N Yoshizawa

National Defense Medical College, Tokorozawa, Saitama, Japan

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Publications (86)261.14 Total impact

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    ABSTRACT: Two cases of rapidly progressive glomerulonephritis (RPGN) with skin vasculitis-associated anti-neutrophil cytoplasmic antibody (ANCA) are examined. Both cases showed purpura on the lower legs on admission and subsequently revealed renal or pulmonary vasculitis. One case responded positively to oral prednisolone alone, but the other case showed high ANCA titer and renal—pulmonary vasculitis. We discuss the diversity of clinical symptoms and the titer of antibody-associated vasculitis.
    Modern Rheumatology 01/2014; 8(1):79-87. · 1.72 Impact Factor
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    ABSTRACT: It is well known that glomerulonephritis can occur after streptococcal infection, which is classically referred to as acute poststreptococcal glomerulonephritis (APSGN). The pathogenic mechanism of APSGN has been described by so-called immune complex theory, which involves glomerular deposition of nephritogenic streptococcal antigen and subsequent formation of immune complexes in situ and/or the deposition of circulating antigen-antibody complexes. However, the exact entity of the causative antigen has remained a matter of debate. We isolated a nephritogenic antigen for APSGN from the cytoplasmic fractions of group A streptococcus (GAS) depending on the affinity for IgG of APSGN patients. The amino acid and the nucleotide sequences of the isolated protein revealed to be highly identical to those of reported plasmin(ogen) receptor of GAS. Thus, we termed this antigen nephritis-associated plasmin receptor (NAPlr). Immunofluorescence staining of the renal biopsy tissues with anti-NAPlr antibody revealed glomerular NAPlr deposition in essentially all patients with early-phase APSGN. Furthermore, glomerular plasmin activity was detected by in situ zymography in the distribution almost identical to NAPlr deposition in renal biopsy tissues of APSGN patients. These data suggest that NAPlr has a direct, nonimmunologic function as a plasmin receptor and may contribute to the pathogenesis of APSGN by maintaining plasmin activity.
    BioMed Research International 01/2012; 2012:417675. · 2.88 Impact Factor
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    ABSTRACT: The nephritis-associated plasmin receptor is a recently identified nephritogenic antigen associated with acute poststreptococcal glomerulonephritis and proposed to play a pathogenic role, but its precise glomerular localization in acute poststreptococcal glomerulonephritis has not been elucidated. We therefore analyzed renal biopsy sections from 10 acute poststreptococcal glomerulonephritis patients by using immunofluorescence staining with anti-nephritis-associated plasmin receptor antibody and various markers of glomerular components. Nephritis-associated plasmin receptor was detected in the glomeruli of all patients, and double staining for nephritis-associated plasmin receptor and collagen IV showed nephritis-associated plasmin receptor to be predominantly on the inner side of the glomerular tufts. Nephritis-associated plasmin receptor-positive areas within glomerular tufts were further characterized with markers for neutrophils, mesangial cells, endothelial cells, and macrophages. In 6 of the patients, nephritis-associated plasmin receptor staining was seen mainly in neutrophils and to a lesser degree in mesangial and endothelial cells. In the other 4 patients, nephritis-associated plasmin receptor staining was seen mainly in mesangial cells and to a lesser degree in neutrophils and endothelial cells. In all patients, macrophages showed little staining. Elevated plasmin activity in glomerular neutrophils was identified by combining in situ zymography staining for plasmin activity and immunofluorescence staining for neutrophils. The glomerular localizations of nephritis-associated plasmin receptor and another nephritogenic antigen, streptococcal pyrogenic exotoxin B, were compared by double immunofluorescence staining and found to be similar. These findings indicate the nephritogenic potential of nephritis-associated plasmin receptor and offer valuable information with respect to the pathogenic mechanism of acute poststreptococcal glomerulonephritis.
    Human pathology 09/2010; 41(9):1276-85. · 3.03 Impact Factor
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    ABSTRACT: We herein report the case of a 12-year-old boy with dense deposit disease (DDD) evoked by streptococcal infection. He had been diagnosed to have asymptomatic hematuria syndrome at the age of 6 during school screening. At 12 years of age, he was found to have macrohematuria and overt proteinuria with hypocomplementemia 2 months after streptococcal pharyngitis. Renal biopsy showed endocapillary proliferative glomerulonephritis with double contours of the glomerular basement membrane. Hypocomplementemia and proteinuria were sustained for over 8 weeks. He was suspected to have dense deposit disease due to intramembranous deposits in the first and the second biopsies. 1 month after treatment with methylprednisolone pulse therapy, proteinuria decreased to a normal level. Microscopic hematuria disappeared 2 years later, but mild hypocomplementemia persisted for more than 7 years. Nephritis-associated plasmin receptor (NAPlr), a nephritic antigen for acute poststreptococcal glomerulonephritis, was found to be positive in the glomeruli for more than 8 weeks. DDD is suggested to be caused by dysgeneration of the alternative pathway due to C3NeF and impaired Factor H activity. A persistent deposition of NAPlr might be one of the factors which lead to complement dysgeneration. A close relationship was suggested to exist between the streptococcal infection and dense deposit disease in this case.
    Clinical nephrology 07/2009; 71(6):703-7. · 1.29 Impact Factor
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    ABSTRACT: A pathogenic role of intraglomerular plasmin bound to nephritogenic antigen (nephritis-associated plasmin receptor, NAPlr) and resistant to physiologic inhibitors such as alpha(2)-antiplasmin (alpha(2)-AP) has recently been proposed in acute poststreptococcal glomerulonephritis (APSGN). To confirm this concept, we analysed the urinary profile of plasmin cascade in APSGN patients. Urine samples from 10 patients with APSGN, 12 patients with IgA nephropathy (IgAN), 10 patients with streptococcal infection without nephritis (SI) and 10 healthy control subjects were analysed. The alpha(2)-AP-resistant plasmin activity was assessed by a chromogenic assay after alpha(2)-AP was added to each urine sample. Urinary plasminogen activator (PA) and plasmin were further analysed by polyacrylamide gel zymography. Urinary NAPlr was assessed by western blot analysis in selected samples. Urinary alpha(2)-AP-resistant plasmin activity corrected for creatinine concentration (units/g x creatinine) was significantly higher in patients with APSGN (2.99 +/- 0.63) than in patients with IgAN (1.02 +/- 0.20, P < 0.01), SI (0.79 +/- 0.17, P < 0.01), or in healthy control subjects (0.73 +/- 0.18, P < 0.01). This tendency was confirmed by casein gel zymography. However urinary PA activity assessed by plasminogen-casein gel zymography did not differ between groups. NAPlr was detected in the urine of APSGN patients. We found elevated urinary plasmin activity resistant to alpha(2)-AP, which may be due to urinary excretion of NAPlr in patients with APSGN. This result supports the pathogenic role of the NAPlr-plasmin complex in the development of APSGN. Furthermore, alpha(2)-AP-resistant urinary plasmin activity may be useful as a diagnostic marker for APSGN.
    Nephrology Dialysis Transplantation 08/2008; 23(7):2254-9. · 3.37 Impact Factor
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    ABSTRACT: The profibrotic effect of plasminogen activator inhibitor-1 (PAI-1) in renal fibrosis is widely recognized, but its mechanism remains controversial especially in chronic progressive kidney disease. In the present study, pioglitazone (Pio) and candesartan (CD), which are reported to inhibit PAI-1, were administered to spontaneously hypercholesterolemic (SHC) rats, a model of chronic progressive kidney disease. Therapeutic effects and effects on the intrarenal plasmin cascade were examined. Eight-wk-old SHC rats were used as controls. Oral administration of vehicle alone, Pio, or CD was performed starting at 8 wk of age and was continued for 24 wk. The degree of renal fibrosis was evaluated by sirius red staining of kidney sections and by total collagen assay of renal homogenates. The renal PAI-1 protein level was assessed by Western blotting, and plasmin activity was analyzed by chromogenic assay and casein gel zymography. Urinary protein and blood urea nitrogen were significantly increased in the vehicle-treated group, but the increase was attenuated in the Pio- and CD-treated groups. This correlated well with the degree of fibrosis as assessed by sirius red staining and total collagen assay. The PAI-1 protein level was also increased significantly in the vehicle-treated group, and the increase was attenuated in the Pio- and CD-treated groups. Despite the presumed plasmin-inhibitory function of PAI-1, plasmin activity changed in parallel with PAI-1. These results suggest that Pio and CD inhibit PAI-1 and exert renoprotective effects against chronic progressive renal disease, but its action is independent of the regulatory function on plasmin activity.
    American journal of physiology. Renal physiology 11/2007; 293(4):F1292-8. · 3.61 Impact Factor
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    ABSTRACT: Glomerular hypercellularity due to resident glomerular cell proliferation and leucocyte infiltration has been described in acute post-streptococcal glomerulonephritis (APSGN). APSGN usually resolves without progression. However, the mechanism of resolution remains to be determined. Renal biopsy tissues from 15 patients with APSGN (obtained 1-31 days after disease onset) and five control patients with minor glomerular abnormality were evaluated with respect to glomerular resolution. Apoptotic cells were assessed by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labelling (TUNEL) as well as by immunostaining of single-stranded DNA (ssDNA). The number of glomerular cells was high in the early-phase of APSGN and decreased over time. No TUNEL+ glomerular cells were found in control subjects, whereas prominent glomerular TUNEL+ cells were observed in APSGN patients, particularly in the early phase of the disease. The number of glomerular TUNEL+ cells decreased exponentially but was still prominent in renal tissue biopsied at 31 days after disease onset. Double staining for ssDNA and glomerular cell markers showed that glomerular apoptotic cells were predominantly mesangium and endothelial cells, with some neutrophils and macrophages. These results suggest that apoptosis exists in the glomerulus in patients with APSGN from the early to the late stages of the disease and contributes to the resolution of glomerular hypercellularity.
    Nephrology Dialysis Transplantation 04/2007; 22(3):740-8. · 3.37 Impact Factor
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    ABSTRACT: Acute post-streptococcal glomerulonephritis (APSGN) is induced by glomerular deposition of nephritogenic streptococcal antigen-antibody complexes. Recently, a streptococcal antigen, nephritis-associated plasminogen receptor (NAPlr) was purified from ruptured streptococcal cell supernatants (RCS). However, the cellular and molecular mechanisms of NAPlr action on the glomerular vas culature are still unknown. Expression of cell adhesion molecules were measured by cellular ELISA (enzyme-linked immunosorbent assay), immunofluorescence microscopy and Western blot analysis. RCS and NAPlr significantly decreased the PECAM-1 expression in human glomerular endothelial cells (HGECs) as compared to that in the control cells. Plasminogen treatment reversed the RCS or NAPlr-induced decrease of PECAM-1 expression and increase of MCP-1 expression. Immunofluorescent microscopy and Western blot analysis also showed that PECAM-1 expression in HGECs was downregulated upon treatment with RCS or NAPlr and this effect was reversed by plasminogen treatment. Furthermore, we found that tumor necrosis factor-alpha production in culture medium of HGECs was increased at the lower level when the culture system was treated with RCS. RCS and NAPlr modulated PECAM-1 expression and MCP-1 production in HGECs, indicating the involvement of NAPlr in inflammatory cell accumulation in glomerular tufts and functional abnormality of glomerular microvasculature such as hyperpermeability.
    Nephron Experimental Nephrology 02/2007; 105(2):e53-64. · 2.01 Impact Factor
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    N Yoshizawa, K Yamakami, T Oda
    Kidney International 04/2006; 69(5):942-3; author reply 942. · 8.52 Impact Factor
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    ABSTRACT: We report the case of a 25-year-old man with abdominal pain, purpura on the legs and proteinuria occurring 2 weeks after acute tonsillitis, and admitted to our hospital with suspected Henoch-Schönlein purpura nephritis (HSPN). He had increased anti-streptolysin O (ASO) titer and hypocomplementemia. A renal biopsy specimen showed endocapillary proliferative changes, which are typical of acute poststreptococcal glomerulonephritis (APSGN). However, immunofluorescence study revealed predominant IgA and C3 deposits in mesangial lesions, indicating a diagnosis of HSPN. Because of massive proteinuria initially, the treatment with a combination of prednisolone, cyclophosphamide, dipyridamole and warfarin was started along with 3 plasma exchanges. Angiotensin-converting enzyme inhibitor was also given. Response to the treatment was favorable. A follow-up biopsy was performed 8 months after the first biopsy. The renal biopsy specimen showed a figure of typical HSPN. To further investigate the cause of glomerular changes in our patient, an immunofluorescent study of nephritogenic nephritis-associated plasmin receptor (NAPlr) of group A, beta-hemolytic streptococci was performed. NAPlr was significantly positive in the glomeruli in the first biopsy specimen, but not in the second. His clinical course and pathological findings suggest that NAPlr may be related to the pathogenesis in a part of patients with HSPN, especially in patients with high ASO titer and hypocomplementemia.
    Clinical nephrology 03/2006; 65(2):124-8. · 1.29 Impact Factor
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    ABSTRACT: We report the case of a 47-year-old man with the simultaneous occurrence of clinical and laboratory features consistent with acute poststreptococcal glomerulonephritis (APSGN), hemolytic uremic syndrome (HUS), and nephrotic syndrome. Acute nephritic syndrome occurred 3 weeks after having pharyngeal pain and diarrhea. He presented with edema and hypertension on admission. Laboratory evaluation showed hemolytic anemia with fragmentation, thrombocytopenia, elevated lactic dehydrogenase level, low haptoglobin level, low complement C3 level, and elevated antistreptolysin-O titer. Serum creatinine level was 1.22 mg/dL (108 micromol/L), and urinalysis showed marked proteinuria, with protein of 8.7 g/d, and hematuria. The renal biopsy specimen was characteristic of APSGN, but not HUS. Moderate expansion of the mesangial matrix, moderate proliferation of epithelial and endothelial cells, and marked infiltration of neutrophils was seen by means of light microscopy, and many subepithelial humps were seen by means of electron microscopy. Neither fibrin deposition nor evidence of thrombotic microangiopathy was found. Complement C3 deposition along the capillary wall and tubules was seen in an immunofluorescence study. The patient was administered plasma infusion at 320 mL/d and antihypertensive drugs. Serum complement C3 and haptoglobin levels returned to normal within 3 weeks. This is a rare case of the simultaneous occurrence of APSGN, HUS, and nephrotic syndrome.
    American Journal of Kidney Diseases 11/2005; 46(4):e59-63. · 5.29 Impact Factor
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    ABSTRACT: A nephritogenic antigen for acute poststreptococcal glomerulonephritis (APSGN) was isolated recently from group A streptococcus and termed nephritis-associated plasmin receptor (NAPlr). In vitro experimental data indicate that the pathogenic role of NAPlr occurs through its ability to bind to plasmin and maintain its proteolytic activity. However, the mechanism whereby this antigen induces glomerular damage in vivo has not been fully elucidated. Renal biopsy tissues from 17 patients with APSGN, 8 patients with rapidly progressive glomerulonephritis, and 10 normal kidneys were analyzed in this study. Plasmin-like activity was assessed on cryostat sections by in situ zymography with a plasmin-sensitive synthetic substrate. Serial sections were simultaneously assessed for NAPlr deposition by immunofluorescence staining. Glomerular plasmin-like activity was absent or weak in normal controls and in patients with rapidly progressive glomerulonephritis, although tubulointerstitial activity was occasionally detected. Prominent glomerular plasmin-like activity was found in patients who had APSGN and in whom glomerular NAPlr was positive, whereas it was absent or weak in patients who had APSGN and in whom glomerular NAPlr was negative. The distribution of glomerular plasmin-like activity was identical to that of NAPlr deposition but was generally different from that of fibrin(ogen) deposition as assessed by double staining. The activity was abolished by the addition of aprotinin to the reaction mixture but was not altered by the addition of a matrix metalloprotease inhibitor, a cysteine protease inhibitor, or inhibitors of plasminogen activators. Thus, upregulated glomerular plasmin-like activity in relation to NAPlr deposition in APSGN was identified. This result supports the nephritogenic character of NAPlr and offers insight into the mechanism whereby this antigen induces nephritis.
    Journal of the American Society of Nephrology 02/2005; 16(1):247-54. · 8.99 Impact Factor
  • Journal of Health Science - J HEALTH SCI. 01/2005; 51(1):55-61.
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    ABSTRACT: The role of nephritis-associated antigen as a virulence factor for acute poststreptococcal glomerulonephritis (APSGN) remains to be fully clarified. Nephritis-associated plasmin receptor (NAPlr) was previously isolated from group A streptococcus (GAS) and shown to bind plasmin(ogen). The nucleotide sequence of the naplr gene from GAS isolates obtained from patients with APSGN was determined. The sequence of the putative open reading frame (1011 bp) showed 99.8% identity among isolated strains. Homology screen revealed an exact match with streptococcal glyceraldehyde-3-phosphate dehydrogenase (GAPDH). NAPlr exhibited GAPDH activity in zymography, and it activated the complement pathway in vitro. In APSGN kidney biopsy specimens, NAPlr was observed mainly in the early stage of the disease (1 to 14 d after onset) but was not colocalized with either C3 or IgG as assessed by double immunofluorescence staining. Sera of patients with APSGN, patients with GAS infection without renal involvement, nonrenal pediatric patients, and healthy adults as controls were assayed for anti-NAPlr antibody titers. Anti-NAPlr antibodies were present most frequently in APSGN sera, and antibody titers were also significantly higher than in patients with GAS infection alone or in other control patients. Moreover, antibody titers remained elevated during the entire 10-yr follow-up period.
    Journal of the American Society of Nephrology 08/2004; 15(7):1785-93. · 8.99 Impact Factor
  • Kazuo Yamakami, Nobuyuki Yoshizawa
    Nippon Saikingaku Zasshi 06/2003; 58(2):451-65.
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    ABSTRACT: BALB/c mice are susceptible to developing an infection with Leishmania major as a result of a fatal T helper 2 (Th2)-type response. However, mice infected with a low dose of parasites are reported to be able to overcome the lesions associated with a T helper 1 (Th1)-type response. To clarify why a difference in the dose of parasites induces a difference in the polarization of the Th phenotype, we first attempted to measure cytokine production. Soon after infection, the mice given high doses of parasites produced elevated levels of both Th1 [interferon-gamma (IFN-gamma)] and Th2 [interleukin (IL)-4 and IL-10] cytokines. However, when assessed at 1 and 2 weeks after infection, no significant difference in the balance of Th1 and Th2 cytokines could be detected between mice infected with low or high doses of L. major. These results support the notion that the Th2 cytokine levels at an early phase of infection could be a key factor for the induction of a Th2 response. In order to assess the efficacy of Th2 cytokines, the mice infected with low doses of L. major were co-administered IL-4 plasmid and IL-10 plasmid. Consequently, the mice (which originally exhibited a Th1 response) showed progressive disease and developed a Th2 response. However, administration of these plasmids at 7 days postinfection could not alter the Th polarization. Furthermore, production of IL-12 from the spleen cells stimulated by L. major was suppressed in the presence of IL-4 and IL-10. These results strongly suggest that the susceptibility to L. major in BALB/c mice depends on the persistence of Th2 cytokine levels at an early phase of infection.
    Immunology 05/2002; 105(4):515-23. · 3.71 Impact Factor
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    ABSTRACT: This study aims to examine the distribution of hemolytic complement activity, the prevalence of hypocomplementemia and the disorders causing hypocomplementemia among individuals taking part in a mass screening program. The subjects consisted of 1340 male Japanese participating in a mass screening program at a Ground Self-Defense Force base in Asaka. We measured the hemolytic complement activity (CH50) after overnight fasting. The CH50 levels for hypercomplementemia and hypocomplementemia were defined as those outside the range of mean +/- 2 SD, respectively. We next measured the concentration of complement components: CIq, C4, B, C3, C5, C9, and C1-inhibitor for men with hypocomplementemia. Rheumatoid factor, ANA, HBsAg, HbsAb, and HCVAb were also measured. The mean +/- SD of age was 43.7 +/- 5.7. The CH50 levels ranged from 7.2 to 66.4 U/ml (mean +/- SD = 37.1 +/- 4.0 U/ml). Twenty-one and 37 men were classified as having hypocomplementemia (CH50 < 29.1 U/ml) and hypercomplementemia (CH50 > 45.1 U/ml), respectively. The age of the individuals with hypocomplementemia was 43.9 +/- 5.6 (Mean +/- SD) years. Three men with C9 deficiencies, 2 men with C5 deficiencies and 7 men with cold activation were identified among the 21 hypocomplementemic men. Three hepatitis C and 2 hepatitis B patients were also found among the 21 hypocomplementemic men. Other disorders found among the hypocomplementemic men were 3 glomerulonephritides and 1 possible SLE. We examined the distribution of CH50 levels in 1340 adult male Japanese. We identified 21 men with hypocomplementemia, and also found 5 cases of complement component deficiencies among 21 hypocomplementemic men. In addition the measurement of the complement activity may have also helped detect the presence of hepatitis, hypocomplementemic glomerulonephritis and collagen disease at an early stage.
    Nippon Eiseigaku Zasshi (Japanese Journal of Hygiene) 10/2001; 56(3):588-94.
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    ABSTRACT: We investigated the relation between coffee drinking and serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) concentrations among 7313 Japanese men receiving a health examination, excluding former alcohol drinkers and men with a history of chronic liver disease. Serum AST > 40 and/or ALT > 40 U/L was defined as liver inflammation. Adjustment was made for alcohol use, smoking, body mass index, serum marker for hepatitis virus infection, and other possible confounders. Adjusted odds ratios of liver inflammation were 1.00 (reference), 0.80, 0.69, and 0.61 for men drinking < 1, 1-2, 3-4, and > or = 5 cups of coffee daily, respectively. Among 6898 men without liver inflammation, serum AST and ALT were inversely associated with coffee consumption, and alcohol-related rise in AST was attenuated with coffee drinking. These findings suggest coffee may have an effect of suppressing the rise of serum aminotransferase, partly by inhibiting the alcohol-related elevation. Studies regarding biological mechanism are warranted.
    Journal of Clinical Epidemiology 09/2001; 54(8):823-9. · 5.33 Impact Factor
  • T Watanabe, N Yoshizawa
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    ABSTRACT: Recurrence of acute poststreptococcal glomerulonephritis (APSGN) is a rare phenomenon. We present an 8-year-old boy with a second episode of APSGN 12 months following a complete clinical recovery from his initial attack. Renal histology, obtained from renal biopsies of the patient during the second attack, showed diffuse endocapillary proliferation, granular deposition of C3, IgG, IgA, and fibrinogen along capillary walls, and subepithelial electron-dense deposits. A new streptococcal cytoplasmic antigen (nephritis-associated plasmin receptor protein, NAP1r), which was recently identified as the pathogenic antigen in APSGN, was detected in the glomeruli of an early kidney biopsy specimen from the patient during the second attack of APSGN, using fluorescein isothiocyanate-labeled rabbit anti-NAP1r. However, antibodies against NAP1r, examined by Western blotting, were not present in sera from the patient. These results suggest that recurrence of APSGN in some patients may be caused by an absence of a natural immune response to NAP1r.
    Pediatric Nephrology 08/2001; 16(7):598-600. · 2.94 Impact Factor
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    ABSTRACT: Fyn is a Src family protein tyrosine kinase associated with TCR/CD3 complex. Fyn appears to play a role in the activation of T cells based on its enzymatic activation and tyrosine phosphorylation following the ligation of TCR/CD3, and it also plays a critical role in the calcium flux and interleukin-2 (IL-2) production. The protective response against murineLeishmania major infection is associated with the T helper-type 1 (Th1) responses and the ability to modulate Th1 cytokines such as IL-2 and interferon-γ, respectively. The role of Fyn tyrosine kinasein vivo was directly examined by the response to infection withL. major in C57BL/6fyn-deficient mice. Despite the absence of Fyn, the mice remained resistant to this infection with only mild lesion development, and, they demonstrated Th1 responses as assessed by the delayed-type hyper-sensitivity response and cytokine milieu. The findings in thefyn-deficient mice failed to support a relationship between the anticipated functions of Fynin vitro and the immune response toL. major infectionin vivo. As a result, in leishmanial disease, Fyn probably plays a minor role in the protective immune response and is, therefore, not a key factor in such a response.
    Environmental Health and Preventive Medicine 07/2001; 6(2):132-5.

Publication Stats

595 Citations
261.14 Total Impact Points

Institutions

  • 1987–2014
    • National Defense Medical College
      • • Division of Public Health
      • • Department of Internal Medicine
      • • Division of Pathology
      Tokorozawa, Saitama, Japan
  • 2008
    • Saitama Medical University
      Saitama, Saitama, Japan
  • 2001
    • Niigata City General Hospital
      Niahi-niigata, Niigata, Japan
  • 1974
    • Devry College of New York, USA
      New York City, New York, United States