Significance of M2 macrophages in glomerulonephritis with crescents

Jun, Li; Yu, Ya-Fen; Liu, Changhua; Wang, Cuimei

doi:10.1016/j.prp.2017.04.011

Cited by 44 publications

(33 citation statements)

References 21 publications

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“…While tubulointerstitial CD163 + macrophages significantly correlated with serum creatinine, serum urea and creatinine clearance, glomerular CD163 + macrophages negatively correlated with plasma C3 and C4 (22,23). Additionally, CD163 was found mainly expressed in active crescentic glomerulonephritis, proliferative glomerular lesions and areas of tubulointerstitial injury (21)(22)(23)(24). In another study including patients with pauci-immune necrotizing glomerulitis, CD68 + and CD163 + macrophages predominated at sites of fibrinoid necrosis (25).…”

Section: Discussionmentioning

confidence: 94%

Association of Urine sCD163 With Proliferative Lupus Nephritis, Fibrinoid Necrosis, Cellular Crescents and Intrarenal M2 Macrophages

et al. 2020

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CD163 is a marker for alternatively activated macrophages, which have been implicated in the pathogenesis of lupus nephritis (LN). In our preliminary screening of urine proteins in LN, urine soluble CD163 (sCD163) was significantly elevated in patients with active LN. To evaluate the potential of sCD163 as a biomarker in LN, urine sCD163 was assayed in patients with active LN, active non-renal lupus patients (ANR), inactive SLE and healthy controls (HC), using ELISA and normalized to urine creatinine. The correlation of urine sCD163 with clinical parameters and renal pathological attributes was further investigated in LN patients with concurrent renal biopsies. A total of 228 SLE patients and 56 HC were included from three cohorts. Results demonstrated that urine sCD163 was significantly elevated in active LN when compared with HC, inactive SLE, or ANR in African-American, Caucasian and Asian subjects (all P < 0.001). In LN patients with concurrent renal biopsies, urine sCD163 was significantly increased in patients with proliferative LN when compared with non-proliferative LN (P < 0.001). Urine sCD163 strongly correlated with SLEDAI, rSLEDAI, activity index (AI) of renal pathology, fibrinoid necrosis, cellular crescents, and interstitial inflammation on biopsies (all P < 0.01). Macrophages, particularly M2 macrophages, the predominant cells expressing CD163 within LN kidneys, represented a potential source of elevated urine sCD163, based on single-cell RNA sequencing analysis. To conclude, urine sCD163 discriminated patients with active LN from other SLE patients and was significantly elevated in proliferative LN. It strongly correlated with concurrent AI and several specific pathological attributes, demonstrating its potential in predicting renal pathology.

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Section: Discussionmentioning

confidence: 94%

Association of Urine sCD163 With Proliferative Lupus Nephritis, Fibrinoid Necrosis, Cellular Crescents and Intrarenal M2 Macrophages

et al. 2020

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“…Current data suggest that M2 macrophages are involved in tissue repair in rhabdomyolysis-induced acute kidney injury, adriamycin nephropathy, acute tubule interstitial nephritis, ischemia-reperfusion injury and unilateral ureteral obstruction (UUO) animal models [ 10–14 ]. In our previous study, we found that M2 macrophages are involved in the pathogenesis of acute tubulointerstitial lesions in glomerulonephritis patients with crescents, acute tubulointerstitial injury of acute tubular necrosis and acute interstitial nephritis patients with good prognosis [ 15 , 16 ]. In this study, CD163-positive macrophages also accumulated in areas of acute tubular injury and positively correlated with urinary NAG and β2-microglobulin, which implied CD163-positive macrophages may be involved in acute tubular injury in pSS.…”

Section: Discussionmentioning

confidence: 99%

Significance of M2 macrophage in tubulointerstitial disease secondary to primary Sjogren's disease

Liu

et al. 2018

Renal Failure

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Objective: M2 Macrophages could improve tubulointerstitial disease in animal models. HIF-1αpromotes macrophage polarization and is involved in tubular injury. The study aims to observe the clinicopathologic significance of M2 macrophage and HIF-1α in tubulointerstitial injury secondary to primary Sjogren's disease. Methods: Renal tissue samples from patients with tubulointerstitial disease secondary to primary Sjogren's disease (SS, n = 10), chronic tubulointerstitial nephritis secondary to drug (CIN, n = 8) were included in this study. The expression of CD163, CD68 and HIF-1α were examined by immunohistochemistry or immunofluorescence. Results: (1) Renal involvement was the first manifestation in seven of ten (7/10) patients with pSS, including proteinuria, renal dysfunction, renal tubular acidosis and multiple renal stone; and two patient had intractable hypokalemia. (2) There were numerous CD163- positive cells and CD68- positive cells infiltration in tubulointerstitial injury of pSS, especially in patients with hypokalemia. CD163 positive cells and HIF-1αwere mainly expressed in acute tubulointerstitial injury of pSS, which positively correlated to N-acetyl-β-D-glucosaminidase and β2-microglobulin. (3) Compared with CIN, patients with pSS had higher serum globulin level, erythrocyte sedimentation rate (ESR) and lower urinary osmotic pressure. (4) During follow-up of one year, six patients with pSS and acute tubular injury acquired improved renal function on therapy of steroid and total glucosides of peony. The remaining four patients with pSS had stable renal function. Conclusion: M2 macrophages are involved in acute tubular injury in patients with primary Sjogren's disease. Early intervention can improve renal function of tubulointerstitial injury secondary to primary Sjogren's disease.

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“…CD206 is a marker of M2 macrophages, which are generally associated with anti-in ammatory phenotypes. Activated CD206 + M2b macrophages have been shown, however, to be pathogenic in a spontaneous model of lupus nephritis [18] and they represent the largest myeloid in ltrates in human lupus nephritis [19,20]. On the other hand, CD206 expression on macrophages was induced by a therapeutic treatment with mesenchymal stem cells in an IL-6 dependent manner in the B6.lpr model [21].…”

Section: Discussionmentioning

confidence: 99%

D-mannose ameliorates autoimmune phenotypes in mouse models of lupus

Wang

Teng

Abboud

et al. 2020

Preprint

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Background: Systemic lupus erythematosus is a disorder of immune regulation characterized by overproduction of autoantibodies. D-mannose is a C-2 epimer of glucose that exhibits immunoregulatory effects in models of autoimmune diseases, such as type 1 diabetes, induced rheumatoid arthritis, and airway inflammation. This study was conducted to evaluate the efficacy of D-mannose treatment in mouse models of lupus.Methods: The effect of D-Mannose was evaluated by flow cytometry on the in vitro activation of C57BL/6 (B6) murine bone marrow derived dendritic cells and their ability to induce antigen specific CD4+ T cell proliferation and activation. The effect of D-mannose administration in vivo on the frequency of Foxp3+ regulatory T cells in B6 mice was assessed by flow cytometry. D-mannose was administered to two models of lupus: the chronic graft-versus-host disease (cGVHD) induced model and the B6.lpr spontaneous model. Autoantibody production was measured by ELISA and immune activation by flow cytometry. Results were compared by two-tailed statistics: unpaired or paired t tests, or Mann-Whitney U tests depending on whether the data was normally distributed.Results: D-mannose inhibited the maturation of bone marrow dendritic cells and their induction of antigen-specific T cell proliferation and activation in vitro. In vivo, D-mannose increased the frequency of Foxp3+ regulatory T cells in unmanipulated control mice. In the cGVHD model of induced lupus, D-mannose treatment decreased autoantibody production, with a concomitant reduction of the frequency of effector memory and follicular helper T cells as well as germinal center B cells and plasma cells. These results were partially validated in the B6.lpr model of spontaneous lupus. Conclusion: Overall, our results suggest that D-mannose ameliorates autoimmune activation in models of lupus, at least partially due to its expansion of Treg cells, the induction of immature conventional dendritic cells and the downregulation of effector T cells activation. D-Mannose showed however a weaker immunomodulatory effect in lupus than in other autoimmune diseases.

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Significance of M2 macrophages in glomerulonephritis with crescents

Cited by 44 publications

References 21 publications

Association of Urine sCD163 With Proliferative Lupus Nephritis, Fibrinoid Necrosis, Cellular Crescents and Intrarenal M2 Macrophages

Association of Urine sCD163 With Proliferative Lupus Nephritis, Fibrinoid Necrosis, Cellular Crescents and Intrarenal M2 Macrophages

Significance of M2 macrophage in tubulointerstitial disease secondary to primary Sjogren's disease

D-mannose ameliorates autoimmune phenotypes in mouse models of lupus

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