Antibodies to laminin in American cutaneous leishmaniasis

Avila, JoséLuis; Rojas, Miguel; Rieber, Manuel

doi:10.1128/iai.43.1.402-406.1984

Cited by 50 publications

(27 citation statements)

References 12 publications

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“…Laminin, a large glycoprotein found exclusively in basement membranes (8) was able to bind most of the tissuereacting antibodies present in these sera (6). Similar laminin-reacting antibodies have been detected in patients with American cutaneous and mucocutaneous leishmaniasis (9) and with poststreptococcal glomerulonephritis (10). However, these antibodies have been found to crossreact with various forms of the parasites (2,3,6,11), as well as with animal erythrocytes (3,(11)(12)(13) and structurally distinct basement membrane proteins such as laminin and nidogen (13).…”

mentioning

confidence: 75%

Circulating antibodies to mouse laminin in Chagas disease, American cutaneous leishmaniasis, and normal individuals recognize terminal galactosyl(alpha 1-3)-galactose epitopes.

Towbin¹,

Rosenfelder²,

Wieslander³

et al. 1987

The Journal of Experimental Medicine

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164

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Sera from patients with American cutaneous leishmaniasis and Chagas disease and from monkeys infected with either Trypanosoma cruzi or Trypanosoma rhodesiense show, in RIAs, strong binding to mouse laminin. A distinct although weaker binding activity is also detected in normal human sera. The antibodies recognize a common carbohydrate epitope present on mouse laminin, which was assigned to a terminal galactosyl(alpha 1-3)-galactose group. Distinct crossreactions were observed with some other basement membrane proteins, rabbit glycosphingolipids, defucosylated human B blood group substance and components produced by some human tumor cells. Only little activity was, however, found on laminin obtained from human placenta. The data indicate that the antibodies arising in infectious diseases are stimulated by similar carbohydrate epitopes present on the surface of parasites. Tissue-specific occurrence of such epitopes may exist and explain the involvement of distinct tissues in autoimmune disorders.

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mentioning

confidence: 75%

Circulating antibodies to mouse laminin in Chagas disease, American cutaneous leishmaniasis, and normal individuals recognize terminal galactosyl(alpha 1-3)-galactose epitopes.

Towbin¹,

Rosenfelder²,

Wieslander³

et al. 1987

The Journal of Experimental Medicine

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164

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“…Patients with localized cutaneous leishmaniasis (LCL) [20], chronic Chagas' disease [21], T. rangeli infection [22] and visceral leishmaniasis [23] were as previously described. Sera from 136 patients with 18 other infectious or inflammatory diseases previously described were also studied [24].…”

Section: Study Population and Clinical Samplesmentioning

confidence: 99%

Cholesterol sulphate-reactive autoantibodies are specifically increased in chronic chagasic human patients

Avila

Rojas

Ávila

1996

Clinical and Experimental Immunology

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SUMMARYAn antibody reactive with cholesterol sulphate (CS) was characterized in human sera by ELISA, erythrocyte and liposome absorption. This antibody was found evenly distributed between the IgA and IgM classes, and whilst this was present at low titres in the serum of 16% of healthy individuals studied, it was significantly elevated in 78% of Trypanosoma cruzi-infected subjects. No association was found between antibody levels and the degree of myocardial damage. No significant difference in immunoreactivity was found between healthy and chagasic subjects using dehydroepiandrosterone sulphate and pregnenolone sulphate and cholesterol, ergosterol, lanosterol, stigmastanol,¯-stigmasterol, pregnenolone, prednisolone and dehydroepiandrosterone as antigens, suggesting that in chagasic sera the whole sterol molecule is important for optimal antibody binding. CS-reactive antibodies were easily purified by absorption either with CS-bearing liposomes or with dextran sulphate gel and further elution with 1 . 5 M NaCl. The optimal pH of CS-antibody interaction was 4 . 0 with 85% binding at pH 7 . 0. Polylysine strongly decreased the binding of these antibodies to the corresponding antigen. Furthermore, these antibodies were strongly absorbed by rabbit and guinea pig erythrocyte but not by rat or human erythrocyte. In contrast with anti-sulphatide antibodies, no significant increase in CS-reactive antibodies was found in dilated cardiomyopathies. Whilst CS itself was not detected in T. cruzi lipid extracts, there is an unidentified sulphated sterol, which migrates close to standard CS and which strongly binds chagasic but not control sera. This latter sterol might be acting in chagasic patients as a powerful antigen, triggering specific autoantibody production.

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“…Antibodies against laminin were determined by the enzymelinked immunosorbent assay (ELISA) following the method described by Avila et al (1984) and Bacman et al (1990). Results of ELISA revealed an optical density of 0.8 for antilaminin IgG, and 0.01 for the IgG from the preimmune, and from the normal rabbit serum used as controls.…”

Section: Immunological Characterization Ofiggmentioning

confidence: 99%

Participation of cytoskeleton in the effect of antilaminin IgG on cardiac cholinoceptors

Bacman¹,

Borda²,

Denduchis³

et al. 1994

British J Pharmacology

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We have previously demonstrated a molecular relationship between laminin and cardiac cholinoceptors. We have now explored the participation of cytoskeletal proteins in the interaction between an antilaminin IgG with cardiac cholinoceptors. Antilaminin IgG, whilst it specifically reacts with laminin molecules was able to induce cardiac cholinoceptor activation; acting like an agonist, decreasing cyclic AMP concentrations, reducing heart contractility and increasing phosphoinositide turnover. Antilaminin IgG also interfered with the binding of a radiolabelled muscarinic antagonist, [3H]‐quinuclidinyl benzilate. Colchicine and cytochalasin B, drugs that are able to prevent microfilament and microtubule polimerization, impaired the binding of antilaminin IgG to muscarinic cholinoceptors. Cytochalasin B but not colchicine modified the muscarinic cholinoceptor effects mediated by regulatory G proteins (cyclic AMP and contractility) induced by antilaminin IgG. It was demonstrated, by immunofluorescence, that none of these disrupting drugs altered the specific recognition of the antibody by its antigen. These data indirectly suggest the participation of the cytoskeleton in the laminin and cholinergic receptor association.

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Antibodies to laminin in American cutaneous leishmaniasis

Cited by 50 publications

References 12 publications

Circulating antibodies to mouse laminin in Chagas disease, American cutaneous leishmaniasis, and normal individuals recognize terminal galactosyl(alpha 1-3)-galactose epitopes.

Circulating antibodies to mouse laminin in Chagas disease, American cutaneous leishmaniasis, and normal individuals recognize terminal galactosyl(alpha 1-3)-galactose epitopes.

Cholesterol sulphate-reactive autoantibodies are specifically increased in chronic chagasic human patients

Participation of cytoskeleton in the effect of antilaminin IgG on cardiac cholinoceptors

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