Sera of patients with systemic lupus erythematosus react with plasmodial antigens and can inhibit thein vitrogrowth ofPlasmodium falciparum

Abstract

The acquisition of protective immunity in malaria is a slow process during which autoantibodies are produced. The present work aimed at studying a possible interference of autoimmune responses on malaria immune protection. This was done by investigating the presence of autoantibodies in the sera of malarious patients, by searching for reactivity of autoantibodies from autoimmune patients against plasmodial antigens, and by studying the effect of such antibodies on the in vitro growth of Plasmodium falciparum. Sera from systemic lupus erythematosus (SLE) and malaria patients were tested against autologous and plasmodial antigens. Out of the 109 SLE sera tested, 48 (44%) reacted against the parasite. In addition, 26 (47%) out of 55 randomly selected sera, mainly those containing anti-DNA and antinuclear autoantibodies, were able to inhibit parasite growth to some extent. Conversely, a high frequency (81%) of sera of malaria patients exhibited reactivity against autoantigens. The results show that patients with autoimmune processes can produce antibodies that recognize plasmodial antigens in the absence of plasmodial infection, that malaria patients can produce autoantibodies, that SLE sera can inhibit plasmodial growth in vitro, and that the presence of anti-DNA and antinuclear antibodies may be important in such anti-plasmodial activity. It is concluded that autoimmune responses may have influence on the protective immunity against malaria.

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

“…As previous works used only purified IgG preparations (Singh et al 2001, Zanini et al 2009), the present study is the first to show that monoclonal auto-Ab can inhibit in vitro P. falciparum growth. �his result was expected, because monoclonal antibody crossreactions between plasmodial and mammalian cells were reported more than two decades ago (Daniel-Ribeiro et al 1984b, Li et al 1995, Crandall et al 1996.…”

“…However, the strongest evidence supporting the protective role of autoimmunity in plasmodial infection has been provided by two independent studies, which showed that sera and IgG antibodies from SLE patients can react with and inhibit the in vitro growth of P. falciparum (Singh et al 2001, Zanini et al 2009). �he present paper expands these findings by showing that sera from patients with other AID, containing auto-Ab of different specificities, can also react against P. falciparum and inhibit the parasite's in vitro growth.…”

“…In addition, it has been demonstrated that sera from SLE patients can react with plasmodial antigens and inhibit the in vitro growth of Plasmodium falciparum (Singh et al 2001, Zanini et al 2009. �aken together, these data suggest that autoimmune responses confer anti-parasite activity, which can be mediated through auto-Ab and/or serum factors that may cooperate with the host immune response during plasmodial infections.…”

“…-IFA� was performed as previously described (Zanini et al 2009). Briefly, slides containing 20 asynchronously cultured, P. falciparum-parasitised red blood cells (pRBC) (NF54 strain) per microscopic field (�rager & Jensen 1976), were incubated with sera that was serially diluted in phosphate-buffered saline (PBS), followed by the addition of fluorescein isothiocyanate (FI�C)-conjugated goat anti-human IgG (Sigma, St. Louis, MO, USA) diluted in PBS-Evans Blue solution for 30 min at 37ºC.…”

“…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).…”