Skip to main content
SpringerLink
Log in

Renal Macrophages and Dendritic Cells in SLE Nephritis

  • Systemic Lupus Erythematosus (G Tsokos, Section Editor)
  • Published:
Current Rheumatology Reports Aims and scope Submit manuscript

Abstract

Purpose of Review

The purpose of the study was to review the characteristics of renal macrophages and dendritic cells during homeostasis and disease, with a particular focus on lupus nephritis.

Recent Findings

Resident renal macrophages derive from embryonic sources and are long-lived and self-renewing; they are also replaced from the bone marrow with age. The unique characteristics of macrophages in each tissue are imposed by the microenvironment and reinforced by epigenetic modifications. In acute renal injury, inflammatory macrophages are rapidly recruited and then replaced by those with a wound healing/resolution phenotype. In lupus nephritis, dendritic cells infiltrate the kidneys and function to present antigen and organize tertiary lymphoid structures that amplify inflammation. In addition, both infiltrating and resident macrophages contribute to ongoing injury. These cells have a mixed inflammatory and alternatively activated phenotype that may reflect failed resolution, potentially leading to tissue fibrosis and irreversible damage.

Summary

A further understanding of the renal inflammatory cells that mediate tissue injury and fibrosis should lead to new therapies to help preserve renal function in patients with lupus nephritis.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Log in via an institution

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Institutional subscriptions

Fig. 1

Similar content being viewed by others

References

Papers of particular interest, published recently, have been highlighted as: • Of importance •• Of major importance

  1. Varol C, Mildner A, Jung S. Macrophages: development and tissue specialization. Annu Rev Immunol. 2015;33:643–75.

    Article  CAS  PubMed  Google Scholar 

  2. •• Murray PJ. Macrophage polarization. Annu Rev Physiol. 2017;79:541–66. This recent review highlights current knowledge of macrophage polarization, heterogeneity, and plasticity, and how macrophage polarization regulates the physiology of normal and damaged tissues.

    Article  CAS  PubMed  Google Scholar 

  3. Ginhoux F, Jung S. Monocytes and macrophages: developmental pathways and tissue homeostasis. Nat Rev Immunol. 2014;14(6):392–404.

    Article  CAS  PubMed  Google Scholar 

  4. •• Cros J, Cagnard N, Woollard K, Patey N, Zhang SY, Senechal B, et al. Human CD14dim monocytes patrol and sense nucleic acids and viruses via TLR7 and TLR8 receptors. Immunity. 2010;33(3):375–86. This study describes the patrolling behavior of CD14dim monocytes, and how they produce inflammatory cytokines through sensing of nucleic acids by TLR7 and TLR8. This represents a useful cellular target in select inflammatory and autoimmune diseases.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  5. •• Villani AC, Satija R, Reynolds G, Sarkizova S, Shekhar K, Fletcher J, et al. Single-cell RNA-seq reveals new types of human blood dendritic cells, monocytes, and progenitors. Science. 2017;356(6335). Using an unbiased single-cell RNA-sequencing strategy, this study profiles blood from healthy donors and discovers novel DC and monocyte subsets that revise the taxonomy.

  6. •• Yona S, Kim KW, Wolf Y, Mildner A, Varol D, Breker M, et al. Fate mapping reveals origins and dynamics of monocytes and tissue macrophages under homeostasis. Immunity. 2013;38(1):79–91. This study uses CX3CR1 reporter mice to map the murine mononuclear phagocyte compartment, demonstrating that most tissue macrophages are established before birth, independent of adult monocyte input.

    Article  CAS  PubMed  Google Scholar 

  7. Schulz C, Gomez Perdiguero E, Chorro L, Szabo-Rogers H, Cagnard N, Kierdorf K, et al. A lineage of myeloid cells independent of Myb and hematopoietic stem cells. Science. 2012;336(6077):86–90.

    Article  CAS  PubMed  Google Scholar 

  8. • Perdiguero EG, Geissmann F. The development and maintenance of resident macrophages. Nat Immunol. 2016;17(1):2–8. This review discusses current knowledge on macrophage development and highlights resident macrophages generated in the yolk sac to be distinct from passenger macrophages and myeloid cells that originate and renew from the bone marrow.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  9. Epelman S, Lavine KJ, Randolph GJ. Origin and functions of tissue macrophages. Immunity. 2014;41(1):21–35.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  10. •• Gosselin D, Link VM, Romanoski CE, Fonseca GJ, Eichenfield DZ, Spann NJ, et al. Environment drives selection and function of enhancers controlling tissue-specific macrophage identities. Cell. 2014;159(6):1327–40. This study shows how specific tissue environments drive distinct gene expression profiles by activation of a tissue-specific enhancer repertoire, thereby influencing macrophage phenotypes.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  11. Lavin Y, Mortha A, Rahman A, Merad M. Regulation of macrophage development and function in peripheral tissues. Nat Rev Immunol. 2015;15(12):731–44.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  12. •• Lavin Y, Winter D, Blecher-Gonen R, David E, Keren-Shaul H, Merad M, et al. Tissue-resident macrophage enhancer landscapes are shaped by the local microenvironment. Cell. 2014;159(6):1312–26. This is the first study to describe the epigenetic profile of tissue-resident macrophages, and how this is shaped by the local microenvironment.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  13. • Amit I, Winter DR, Jung S. The role of the local environment and epigenetics in shaping macrophage identity and their effect on tissue homeostasis. Nat Immunol. 2016;17(1):18–25. This review discusses the role the local microenvironment plays in shaping tissue-macrophage identity.

    Article  CAS  PubMed  Google Scholar 

  14. • Glass CK, Natoli G. Molecular control of activation and priming in macrophages. Nat Immunol. 2016;17(1):26–33. This review highlights recent findings on mechanisms underlying signal-dependent activation and priming of macrophages and discusses the impact of genetic variation on these processes.

    Article  CAS  PubMed  Google Scholar 

  15. •• Sahu R, Bethunaickan R, Singh S, Davidson A. Structure and function of renal macrophages and dendritic cells from lupus-prone mice. Arthritis Rheumatol. 2014;66(6):1596–607. Here, our group highlights the heterogeniety of renal macrophage/DC infiltrates in chronic lupus nephritis in a mouse model and provides an initial phenotypic and functional analysis that aids in defining the roles for each subset in nephritis.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  16. • Kawakami T, Lichtnekert J, Thompson LJ, Karna P, Bouabe H, Hohl TM, et al. Resident renal mononuclear phagocytes comprise five discrete populations with distinct phenotypes and functions. J Immunol. 2013;191(6):3358–72. This study defines five disctinct resident renal mononuclear phagopcyte subpopulations in the normal mouse kidney using an array of surface markers, which goes beyond the conventional classification.

    Article  CAS  PubMed  Google Scholar 

  17. • Bethunaickan R, Berthier CC, Ramanujam M, Sahu R, Zhang W, Sun Y, et al. A unique hybrid renal mononuclear phagocyte activation phenotype in murine systemic lupus erythematosus nephritis. J Immunol. 2011;186(8):4994–5003. In this study, our group describes a unique renal mononuclear phagocyte that contributes to tissue damage in lupus nephritis by mediating both local inflammation and excessive tissue remodeling.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  18. Ramanujam M, Bethunaickan R, Huang W, Tao H, Madaio MP, Davidson A. Selective blockade of BAFF for the prevention and treatment of systemic lupus erythematosus nephritis in NZM2410 mice. Arthritis Rheum. 2010;62(5):1457–68.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  19. Menezes S, Melandri D, Anselmi G, Perchet T, Loschko J, Dubrot J, et al. The heterogeneity of Ly6Chi monocytes controls their differentiation into iNOS+ macrophages or monocyte-derived dendritic cells. Immunity. 2016;45(6):1205–18.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  20. Goudot C, Coillard A, Villani AC, Gueguen P, Cros A, Sarkizova S, et al. Aryl hydrocarbon receptor controls monocyte differentiation into dendritic cells versus macrophages. Immunity. 2017;47(3):582–596.e6.

  21. •• Huen SC, Cantley LG. Macrophages in renal injury and repair. Annu Rev Physiol. 2017;79:449–69. This recent review highlights current understanding of how macrophages mechanistically contribute to injury and repair in acute kidney injury (AKI).

    Article  CAS  PubMed  Google Scholar 

  22. Mildner A, Schonheit J, Giladi A, David E, Lara-Astiaso D, Lorenzo-Vivas E, et al. Genomic characterization of murine monocytes reveals C/EBPbeta transcription factor dependence of Ly6C- cells. Immunity. 2017;46(5):849–862.e7.

  23. • Auffray C, Fogg D, Garfa M, Elain G, Join-Lambert O, Kayal S, et al. Monitoring of blood vessels and tissues by a population of monocytes with patrolling behavior. Science. 2007;317(5838):666–70. This seminal study establishes our knowledge of the patrolling behavior of Ly6C lo monocytes and describes the functional differences between the monocyte subsets.

    Article  CAS  PubMed  Google Scholar 

  24. •• Carlin LM, Stamatiades EG, Auffray C, Hanna RN, Glover L, Vizcay-Barrena G, et al. Nr4a1-dependent Ly6C(low) monocytes monitor endothelial cells and orchestrate their disposal. Cell. 2013;153(2):362–75. This study describes recruitment of patrolling Ly6C low monocytes to the endothelium and into the kidneys and shows that this is dependent on TLR7 expression in renal cells.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  25. Quintar A, McArdle S, Wolf D, Marki A, Ehinger E, Vassallo M, et al. Endothelial protective monocyte patrolling in large arteries intensified by western diet and atherosclerosis. Circ Res. 2017;120(11):1789–99.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  26. Williams JW, Randolph GJ, Zinselmeyer BHA. Polecat’s view of patrolling monocytes. Circ Res. 2017;120(11):1699–701.

    Article  CAS  PubMed  Google Scholar 

  27. Celhar T, Pereira-Lopes S, Thornhill SI, Lee HY, Dhillon MK, Poidinger M, et al. TLR7 and TLR9 ligands regulate antigen presentation by macrophages. Int Immunol. 2016;28(5):223–32.

    Article  CAS  PubMed  Google Scholar 

  28. • Yoshimoto S, Nakatani K, Iwano M, Asai O, Samejima K, Sakan H, et al. Elevated levels of fractalkine expression and accumulation of CD16+ monocytes in glomeruli of active lupus nephritis. Am J Kidney Dis. 2007;50(1):47–58. This study describes the association of SLE disease severity with glomerular fractalkine expression and CD16 + /CX3CR1 + monocyte accumulation in humans.

    Article  CAS  PubMed  Google Scholar 

  29. •• Stamatiades EG, Tremblay ME, Bohm M, Crozet L, Bisht K, Kao D, et al. Immune monitoring of trans-endothelial transport by kidney-resident macrophages. Cell. 2016;166(4):991–1003. This study identifies the unique immune monitoring property of kidney macrophages and a mechanism by which they initiate inflammatory responses to small immune complexes in the kidney.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  30. •• Kassianos AJ, Wang X, Sampangi S, Muczynski K, Healy H, Wilkinson R. Increased tubulointerstitial recruitment of human CD141(hi) CLEC9A(+) and CD1c(+) myeloid dendritic cell subsets in renal fibrosis and chronic kidney disease. Am J Physiol Renal Physiol. 2013;305(10):F1391–401. This study identifies activated mDC subsets to be positioned strategically, after being recruited to the tubulointerstitium, to play a role in the development of fibrosis and thereby contribute to renal fibrosis and chronic kidney disease.

    Article  CAS  PubMed  Google Scholar 

  31. •• Xue J, Schmidt SV, Sander J, Draffehn A, Krebs W, Quester I, et al. Transcriptome-based network analysis reveals a spectrum model of human macrophage activation. Immunity. 2014;40(2):274–88. This study proposes a refined activation-independent core signature for human and murine macrophages, and reveals a spectrum of macrophage activation states extending beyond the current M1 vs. M2 polarization model, identifying central transcriptional regulators associated with all macrophage activation complemented by regulators related to stimulus-specific programs.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  32. Van den Bossche J, Baardman J, Otto NA, van der Velden S, Neele AE, van den Berg SM, et al. Mitochondrial dysfunction prevents repolarization of inflammatory macrophages. Cell Rep. 2016;17(3):684–96.

    Article  PubMed  Google Scholar 

  33. Galvan-Pena S, O'Neill LA. Metabolic reprograming in macrophage polarization. Front Immunol. 2014;5:420.

    PubMed  PubMed Central  Google Scholar 

  34. •• Jha AK, Huang SC, Sergushichev A, Lampropoulou V, Ivanova Y, Loginicheva E, et al. Network integration of parallel metabolic and transcriptional data reveals metabolic modules that regulate macrophage polarization. Immunity. 2015;42(3):419–30. This study provides a comphrehensive view of the integrated transcriptional and central metabolic changes during murine macrophage polarization and uncovers targets for control and intervention of this polarization process.

    Article  CAS  PubMed  Google Scholar 

  35. Phan AT, Goldrath AW, Glass CK. Metabolic and epigenetic coordination of T cell and macrophage immunity. Immunity. 2017;46(5):714–29.

    Article  CAS  PubMed  Google Scholar 

  36. Liu PS, Wang H, Li X, Chao T, Teav T, Christen S, et al. Alpha-ketoglutarate orchestrates macrophage activation through metabolic and epigenetic reprogramming. Nat Immunol. 2017;18(9):985–94.

    CAS  PubMed  Google Scholar 

  37. •• O'Neill LA, Kishton RJ, Rathmell J. A guide to immunometabolism for immunologists. Nat Rev Immunol. 2016;16(9):553–65. This review highlights the complex interplay between metabolic reprogramming and immunity and provides a clear overview of our knowledge of immunometabolism to date.

    Article  PubMed  PubMed Central  Google Scholar 

  38. • Mills EL, Kelly B, Logan A, Costa AS, Varma M, Bryant CE, et al. Succinate dehydrogenase supports metabolic repurposing of mitochondria to drive inflammatory macrophages. Cell. 2016;167(2):457–70 e13. This study describes how the metabolic alterations that occur upon activation of macrophages repurpose mitochondria from ATP synthesis to ROS production in order to promote a pro-inflammatory state.

    Article  CAS  PubMed  Google Scholar 

  39. Helm O, Held-Feindt J, Schafer H, Sebens S. M1 and M2: there is no “good” and “bad”—how macrophages promote malignancy-associated features in tumorigenesis. Oncoimmunology. 2014;3(7):e946818.

    Article  PubMed  PubMed Central  Google Scholar 

  40. •• Martinez J, Cunha LD, Park S, Yang M, Lu Q, Orchard R, et al. Noncanonical autophagy inhibits the autoinflammatory, lupus-like response to dying cells. Nature. 2016;533(7601):115–9. This study identifies a noncanonical authophagic process, LC-3-associated phagocytosis (LAP), in the control of autoinflammatory lupus-like disease and suggests a link between failed clearance of dying cells, LAP, and SLE pathogenesis.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  41. Martinez J, Malireddi RK, Lu Q, Cunha LD, Pelletier S, Gingras S, et al. Molecular characterization of LC3-associated phagocytosis reveals distinct roles for Rubicon, NOX2 and autophagy proteins. Nat Cell Biol. 2015;17(7):893–906.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  42. Tabas I, Bornfeldt KE. Macrophage phenotype and function in different stages of atherosclerosis. Circ Res. 2016;118(4):653–67.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  43. •• Gieseck RL, 3rd, Wilson MS, Wynn TA. Type 2 immunity in tissue repair and fibrosis. Nat Rev Immunol. 2017. This review highlights mechanisms by which type 2 immunity contributes to tissue regeneration and fibrosis following injury, and the involvement of macrophages in the resolution of inflammation and repair.

  44. Hesketh M, Sahin KB, West ZE, Murray RZ. Macrophage phenotypes regulate scar formation and chronic wound healing. Int J Mol Sci. 2017;18(7)

  45. •• Lee S, Huen S, Nishio H, Nishio S, Lee HK, Choi BS, et al. Distinct macrophage phenotypes contribute to kidney injury and repair. J Am Soc Nephrol. 2011;22(2):317–26. This study shows that macrophages can undergo a phenotypic switch from pro-inflammatory to a trophic phenotype that supports the transition from kidney tubular injury to tubule repair/recovery.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  46. Brandt S, Mertens PR. The kidney regulates regeneration, but don’t upset the balance. Int Urol Nephrol. 2016;48(8):1371–6.

    Article  CAS  PubMed  Google Scholar 

  47. Adhyatmika A, Putri KS, Beljaars L, Melgert BN. The elusive antifibrotic macrophage. Frontiers in medicine. 2015;2:81.

    Article  PubMed  PubMed Central  Google Scholar 

  48. Cao Q, Harris DC, Wang Y. Macrophages in kidney injury, inflammation, and fibrosis. Physiology (Bethesda). 2015;30(3):183–94.

    CAS  Google Scholar 

  49. Braga TT, Correa-Costa M, Guise YF, Castoldi A, de Oliveira CD, Hyane MI, et al. MyD88 signaling pathway is involved in renal fibrosis by favoring a TH2 immune response and activating alternative M2 macrophages. Mol Med. 2012;18:1231–9.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  50. • Eming SA, Wynn TA, Martin P. Inflammation and metabolism in tissue repair and regeneration. Science. 2017;356(6342):1026–30. This review highlights current knowledge as well as novel concepts of inflammation and cell metabolism in tissue repair, regeneration, and fibrosis, and discusses potential clinical therapeutic approaches to improve wound healing.

    Article  CAS  PubMed  Google Scholar 

  51. Headland SE, Norling LV. The resolution of inflammation: principles and challenges. Semin Immunol. 2015;27(3):149–60.

    Article  CAS  PubMed  Google Scholar 

  52. Lopez-Guisa JM, Cai X, Collins SJ, Yamaguchi I, Okamura DM, Bugge TH, et al. Mannose receptor 2 attenuates renal fibrosis. J Am Soc Nephrol. 2012;23(2):236–51.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  53. Maruotti N, Annese T, Cantatore FP, Ribatti D. Macrophages and angiogenesis in rheumatic diseases. Vascular cell. 2013;5(1):11.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  54. •• Hill GS, Delahousse M, Nochy D, Remy P, Mignon F, Mery JP, et al. Predictive power of the second renal biopsy in lupus nephritis: significance of macrophages. Kidney Int. 2001;59(1):304–17. This report describes the predictive power of a second (repeat) renal biopsy on risk of progression to renal failure and the association of macrophage with poorer prognosis.

    Article  CAS  PubMed  Google Scholar 

  55. Yang N, Isbel NM, Nikolic-Paterson DJ, Li Y, Ye R, Atkins RC, et al. Local macrophage proliferation in human glomerulonephritis. Kidney Int. 1998;54(1):143–51.

    Article  CAS  PubMed  Google Scholar 

  56. • Dias CB, Malafronte P, Lee J, Resende A, Jorge L, Pinheiro CC, et al. Role of renal expression of CD68 in the long-term prognosis of proliferative lupus nephritis. J Nephrol. 2017;30(1):87–94. This study identifies an association between renal CD68 (macrophage) expression and progression of chronic kidney disease in patients with proliferative lupus nephritis.

    Article  CAS  PubMed  Google Scholar 

  57. Lindenmeyer M, Noessner E, Nelson PJ, Segerer S. Dendritic cells in experimental renal inflammation—part I. Nephron Exp Nephrol. 2011;119(4):e83–90.

    Article  PubMed  Google Scholar 

  58. Noessner E, Lindenmeyer M, Nelson PJ, Segerer S. Dendritic cells in human renal inflammation—part II. Nephron Exp Nephrol. 2011;119(4):e91–8.

    Article  PubMed  Google Scholar 

  59. Woltman AM, de Fijter JW, Zuidwijk K, Vlug AG, Bajema IM, van der Kooij SW, et al. Quantification of dendritic cell subsets in human renal tissue under normal and pathological conditions. Kidney Int. 2007;71(10):1001–8.

    Article  CAS  PubMed  Google Scholar 

  60. • Berthier CC, Bethunaickan R, Gonzalez-Rivera T, Nair V, Ramanujam M, Zhang W, et al. Cross-species transcriptional network analysis defines shared inflammatory responses in murine and human lupus nephritis. J Immunol. 2012;189(2):988–1001. This study identifies key shared transcriptional pathways between mouse and human lupus nephrtitis.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  61. Misharin AV, Cuda CM, Saber R, Turner JD, Gierut AK, Haines GK, 3rd, et al. Nonclassical Ly6C(−) monocytes drive the development of inflammatory arthritis in mice. Cell Rep 2014;9(2):591–604.

  62. • Celhar T, Hopkins R, Thornhill SI, De Magalhaes R, Hwang SH, Lee HY, et al. RNA sensing by conventional dendritic cells is central to the development of lupus nephritis. Proc Natl Acad Sci U S A. 2015;112(45):E6195–E6204. This study highlights the importance of conventional DCs and their RNA-sensing capacities through TLR7 expression for kidney pathogenesis in murine lupus nephritis.

  63. Wolf Y, Shemer A, Polonsky M, Gross M, Mildner A, Yona S, et al. Autonomous TNF is critical for in vivo monocyte survival in steady state and inflammation. J Exp Med. 2017;214(4):905–17.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  64. Bethunaickan R, Sahu R, Liu Z, Tang YT, Huang W, Edegbe O, et al. Anti-TNF treatment of IFN induced lupus nephritis reduces the renal macrophage response but does not alter glomerular immune complex formation. Arthritis Rheum. 2012;

  65. Ondee T, Surawut S, Taratummarat S, Hirankarn N, Palaga T, Pisitkun P, et al. Fc gamma receptor IIB deficient mice: a lupus model with increased endotoxin tolerance-related sepsis susceptibility. Shock (Augusta, Ga). 2017;47(6):743–52.

    Article  CAS  Google Scholar 

  66. • Iwata Y, Bostrom EA, Menke J, Rabacal WA, Morel L, Wada T, et al. Aberrant macrophages mediate defective kidney repair that triggers nephritis in lupus-susceptible mice. J Immunol. 2012;188(9):4568–80. This study describes how transient injury can lead to defective repair, nonresolving inflammation, and early onset lupus nephritis due to defective healing by aberrant macrophages in lupus prone mice.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  67. Zhang W, Xu W, Xiong S. Blockade of Notch1 signaling alleviates murine lupus via blunting macrophage activation and M2b polarization. J Immunol. 2010;184(11):6465–78.

    Article  CAS  PubMed  Google Scholar 

  68. Li F, Yang Y, Zhu X, Huang L, Xu J. Macrophage polarization modulates development of systemic lupus erythematosus. Cellular physiology and biochemistry: international journal of experimental 2015;37(4):1279–1288.

  69. Sung SJ, Ge Y, Dai C, Wang H, SM F, Sharma R, et al. Dependence of glomerulonephritis induction on novel intraglomerular alternatively activated bone marrow-derived macrophages and mac-1 and PD-L1 in lupus-prone NZM2328 mice. J Immunol. 2017;198(7):2589–601.

    Article  CAS  PubMed  Google Scholar 

  70. Kadiombo AT, Maeshima A, Kayakabe K, Ikeuchi H, Sakairi T, Kaneko Y, et al. Involvement of infiltrating macrophage-derived activin A in the progression of renal damage in MRL-lpr mice. Am J Physiol Renal Physiol. 2017;312(2):F297–f304.

    Article  CAS  PubMed  Google Scholar 

  71. • Olmes G, Buttner-Herold M, Ferrazzi F, Distel L, Amann K, Daniel C. CD163+ M2c-like macrophages predominate in renal biopsies from patients with lupus nephritis. Arthritis Res Ther. 2016;18:90. This study describes M2-like macrophages to be the dominant subpopulation in human lupus nephritis, where particularly M2a subpopulations were associated with disease progression.

    Article  PubMed  PubMed Central  Google Scholar 

  72. Li J, YF Y, Liu CH, Wang CM. Significance of M2 macrophages in glomerulonephritis with crescents. Pathol Res Pract. 2017;213(9):1215–20.

    Article  CAS  PubMed  Google Scholar 

  73. Li J, Liu CH, DL X, Gao B. Significance of CD163-positive macrophages in proliferative glomerulonephritis. Am J Med Sci. 2015;350(5):387–92.

    Article  PubMed  Google Scholar 

  74. Schiffer L, Bethunaickan R, Ramanujam M, Huang W, Schiffer M, Tao H, et al. Activated renal macrophages are markers of disease onset and disease remission in lupus nephritis. J Immunol. 2008;180(3):1938–47.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

Download references

Author information

Authors and Affiliations

  1. Center for Autoimmunity and Musculoskeletal Diseases, Feinstein Institute for Medical Research, 350 Community Drive, Manhasset, New York, NY, 11030, USA

    Naomi I. Maria & Anne Davidson

Authors
  1. Naomi I. Maria
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Anne Davidson
    View author publications

    You can also search for this author in PubMed Google Scholar

Corresponding author

Correspondence to Anne Davidson.

Ethics declarations

Conflict of Interest

The authors declare that they have no conflict of interest.

Human and Animal Rights and Informed Consent

This article does not contain any studies with human or animal subjects performed by any of the authors.

Additional information

This article is part of the Topical Collection on Systemic Lupus Erythematosus

Rights and permissions

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Maria, N.I., Davidson, A. Renal Macrophages and Dendritic Cells in SLE Nephritis. Curr Rheumatol Rep 19, 81 (2017). https://doi.org/10.1007/s11926-017-0708-y

Download citation

  • Published:

  • DOI: https://doi.org/10.1007/s11926-017-0708-y

Keywords

Search

Navigation