Endemic Filariasis on a Pacific Island

II. Immunologic Aspects: Immunoglobulin, Complement, and Specific Antifilarial IgG, IgM and IgE Antibodies

Eric A. OttesenLaboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20205

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Peter F. WellerLaboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20205

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Milford N. LundeLaboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20205

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Rabia HussainLaboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20205

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Sixty-eight individuals from a Pacific island hyperendemic for subperiodic bancroftian filariasis were selected from a larger study population to include the entire clinical spectrum of filarial infection in that region and also an “endemic control” group without clinical or parasitologic evidence of filarial infection. Analysis of their blood leukocyte and humoral immune responses yielded the following major findings: 1) levels of specific antifilarial antibodies of three different immunoglobulin classes (IgG and IgM measured by ELISA and IgE determined by radioimmunoassay) were significantly greater in the “endemic control” population than in the patients with filariasis, an observation true for both children and adults; 2) the endemic controls also had significantly higher levels of serum IgM and C3 than did the filariasis patients; 3) while individuals with “filarial fevers” and “chronic (lymphatic) pathology” did have significantly lower IgG antibody responses to filarial antigen than the controls, the lowest antibody levels were found in the patients with microfilaremia; 4) symptomatic patients (i.e., those with filarial fevers or lymphatic obstruction) regularly showed higher specific antibody responses to filarial antigens than asymptomatic, infected individuals, although the difference did not reach statistical significance. These findings are in concert with our previously reported, intriguing observation that lymphocyte proliferative responsiveness to filarial antigens was much greater in individuals of the ‘non-infected’ endemic control population than in patients with filariasis; furthermore, they indicate the important issues that must be approached and resolved to define the immunologic determinants leading both to the various filarial clinical syndromes and to protective immunity.

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