title: Increased polyclonal immunoglobulin reactivity toward human and bacterial proteins is associated with clinical protection in human Plasmodium infection.
abstract: BACKGROUND
  Polyclonal B-cell activation is well known to occur in Plasmodium infections, but its role in pathogenesis or protection remains unclear. However, protective properties of natural antibodies have previously been demonstrated in other contexts.
  
  
  METHODS
  Sera from asymptomatic and symptomatic Plasmodium-infected subjects locally detected in a survey study in the Brazilian Amazon, and from unexposed and exposed but presently uninfected control subjects, were assayed by a standardized quantitative immunoblot method allowing simultaneous detection of IgG or IgM reactivity to a large number of parasite-unrelated proteins.
  
  
  RESULTS
  In subjects free of coinfection with hepatitis B virus, IgG reactivity to human brain antigens and Escherichia coli proteins was strikingly enhanced in asymptomatic Plasmodium-infected individuals when compared to such with clinical malaria symptoms, or to uninfected control subjects. This difference was most characteristic for limited exposure times (less than ten years locally, or 20 years in endemic areas). It was more significant than a similar trend found for IgG to Plasmodium falciparum antigens, and unrelated to parasitaemia levels. Asymptomatic subjects with comparatively short exposure characteristically showed relatively elevated IgG versus IgM reactivity. Polyclonal IgG reactivity appears triggered by previous P. falciparum but not Plasmodium vivax malaria.
  
  
  CONCLUSIONS
  The observed difference in polyclonal antibody production seems related to intrinsic activation states of infected individuals, rather than to parasite-antigen specific immune responses. However, it appears influenced by preceding stimuli. This supports the idea that acquired clinical immunity may not exclusively depend on antigen-specific responses, but also on the individual polyclonal reaction.
authors.affiliation: Instituto Gulbenkian de Ciência, Apartado 14, 2781-901 Oeiras, Portugal. cfesel@igc.gulbenkian.pt
authors.forename: Constantin
authors.initials: C
authors.lastname: Fesel
authors.forename: Luis F
authors.initials: LF
authors.lastname: Goulart
authors.forename: Adolfo
authors.initials: A
authors.lastname: Silva Neto
authors.forename: Alysson
authors.initials: A
authors.lastname: Coelho
authors.forename: Cor Jesus F
authors.initials: CJ
authors.lastname: Fontes
authors.forename: Erika M
authors.initials: EM
authors.lastname: Braga
authors.forename: Nelson M
authors.initials: NM
authors.lastname: Vaz
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000818:Animals; D000907:Antibodies, Bacterial / Q000097:blood / Q000276:immunology; D000913:Antibodies, Protozoan / Q000097:blood / Q000276:immunology; D001921:Brain / Q000276:immunology; D001938:Brazil / Q000453:epidemiology; D002648:Child; D029968:Escherichia coli Proteins / Q000276:immunology; D006514:Hepatitis B Surface Antigens / Q000097:blood / Q000276:immunology; D006801:Humans; D007113:Immunity, Innate / Q000276:immunology*; D007074:Immunoglobulin G / Q000097:blood / Q000276:immunology; D007075:Immunoglobulin M / Q000097:blood / Q000276:immunology; D007136:Immunoglobulins / Q000097:blood / Q000276:immunology*; D016778:Malaria, Falciparum / Q000453:epidemiology / Q000276:immunology*; D016780:Malaria, Vivax / Q000453:epidemiology / Q000276:immunology*; D008875:Middle Aged; D018512:Parasitemia / Q000097:blood / Q000276:immunology; D010963:Plasmodium falciparum / Q000276:immunology / Q000302:isolation & purification; D010966:Plasmodium vivax / Q000276:immunology / Q000302:isolation & purification; D025341:Principal Component Analysis / Q000379:methods
chemical_list: D000907:Antibodies, Bacterial; D000913:Antibodies, Protozoan; D029968:Escherichia coli Proteins; D006514:Hepatitis B Surface Antigens; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D007136:Immunoglobulins