Patients with IgA nephropathy have circulating anti-basement membrane antibodies reacting with structures common to collagen I, II, and IV.

Cederholm, Bo; Wieslander, Jörgen; Bygren, Per; Heinegård, Dick

doi:10.1073/pnas.83.16.6151

Cited by 49 publications

(21 citation statements)

References 21 publications

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“…Since switch region polymorphism may be associated with differences of the variable heavy chain region genes, it is conceivable that altered SMu and Sa 1 genotypes and phenotypes are secondary to restrictions in the antigen recognition repertoire. In a recent study, plasma from patients with mesangial IgA-GN, but not controls, interacted with a glomerular basement membrane epitope, a finding also consistent with restriction of the recognition mechanism (16). Similar considerations apply to the recent recognition of polymorphism of the Ig heavy chain switch region in other histological types ofglomerulonephritis (9).…”

Section: Discussionsupporting

confidence: 53%

Relation of mesangial IgA glomerulonephritis to polymorphism of immunoglobulin heavy chain switch region.

Demaine¹,

Rambausek²,

Knight³

et al. 1988

J. Clin. Invest.

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Section: Discussionsupporting

confidence: 53%

Relation of mesangial IgA glomerulonephritis to polymorphism of immunoglobulin heavy chain switch region.

Demaine¹,

Rambausek²,

Knight³

et al. 1988

J. Clin. Invest.

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“…The techniques used were essentially those previously described (1). Antigen was coated on polystyrene 96-well microtiter plates (NUNC immunoplate I, NUNC, Roskilde, Denmark).…”

Section: Methodsmentioning

confidence: 99%

“…The IgA antibodies bind equally well to collagens I, II, and IV, and denatured collagens bind antibodies most efficiently (1).…”

mentioning

confidence: 99%

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Circulating complexes containing IgA and fibronectin in patients with primary IgA nephropathy.

Cederholm

Wieslander

Bygren

et al. 1988

Proc. Natl. Acad. Sci. U.S.A.

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IgA antibodies from patients with primary IgA nephropathy bind to collagens I, II, and IV. Here we show that this binding is mediated by the collagen-binding site of fibronectin, which occurs in the circulation in complex with IgA. No antibodies binding directly to collagen were identified.The complexes were isolated by affinity chromatography on gelatin-Sepharose and heparin-Sepharose, both with affinity for fibronectin, followed by adsorption to anti-human IgA immobilized on agarose gel. The presence of fibronectin and IgA antibodies in the isolated complexes is shown by enzymelinked immunosorbent assay, gel electrophoresis, and electrophoretic transfer followed by immunostaining. The presence of an IgA-fibronectin complex in serum and the binding of this complex to collagen demonstrate the necessity of removing fibronectin from serum prior to identifying anti-collagen antibodies.

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“…Several abnormalities ofthe immunologieal status in IgAN. such as polyelonal aetivation of IgA-producing B cells [3], presence of various autoantibodies [4][5][6] and association with other immunologieal disorders [7-y]. have been reported.…”

Section: Introdlctionmentioning

confidence: 99%

Altered production of IgE and IgA induced by IL-4 in peripheral blood mononuclear cells from patients with IgA nephropathy

Yano

Endoh

Miyazaki

et al. 1992

Clinical and Experimental Immunology

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SUMMARYIn order to elucidate the factors responsible for altered inimunoglobuHn production in patients with IgA nephropalhy (IgAN). the in vitro effeets of IL-4 and interferon-gamma (IFN-y) on the synthesis of IgH and IgA by peripheral blood mononuclcar cells (PBMC) were studied. Spontaneous IgE and IgA synthesis by PBMC was signifieantly increased in palienis with IgA nephropathy compared with eontrols. The maximum amounts of IgA and IgE synthesis by PBMC after stimulation with IL-4 were almost the same both in palients with IgAN and in eontrols. The enhaneemenl rale of IL-4-induced IgE and IgA synthesis was signihcanlly lower in IgAN than in the controls, suggesting in vivo preaetivation of PBMC in IgAN patients. IFN-7 suppressed IgA and IgE synthesis by PBMC from IgAN patients as well as controls. However, the suppressive effect on IgE synthesis was less prominent in patients with IgAN, These results suggested ihat altered IL-4 action might be involved in the development oflgA nephropathy. IgE [18]. In recent studies, increased expression of CD23 on peripheral blood lymphocytes has been reported in asthma [19]. atopic dermatitis [20). and in other atopie diseases [21.22] as well as in collagen diseases sueh as systemic lupus erythcmalosus (SLE) and rheumatic arthritis [23], Other reports showed elevated levels of lL-4 in sera from patients with Correspondence: Naohiro Yano, MI), Department oT Internal Medicine, Tokai University, Isehara, Kanagawa, 259-11, Japan, progressive systemic sclerosis [24], and expression of IL-4 mRNA in allergen-induced late-phase cutaneous reactions in atopie subjects [25], A study using I L-4-transgenie miee revealed thai IL-4 induces allcrgic-like inflammatory disease in systemic organs [26]. These studies strongly suggested that IL-4 plays some role in the development ofdiseases wiih allergie changes. The aim of ihe present study was to elueidate the role of IL-4 in altered production of IgE and IgA by peripheral blood mononuciear cells (PBMC) from patients with IgAN. Keywords MATERIALS AND METHODS PatientsTwenty-six patients with IgAN and 22 age-matched patients with non-IgA prolifcrative glomerulonephrilis (PGN) were selected randomly from patients who were diagnosed by open

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Patients with IgA nephropathy have circulating anti-basement membrane antibodies reacting with structures common to collagen I, II, and IV.

Cited by 49 publications

References 21 publications

Relation of mesangial IgA glomerulonephritis to polymorphism of immunoglobulin heavy chain switch region.

Relation of mesangial IgA glomerulonephritis to polymorphism of immunoglobulin heavy chain switch region.

Circulating complexes containing IgA and fibronectin in patients with primary IgA nephropathy.

Altered production of IgE and IgA induced by IL-4 in peripheral blood mononuclear cells from patients with IgA nephropathy

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