Lymphocytes are dispensable for glomerulonephritis but required for renal interstitial fibrosis in matrix defect-induced Alport renal disease

Laboratory Investigation

Volumn 88, Issue 3, 2008, Pages 284-292

  LeBleu, Valerie S ^a   Sugimoto, Hikaru ^a   Miller, Caroline A ^b   Gattone II, Vincent H ^b   Kalluri, Raghu ^a,c  

^a HARVARD MEDICAL SCHOOL   (United States)

^b INDIANA UNIVERSITY SCHOOL OF MEDICINE   (United States)

^c HARVARD MIT DIVISION OF HEALTH SCIENCES AND TECHNOLOGY   (United States)

Author keywords

3(IV) collagen KO; Alport; Crescentic glomerulonephritis; Rag 1 KO; Renal fibrosis

Indexed keywords

COLLAGEN TYPE 4; RAG1 PROTEIN;

ALPORT SYNDROME; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; B LYMPHOCYTE; CONTROLLED STUDY; DISEASE COURSE; GENE DELETION; GLOMERULONEPHRITIS; GLOMERULUS BASEMENT MEMBRANE; IMMUNOCYTOCHEMISTRY; KIDNEY FIBROSIS; KIDNEY FUNCTION; MOUSE; NONHUMAN; PATHOGENESIS; PRIORITY JOURNAL; T LYMPHOCYTE; TH1 CELL;

ALBUMINURIA; ANIMALS; B-LYMPHOCYTES; COLLAGEN TYPE IV; CREATINE; CROSSES, GENETIC; ENZYME-LINKED IMMUNOSORBENT ASSAY; EXTRACELLULAR MATRIX; FIBROSIS; GENE DELETION; GLOMERULAR BASEMENT MEMBRANE; GLOMERULONEPHRITIS; HOMEODOMAIN PROTEINS; IMMUNOHISTOCHEMISTRY; LYMPHOCYTES; MICE; MICE, INBRED C57BL; MICE, KNOCKOUT; NEPHRITIS, HEREDITARY; PROTEINURIA; STATISTICS AS TOPIC; T-LYMPHOCYTES; TIME FACTORS;

EID: 39749178268     PISSN: 00236837     EISSN: 15300307     Source Type: Journal    
DOI: 10.1038/labinvest.3700715     Document Type: Article

References (38)

1. Atkins RC, Nikolic-Paterson DJ, Song Q, et al. Modulators of crescentic glomerulonephritis. J Am Soc Nephrol 1996;7:2271-2278.
2. Mathieson PW. The ins and outs of glomerular crescent formation. Clin Exp Immunol 1997;110:155-157.
3. Morrin PA, Hinglais N, Nabarra B, et al. Rapidly progressive glomerulonephritis. A clinical and pathologic study. Am J Med 1978;65:446-460.
4. Whitworth JA, Morel-Maroger L, Mignon F, et al. The significance of extracapillary proliferation. Clinicopathological review of 60 patients. Nephron 1976;16:1-19.
5. Connolly K, Roubinian JR, Wofsy D. Development of murine lupus in CD4-depleted NZB/NZW mice. Sustained inhibition of residual CD4+ T cells is required to suppress autoimmunity. J Immunol 1992;149:3083-3088.
6. Huang XR, Holdsworth SR, Tipping PG. Evidence for delayed-type hypersensitivity mechanisms in glomerular crescent formation. Kidney Int 1994;46:69-78.
7. Huang XR, Tipping PG, Apostolopoulos J, et al. Mechanisms of T cell-induced glomerular injury in anti-glomerular basement membrane (GBM) glomerulonephritis in rats. Clin Exp Immunol 1997;109:134-142.
8. Jabs DA, Burek CL, Hu Q, et al. Anti-CD4 monoclonal antibody therapy suppresses autoimmune disease in MRL/Mp-lpr/lpr mice. Cell Immunol 1992;141:496-507.
9. Kalluri R, Danoff TM, Okada H, et al. Susceptibility to anti-glomerular basement membrane disease and Good pasture syndrome is linked to MHC class II genes and the emergence of T cell-mediated immunity in mice. J Clin Invest 1997;100:2263-2275.
10. Kitching AR, Holdsworth SR, Tipping PG. Crescentic glomerulonephritis-a manifestation of a nephritogenic Th1 response? Histol Histopathol 2000;15:993-1003.
11. Li S, Holdsworth SR, Tipping PG. Antibody independent crescentic glomerulonephritis in mu chain deficient mice. Kidney Int 1997;51:672-678.
12. Tipping PG, Holdsworth SR. T cells in crescentic glomerulonephritis. J Am Soc Nephrol 2006;17:1253-1263.
13. Tipping PG, Huang XR, Qi M, et al. Crescentic glomerulonephritis in CD4- and CD8-deficient mice. Requirement for CD4 but not CD8 cells. Am J Pathol 1998;152:1541-1548.
14. Ophascharoensuk V, Pippin JW, Gordon KL, et al. Role of intrinsic renal cells vs infiltrating cells in glomerular crescent formation. Kidney Int 1998;54:416-425.
15. Bariety J, Bruneval P, Hill G, et al. Post transplantation relapse of FSGS is characterized by glomerular epithelial cell transdifferentiation. J Am Soc Nephrol 2001;12:261-274.
16. Bariety J, Bruneval P, Meyrier A, et al. Podocyte involvement in human immune crescentic glomerulonephritis. Kidney Int 2005;68:1109-1119.
17. Bariety J, Nochy D, Mandet C, et al. Podocytes undergo phenotypic changes and express macrophagic-associated markers in idiopathic collapsing glomerulopathy. Kidney Int 1998;53:918-925.
18. Kihara I, Yaoita E, Kawasaki K, et al. Origin of hyperplastic epithelial cells in idiopathic collapsing glomerulopathy. Histopathology 1999;34:537-547.
19. Ng YY, Fan JM, Mu W, et al. Glomerular epithelial-myofibroblast transdifferentiation in the evolution of glomerular crescent formation. Nephrol Dial Transplant 1999;14:2860-2872.
20. Orikasa M, Iwanaga T, Kawachi H, et al. Monoclonal antibody against rat podocyte-derived macrophagic cells reacts with crescent-forming cells in an experimental model. Nephrology (Carlton) 2003;8:217-223.
21. Orikasa M, Iwanaga T, Takahashi-Iwanaga H, et al. Macrophagic cells outgrowth from normal rat glomerular culture: possible metaplastic change from podocytes. Lab Invest 1996;75:719-733.
22. Smeets B, Te Loeke NA, Dijkman HB, et al. The parietal epithelial cell: a key player in the pathogenesis of focal segmental glomerulosclerosis in Thy-1.1 transgenic mice. J Am Soc Nephrol 2004;15:928-939.
23. Yaoita E, Kurihara H, Sakai T, et al. Phenotypic modulation of parietal epithelial cells of Bowman's capsule in culture. Cell Tissue Res 2001;304:339-349.
24. Kalluri R, Cosgrove D. Assembly of type IV collagen. Insights from alpha3(IV) collagen-deficient mice. J Biol Chem 2002;75:12719-12724.
25. Cosgrove D, Kalluri R, Miner JH, et al. Choosing a mouse model to study the molecular pathobiology of Alport glomerulonephritis. Kidney Int 2007;71:615-618.
26. Cosgrove D, Meehan DT, Grunkemeyer JA, et al. Collagen COL4A3 knockout: a mouse model for autosomal Alport syndrome. Genes Dev 1996;10:2981-2992.
27. Miner JH, Sanes JR. Molecular and functional defects in kidneys of mice lacking collagen alpha 3(IV): implications for Alport syndrome. J Cell Biol 1996;135:1403-1413.
28. Prodromidi EI, Poulsom R, Jeffery R, et al. Bone Marrow Derived-Cells Contribute to Podocyte Regeneration and Amelioration of Renal Disease in a Mouse Model of Alport Syndrome. Stem Cells 2006;24:2448-2455.
29. Sugimoto H, Mundel TM, Sund M, et al. Bone-marrow-derived stem cells repair basement membrane collagen defects and reverse genetic kidney disease. Proc Natl Acad Sci USA 2006;103:7321-7326.
30. Mombaerts P, Iacomini J, Johnson RS, et al. RAG-1-deficient mice have no mature B and T lymphocytes. Cell 1992;68:869-877.
31. Moeller MJ, Soofi A, Hartmann I, et al. Podocytes populate cellular crescents in a murine model of inflammatory glomerulonephritis. J Am Soc Nephrol 2004;15:61-67.
32. Ninichuk V, Gross O, Reichel C, et al. Delayed chemokine receptor 1 blockade prolongs survival in collagen 4A3-deficient mice with Alport disease. J Am Soc Nephrol 2005;16:977-985.
33. Donadelli R, Abbate M, Zanchi C, et al. Protein traffic activates NF-kB gene signaling and promotes MCP-1-dependent interstitial inflammation. Am J Kidney Dis 2000;36:1226-1241.
34. Harris RC, Neilson EG. Toward a unified theory of renal progression. Annu Rev Med 2006;57:365-380.
35. Shimizu H, Maruyama S, Yuzawa Y, et al. Anti-monocyte chemoattractant protein-1 gene therapy attenuates renal injury induced by protein-overload proteinuria. J Am Soc Nephrol 2003;14:1496-1505.
36. Kuroiwa T, Schlimgen R, Illei GG, et al. Distinct T cell/renal tubular epithelial cell interactions define differential chemokine production: implications for tubulointerstitial injury in chronic glomerulonephritides. J Immunol 2000;164:3323-3329.
37. Neilson EG. The nephritogenic T lymphocyte response in interstitial nephritis. Semin Nephrol 1993;13:496-502.
38. Strutz F, Neilson EG. The role of lymphocytes in the progression of interstitial disease. Kidney Int Suppl 1994;45:S106-S110.