Sera of patients with systemic lupus erythematosus react with plasmodial antigens and can inhibit the in vitro growth of Plasmodium 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.

Keywords::

• Systemic Lupus Erythematosus
• autoimmune diseases
• autoantibodies
• malaria
• immune protection

Acknowledgements

We are grateful to Dr. Marilena Fernandes for providing access to SLE patients from the Hospital dos Servidores do Estado do Rio de Janeiro and to the medical residents for examining and interviewing them, and to Dr. Roger Levi (Rio de Janeiro State University) for providing assistance in the performance of the anticardiolipin ELISA test. We are also indebted to the PhD student Yuri Chaves Martins for the help in the preparation of the manuscript. Dr. Cláudio Tadeu Daniel-Ribeiro is recipient of a research productivity fellowship from the Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) and Graziela Maria Zanini received a fellowship from Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES). The work was supported by Instituto Oswaldo Cruz, Fiocruz (PAPES), the CNPq and the Faperj.

Declaration of interests: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.