High prevalence of co-factor independent anticardiolipin antibodies in malaria exposed individuals

Abstract

SUMMARY Anticardiolipin antibodies (aCL) were investigated in 137 individuals chronically exposed to malaria and living in Africa and Asia. They belonged to several groups according to parasite (Plasmodium falciparum or vivax) and clinical manifestations (i.e. asymptomatic parasite carriers, acute uncomplicated attack or severe malaria episodes). aCL were measured in an enzyme immunoassay (ELISA) performed in the presence of either goat serum (aCLs) or gelatin (aCLg). In a group of 53 patients with autoimmune manifestations (i.e. antiphospholipid syndrome and/or lupus), detection of IgG but not IgM aCL was markedly reduced in the presence of gelatin. In malaria donors, high prevalence of serum co‐factor‐independent IgG and IgM were detected, and the presence of goat serum in the assay consistently decreased their detection. aCLg levels were found to be related to the clinical/endemic status of donors. IgG aCLg were found to be higher in asymptomatic P. falciparum carriers than in patients with uncomplicated acute or cerebral malaria. IgM aCLg were higher in the cerebral malaria group than in groups with uncomplicated acute malaria patients or asymptomatic individuals. Data suggest that using a serum co‐factor independent, sensitive ELISA, aCL are commonly detected during malarial infections and related to malarial infection status.

Monoclonal auto-antibodies and sera of autoimmune patients react with Plasmodium falciparum and inhibit its in vitro growth

“…Anti-nuclear, anti-smooth muscle and anti-M1 antibodies are induced during the course of malaria infection and these may be related to the degree of immunity [for review, see Daniel-Ribeiro and Zanini (2000) and Consigny et al (2002)]. �he present work supports these data by showing that sera containing these auto-Abs can react against P. falciparum and that anti-M1 MoAb can inhibit in vitro parasite growth.…”

“…Indeed, auto-Ab with various specificities, such as double and single-stranded DNA (Daniel-Ribeiro et al 1984c, Zouali et al 1986, Zanini et al 2009), erythrocytes (Lefrançois et al 1981, Vivas et al 2008), lymphocytes (de Souza & Playfair 1983, phospholipids (Bate et al 1992, Vivas et al 2008, ribonucleoprotein (Zouali et al 1986, Daniel-Ribeiro et al 1991, Zanini et al 2009), RNA (Kreier & Dilley 1969), smooth muscle (Quakyi et al 1979, Poels et al 1980, Daniel-Ribeiro et al 1991, cardiolipin (Consigny et al 2002) and cytosol proteins (Dugué et al 2004) are evident in the course of malaria infection. It seems that the specificities of the auto-Ab produced differ according to the degree of antiparasite immunity (Poels et al 1980) and that they are not related to organ-specific, partially sequestered autoantigens, such as thyroglobulin (Daniel-Ribeiro 2000).…”

Antiphospholipid Antibodies and the Risk of Stroke in Urban and Rural Tanzania

“…Apart from syphilis, LA and other aPL subpopulations may arise in the course of other infections, 22 including those common in SSA such as HIV, 23 mycobacterial infections, syphilis, 24 malaria, 25 and viral hepatitis. 26 The observation that the prevalence of LA was higher in cases from rural Hai region may be explained by a higher infectious burden in this area, whereas traditional stroke risk factors may be more important in urban Dar-es-Salaam.…”

Unusual thrombotic manifestations secondary to antiphospholipid syndrome and hepatic fascioliasis

“…5,6 In some cases, these antibodies may be transient and disappear within 2 or 3 months. However, in other susceptible individuals they may persist and may trigger the development of a thrombotic complication.…”