SummaryThis study has been undertaken to assess whether anticardiolipin and anti-(32-GPI are two distinct populations of (auto)antibodies, and to clarify whether the β2-GPI region critical for phospholipid binding is also crucial for anti-β2-GPI reactivity.Fourteen of the 62 anticardiolipin (aCL) ELISA positive sera (22.6%) were positive for anti-β2-GPI by immunoblotting, 42 (67.7%) for aCL using TLC immunostaining.IgG fractions from 5 sera gave the same anticardiolipin reactivity detected by TLC immunostaining in the corresponding sera.All anti-β2-GPI-positive sera were reactive with the phenylthio-carbamyl derivative of the protein, indicating that binding of phe-nylisothiocyanate with lysine residues does not modify the molecule antigenicity. In addition, incubation of IgG fractions with the phospholipid binding site did not modify reactivity with β2-GPI.These findings demonstrate that: a) “true” antiphospholipid antibodies are detectable in patients sera; b) aCL and anti-β2-GPI have a different immunological profile; c) the β2-GPI phospholipid-binding site is not the region recognized by the antibodies.
Gangliosides were found to be present in Entamoeba histolytica. They were extracted from lyophilized trophozoites of the pathogenic strain HM-1:IMSS and purified by high performance thin-layer chromatography. Two resorcinol-positive bands, comigrating with GM2 and GD1a were demonstrated, revealing the existence of ganglioside molecules in Entamoeba histolytica. The GM2 content, determined as lipid-bound sialic acid, was 1.5 micrograms/10(8) amoebae, the content of the GD1a comigrating band was 0.32 microgram/10(8) amoebae. The identity of the GM2 comigrating band was confirmed by TLC immunostaining, using the monoclonal anti-GM2 antibody GMB28. Furthermore, six out of ten anti-amoeba positive sera selectively reacted with the GM2 comigrating band, as revealed by immunostaining on TLC plates. Absorption tests revealed that preincubation of anti-amoeba positive sera with standard GM2 was followed by a significant decrease in the reaction with amoeba trophozoites by indirect immunofluorescence. These results demonstrate that a GM2 comigrating component of Entamoeba histolytica may be one of the antigens responsible for the appearance of circulating antibodies in patients with amoebiasis.
In this study the presence of brain antiganglioside antibodies in the cerebrospinal fluid (CSF) of patients with HIV infection was analysed. CSF samples were collected from 45 patients with AIDS and from 45 anti-HIV negative subjects, 15 of whom presented aseptic meningitis. Nineteen AIDS patients had clinically well-documented encephalopathy. Thirteen of these patients had white matter lesions shown by magnetic resonance imaging (MRI). Both IgG and IgM antiganglioside antibodies were detected by immunostaining on thin layer chromatography plates in three CSF samples from AIDS patients with progressive encephalopathy with signs of a diffuse demyelination, as revealed by MRI. Two of these CSF samples reacted specifically with GM3, GM1 and GD1a and one with GD1a. In none of the HIV infected patients without demyelinating encephalopathy, but with opportunistic infections or cerebral lymphoma, nor in the anti-HIV negative control subjects were antiganglioside antibodies detected. No association with JCV DNA, CMV DNA, EBV DNA, detected by nested PCR, nor HIV antigen p24 was found. These findings show the presence of brain antiganglioside antibodies in the CSF of AIDS patients for the first time. However, the findings do not suggest relating the presence of these antibodies to HIV encephalopathy or particular viral agents, but indicate that the antibodies are detectable in subjects with progressive encephalopathy with a diffuse demyelination.
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