Dysfunctions of Pokeweed Mitogen-stimulated T and B Lymphocyte Responses Induced by Gammaglobulin Therapy

Durandy, Anne; Fischer, Alain; Griscelli, C

doi:10.1172/jci110104

Cited by 82 publications

(19 citation statements)

References 46 publications

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“…It is, however, unlikely to be secondary to chronic infections since it was found in patient 3 at birth and in patient 8 who is in good health. Ecto-5'-NT deficiency cannot be a consequence of immunoglobulin replacement therapy (as has been suggested for decreased PWM responses in nonimmunodeficient children treated with gammaglobulin [47]), since is was detected in two of our patients before the initiation of treatment. Although ecto-5'-NT activity is a marker for T lymphocyte differentiation (22,23,48), with thymocytes having virtually absent activity, it is unlikely that low numbers of T cells with ecto-5'-NT activity in CAG and CVI patients can be explained merely by a block in T cell maturation.…”

Section: Resultsmentioning

confidence: 51%

Ecto-5′-Nucleotidase Activity in Human T Cell Subsets. DECREASED NUMBERS OF ECTO-5′-NUCLEOTIDASE POSITIVE CELLS FROM BOTH OKT4+ AND OKT8+ CELLS IN PATIENTS WITH HYPOGAMMAGLOBULINEMIA

Thompson¹,

Saxon²,

O’Connor³

et al. 1983

J. Clin. Invest.

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Section: Resultsmentioning

confidence: 51%

Ecto-5′-Nucleotidase Activity in Human T Cell Subsets. DECREASED NUMBERS OF ECTO-5′-NUCLEOTIDASE POSITIVE CELLS FROM BOTH OKT4+ AND OKT8+ CELLS IN PATIENTS WITH HYPOGAMMAGLOBULINEMIA

Thompson¹,

Saxon²,

O’Connor³

et al. 1983

J. Clin. Invest.

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“…These observation may also indicate an inhibition of anti-idiotypic activity in vivo, as described in vitro [12]. IgG may block macrophage and B cell Fc receptors inhibiting the anti-idiotypic antibody synthesis from B lymphocytes [13]. IgA and IgM remained unchanged for the whole period of treatment.…”

Section: Results and Conclusionmentioning

confidence: 99%

Intravenous Immunoglobulin G in the Treatment of Patients with Chronic Glomerulonephritis: Clinical Experience Lasting 15 Years

Monova¹,

Belovezhdov²,

Altŭnkova³

et al. 2002

Nephron

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In our study, we collected data on 116 patients with biopsy-proven idiopathic or lupus glomerulonephritis who were treated with high doses of intravenous immunoglobulin G (IVIG) (Veinoglobuline or Immunovenin-intact). In all patients a severe nephrotic syndrome (edema, proteinuria >6 g/24 h, serum albumin <22 g/24 h) had been observed. 34 patients had renal failure (serum creatinine up to 504 µmol/l) and 96 hypertension. 98 patients were previously for a long time treated with corticosteroids, immunosuppressors and anticoagulants without any effect. 18 patients had no therapy before IVIG. IVIG had been applied in a dose of 85 mg/kg/24 h 3 times every other day. Depending on the clinical improvement afterwards (in case of therapy resistance or relapse) these boli had been repeated in 84 patients after 1 month (and every 3 months for maintenance of remission) to 7 years. Proteinuria disappeared and full remission occurred in 36 patients. Partial remission was present in 48 patients. 32 patients went into end-stage renal failure and/or died (15 of them of a nonrenal cause). In 13/34 patients with impaired renal function serum creatinine levels go back to normal after treatment. Our results suggested that IVIG therapy may be recommended in patients unresponsive to aggressive conventional treatment.

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“…One possible explanation is that the ability to produce immunoglobulins may be perturbed by IVIG. Durandy et al [23] have indicated that lymphocytes obtained from nonimmunodeficent children treated with intramuscular immunoglobulin have a reduced capacity to proliferate and mature into IgG-and IgM-secreting plasma cells in vitro after stimulation with pokeweed mitogen. In fact, IVIG therapy suppresses polyclonal B cell activation observed in the acute phase of KD [24,25].…”

Section: Discussionmentioning

confidence: 99%

“…In fact, IVIG therapy suppresses polyclonal B cell activation observed in the acute phase of KD [24,25]. An alternative explanation is derived from the cellular immune perturbation caused by KD [23][24][25]. Microbial SAgs bypass normal antigen presentation by binding to class II major histocompatibility complex molecules on antigen-presenting cells and to TCR Vβ elements on T cells, and trigger T cell activation through this interaction [18,[26][27][28][29].…”

Section: Discussionmentioning

confidence: 99%

Development of serum IgM antibodies against superantigens ofStaphylococcus aureusandStreptococcus pyogenesin Kawasaki disease

Matsubara

Fukaya

Miwa

et al. 2006

Clinical and Experimental Immunology

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SummaryTo serologically determine the association of microbial superantigens and the pathogenesis of Kawasaki disease (KD), we conducted a case-control study. Serum IgG and IgM antibodies against staphylococcal enterotoxin A (SEA), SEB, SEC, toxic shock syndrome toxin-1 (TSST-1), and streptococcal pyrogenic exotoxin A (SPEA) were measured by an enzyme-linked immunosorbent assay in 293 serum samples from 65 KD patients on clinical days 1-28 and 120 control samples. The administration of immunoglobulin products, which contain high concentrations of IgG antibodies against all the superantigens, directly elevated antitoxin IgG antibodies in KD patients. In contrast, antitoxin IgM antibodies were not detected in immunoglobulin products. Actually, we found a significant elevation of IgM antibodies against SEA in KD patients in the first (median titre: 0·020, P < < < < 0·01 versus control), second (0·024, P < < < < 0·001), third (0·030, P < < < < 0·001) and fourth (0·038, P < < < < 0·001) weeks, compared to the controls (0·015). Significant differences of IgM antibodies were also true for SEB, TSST-1, and SPEA throughout the first to fourth weeks, and for SEC throughout the second to fourth weeks. The prevalence of KD patients having high IgM titres (> > > > mean + + + + 2SD of control values) to the 5 superantigens was increased with the clinical weeks, and reached 29-43% of KD subjects at the fourth week. This is the first study that describes kinetics of IgM antibodies against superantigens and clarifies the serological significance throughout the clinical course of KD. Our results suggest that multiple superantigens involve in the pathogenesis of KD.

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Dysfunctions of Pokeweed Mitogen-stimulated T and B Lymphocyte Responses Induced by Gammaglobulin Therapy

Abstract: A B S T R A C T Lymphocytes obtained from nonim

Cited by 82 publications

References 46 publications

Ecto-5′-Nucleotidase Activity in Human T Cell Subsets. DECREASED NUMBERS OF ECTO-5′-NUCLEOTIDASE POSITIVE CELLS FROM BOTH OKT4+ AND OKT8+ CELLS IN PATIENTS WITH HYPOGAMMAGLOBULINEMIA

Ecto-5′-Nucleotidase Activity in Human T Cell Subsets. DECREASED NUMBERS OF ECTO-5′-NUCLEOTIDASE POSITIVE CELLS FROM BOTH OKT4+ AND OKT8+ CELLS IN PATIENTS WITH HYPOGAMMAGLOBULINEMIA

Intravenous Immunoglobulin G in the Treatment of Patients with Chronic Glomerulonephritis: Clinical Experience Lasting 15 Years

Development of serum IgM antibodies against superantigens ofStaphylococcus aureusandStreptococcus pyogenesin Kawasaki disease

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