MH, et al. Synaptopodin limits TRPC6 podocyte surface expression and attenuates proteinuria. J Am Soc Nephrol 2016; 27: 3308-19. PMID
40.	Ning L, Suleiman HY, Miner JH. Synaptopodin is dispensable for normal podocyte homeostasis but is protective in the context of acute podocyte injury. J Am Soc Nephrol 2020; 31: 2815-32. DOI PMID
41.	Li H, Wu H, Guo Q, et al. Myeloid-derived suppressor cells promote the progression of primary membranous nephropathy by enhancing Th 17 response. Front Immunol 2020; 11: 1777.
42.	McGeachy MJ, Cua DJ, Gaffen SL. The IL-17 family of cytokines in health and disease. Immunity 2019; 50: 892-906. DOI PMID
43.	Chen L, Ruan G, Cheng Y, Yi A, Chen D, Wei Y. The role of Th17 cells in inflammatory bowel disease and the research progress. Front Immunol 2023; 13: 1055914.
44.	GR L. The balance of Th17 versus Treg cells in autoimmunity. Int J Mol Sci 2018; 19: 730.
45.	Bunte K, Beikler T. Th 17 cells and the IL-23/IL-17 axis in the pathogenesis of periodontitis and immune-mediated inflammatory diseases. Int J Mol Sci 2019; 20: 3394.
46.	Yang X, Zhang J, Ding YL. Association of microRNA-155, interleukin 17A, and proteinuria in preeclampsia. Medicine (Baltimore) 2017; 2017: e6509.
47.	Zhai SB, Sun BC, Zhang Y, Zhao LY, Zhang L. IL-17 aggravates renal injury by promoting podocyte injury in children with primary nephrotic syndrome. Exp Ther Med 2020; 20: 409-17. DOI PMID
48.	Wang L, Li Q, Wang LJ, et al. The role of Th17/IL-17 in the pathogenesis of primary nephrotic syndrome in children. Kidney Blood Press Res 2013; 337: 332-45.
49.	Liu YB, Su L, Lin QX, Han Y, Peng Y, Fan QF. Induction of C-Mip by IL-17 plays an important role in adriamycin-induced podocyte damage. Cell Physiol Biochem 2015; 36: 1274-90.
50.	Xu Y, Lin H, Zheng W, et al. Matrine ameliorates adriamycin-induced nephropathy in rats by enhancing renal function and modulating Th17/Treg balance. Eur J Pharmacol 2016; 791: 491-501. DOI PMID
51.	Li MO, Wan YY, Flavell RA. T cell-produced transforming growth factor-beta1 controls T cell tolerance and regulates Th1- and Th17-cell differentiation. Immunity 2007; 26: 579-91. DOI PMID
52.	Cantarelli C, Jarque M, Angeletti A, et al. A comprehensive phenotypic and functional immune analysis unravels circulating anti-phospholipase A2 receptor antibody secreting cells in membranous nephropathy patients. Kidney Int Rep 2020; 5: 1764-76. DOI PMID
53.	Le Berre L, Bruneau S, Naulet J, et al. Induction of T regulatory cells attenuates idiopathic nephrotic syndrome. J Am Soc Nephrol 2008; 20: 57-67.
54.	Kim MG, Koo TY, Yan JJ, et al. IL-2/anti-IL-2 complex attenuates renal ischemia-reperfusion injury through expansion of regulatory T cells. J Am Soc Nephrol 2013; 24: 1529-36.

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Dampness syndrome aggravates T helper 17/regulatory T imbalance to promote renal injury in rats with experimental membranous nephropathy

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