Role of basophils in the pathogenesis of minimal change nephrotic syndrome: A literature review

A number of studies have verified that minimal change nephrotic syndrome (MCNS) may result from the dysfunction of T cells and B cells, although the precise mechanisms are yet to be elucidated. It is widely recognized that MCNS is a T helper (Th)2-dominant glomerular disease caused by an imbalanced Th1/Th2 immune response. Increased levels of the Th2 cytokines, interleukin (IL)-4 and IL-13, have been demonstrated to be closely associated with disease activity. In addition, basophils can affect the Th1/Th2 balance by enhancing the Th2 response and impairing the Th1 response, which are then involved in the development of numerous diseases. However, whether basophils are vital in the pathogenesis of MCNS remains unknown. Frequent positivity of the human basophil degranulation test in patients with MCNS has been observed. Thus, basophils should be analyzed in order to determine their role in the pathogenesis of MCNS.

[1]  J. Craig,et al.  Corticosteroid therapy for nephrotic syndrome in children. , 2007, The Cochrane database of systematic reviews.

[2]  M. Vogel,et al.  Improved FcγRIIb Targeting Functionally Translates into Enhanced Inhibition of Basophil Activation , 2014, International Archives of Allergy and Immunology.

[3]  T. Huizinga,et al.  Activation of human basophils by combined toll‐like receptor‐ and FcεRI‐triggering can promote Th2 skewing of naive T helper cells , 2014, European journal of immunology.

[4]  A. Pickles,et al.  Redefining phenotypes of wheezing disorders during childhood to elucidate genetic predisposition , 2012 .

[5]  D. Yang,et al.  Elevated Levels of Immunoglobulin E May Indicate Steroid Resistance or Relapse in Adult Primary Nephrotic Syndrome, Especially in Minimal Change Nephrotic Syndrome , 2011, The Journal of international medical research.

[6]  G. Illei,et al.  BASOPHILS AND THE T HELPER 2 ENVIRONMENT CAN PROMOTE THE DEVELOPMENT OF LUPUS NEPHRITIS , 2010, Nature Medicine.

[7]  J. Bach,et al.  The ‘hygiene hypothesis’ for autoimmune and allergic diseases: an update , 2010, Clinical and experimental immunology.

[8]  Liu Zhi-hong Triptolide protects podocytes from IL-13 induced injury in vitro , 2010 .

[9]  M. Mack,et al.  Basophils and mast cells in renal injury. , 2009, Kidney international.

[10]  Richard J. Johnson,et al.  Idiopathic nephrotic syndrome and atopy: is there a common link? , 2009, American journal of kidney diseases : the official journal of the National Kidney Foundation.

[11]  M. Nakahira,et al.  Basophils contribute to TH2-IgE responses in vivo via IL-4 production and presentation of peptide–MHC class II complexes to CD4+ T cells , 2009, Nature Immunology.

[12]  D. MacGlashan Jr.,et al.  Self-Termination/Anergic Mechanisms in Human Basophils and Mast Cells , 2009, International Archives of Allergy and Immunology.

[13]  J. O’Shea,et al.  Lyn kinase controls basophil GATA-3 transcription factor expression and induction of Th2 cell differentiation. , 2009, Immunity.

[14]  Zheng Chun-xia Interleukin-13 indcued podocyte injury via a signal transducer and activator of transcription-6-dependent way , 2009 .

[15]  D. Metcalfe,et al.  Amplification mechanisms for the enhancement of antigen-mediated mast cell activation , 2009, Immunologic research.

[16]  H. Karasuyama,et al.  Newly discovered roles for basophils: a neglected minority gains new respect , 2009, Nature Reviews Immunology.

[17]  D. MacGlashan IgE receptor and signal transduction in mast cells and basophils. , 2008, Current opinion in immunology.

[18]  Ruslan Medzhitov,et al.  A mechanism for the initiation of allergen-induced T helper type 2 responses , 2008, Nature Immunology.

[19]  J. Craig,et al.  Corticosteroid therapy for nephrotic syndrome in children. , 2015, The Cochrane database of systematic reviews.

[20]  S. Sicherer,et al.  Immunotherapy With a Ragweed-Toll-Like Receptor 9 Agonist Vaccine for Allergic Rhinitis , 2007, Pediatrics.

[21]  P. Tan,et al.  Overexpression of interleukin-13 induces minimal-change-like nephropathy in rats. , 2007, Journal of the American Society of Nephrology : JASN.

[22]  Cindy Zhou,et al.  Coincident Activation of Th2 T Cells with Onset of the Disease and Differential Expression of GRO-Gamma in Peripheral Blood Leukocytes in Minimal Change Disease , 2007, American Journal of Nephrology.

[23]  D. Zillikens,et al.  The 21st century renaissance of the basophil? Current insights into its role in allergic responses and innate immunity , 2006, Experimental dermatology.

[24]  K. Ohta,et al.  Expression and Function of Toll-Like Receptors in Human Basophils , 2006, International Archives of Allergy and Immunology.

[25]  Richard J. Johnson,et al.  Hygiene hypothesis and prevalence of glomerulonephritis. , 2005, Kidney international. Supplement.

[26]  J. Schroeder,et al.  Toll-like receptor 2 ligands activate human basophils for both IgE-dependent and IgE-independent secretion. , 2005, The Journal of allergy and clinical immunology.

[27]  S. Akira,et al.  Toll-like receptors in innate immunity. , 2004, International immunology.

[28]  A. Yoshioka,et al.  Up-regulation of interleukin-2 mRNA in children with idiopathic nephrotic syndrome , 2004, Pediatric Nephrology.

[29]  M. Tokumoto,et al.  Up-regulated interleukin-4 production by peripheral T-helper cells in idiopathic membranous nephropathy. , 2004, Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association.

[30]  H. Schulte-Wissermann,et al.  IgE in patients with glomerulonephritis and minimal-change nephrotic syndrome , 1979, European Journal of Pediatrics.

[31]  M. Cho,et al.  Interleukin-8 and Tumor Necrosis Factor-Alpha Are Increased in Minimal Change Disease but Do Not Alter Albumin Permeability , 2003, American Journal of Nephrology.

[32]  M. Endo,et al.  Implication of Elevated Serum IgE Levels in Minimal Change Nephrotic Syndrome , 2002, Nephron.

[33]  G. Tirino,et al.  T-lymphocyte populations and cytokines in childhood nephrotic syndrome. , 2002, American journal of kidney diseases : the official journal of the National Kidney Foundation.

[34]  S. Dower,et al.  Toll-Like Receptor (TLR)2 and TLR4 in Human Peripheral Blood Granulocytes: A Critical Role for Monocytes in Leukocyte Lipopolysaccharide Responses1 , 2002, The Journal of Immunology.

[35]  W. Gong,et al.  Minimal change nephrotic syndrome--a complex genetic disorder. , 2000, Annals of the Academy of Medicine, Singapore.

[36]  P. Mathieson,et al.  Interleukin-4 and interleukin-4 receptor polymorphisms in minimal change nephropathy. , 1999, Clinical science.

[37]  S. Jordan,et al.  Th1 and Th2 cytokine mRNA profiles in childhood nephrotic syndrome: evidence for increased IL-13 mRNA expression in relapse. , 1999, Journal of the American Society of Nephrology : JASN.

[38]  K. Pyun,et al.  Up-regulation of interleukin-4 and CD23/FcepsilonRII in minimal change nephrotic syndrome. , 1999, Pediatric nephrology.

[39]  M. Luqman,et al.  IL-4 production by allergen-stimulated primary cultures: identification of basophils as the major IL-4-producing cell type. , 1996, International immunology.

[40]  W. F. Chen,et al.  Increased production of interleukin 4 in children with simple idiopathic nephrotic syndrome. , 1994, Chinese medical journal.

[41]  A. Koyama,et al.  A glomerular permeability factor produced by human T cell hybridomas. , 1991, Kidney international.

[42]  K. Shu,et al.  Serum IgE in primary glomerular diseases and its clinical significance. , 1988, Nephron.

[43]  K. Chan,et al.  Immunoglobulins (IgG, IgA, IgM, IgE) and complement components (C3, C4) in nephrotic syndrome due to minimal change and other forms of glomerulonephritis, a clue for steroid therapy? , 1987, Nephron.

[44]  H. Kida,et al.  Immunodynamics of minimal change nephrotic syndrome in adults T and B lymphocyte subsets and serum immunoglobulin levels. , 1985, Clinical and experimental immunology.

[45]  J. Benveniste,et al.  [Frequent positivity of the human basophil degranulation test in idiopathic nephrotic syndromes (minimal glomerular changes and segmental and focal glomerulosclerosis)]. , 1984, Nephrologie.

[46]  G. Lagrue,et al.  Allergy and lipoid nephrosis. , 1983, Advances in nephrology from the Necker Hospital.

[47]  G. Lagrue,et al.  [Nephrotic syndrome and hypersensitivity to pollens (author's transl)]. , 1982, La Nouvelle presse medicale.

[48]  N. Mallick,et al.  Circulating immune complexes in idiopathic glomerular disease. , 1982, Kidney international.

[49]  J. Benveniste,et al.  BASOPHIL SENSITISATION IN IDIOPATHIC NEPHROTIC SYNDROME , 1982, The Lancet.

[50]  Roger Williams,et al.  PARACETAMOL HEPATOXICITY , 1976, The Lancet.

[51]  S. Johansson,et al.  Description and immunological findings , 1975 .

[52]  S. Johansson,et al.  Seasonal nephrotic syndrome. Description and immunological findings. , 1975, Clinical allergy.

[53]  R. Shalhoub Pathogenesis of lipoid nephrosis: a disorder of T-cell function. , 1974, Lancet.

[54]  Carpenter Wt A new setting for informed consent. , 1974 .

[55]  J. Cameron,et al.  IgE and the nephrotic syndrome. , 1971, Lancet.

[56]  J. Soothill,et al.  Nephrotic syndrome with pollen hypersensitivity. , 1959, Lancet.

[57]  Rytand Da Onset of the nephrotic syndrome during a reaction to bee sting. , 1955 .

[58]  D. A. Rytand Onset of the nephrotic syndrome during a reaction to bee sting. , 1955, Stanford medical bulletin.