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Free access | 10.1172/JCI109852
Department of Bacterial Diseases, Walter Reed Army Institute of Research, Washington, D. C. 20012
Department of Immunology, Walter Reed Army Institute of Research, Washington, D. C. 20012
Department of Gastroenterology, Walter Reed Army Institute of Research, Washington, D. C. 20012
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Department of Bacterial Diseases, Walter Reed Army Institute of Research, Washington, D. C. 20012
Department of Immunology, Walter Reed Army Institute of Research, Washington, D. C. 20012
Department of Gastroenterology, Walter Reed Army Institute of Research, Washington, D. C. 20012
Find articles by Smith, L. in: JCI | PubMed | Google Scholar
Department of Bacterial Diseases, Walter Reed Army Institute of Research, Washington, D. C. 20012
Department of Immunology, Walter Reed Army Institute of Research, Washington, D. C. 20012
Department of Gastroenterology, Walter Reed Army Institute of Research, Washington, D. C. 20012
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Department of Bacterial Diseases, Walter Reed Army Institute of Research, Washington, D. C. 20012
Department of Immunology, Walter Reed Army Institute of Research, Washington, D. C. 20012
Department of Gastroenterology, Walter Reed Army Institute of Research, Washington, D. C. 20012
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Department of Bacterial Diseases, Walter Reed Army Institute of Research, Washington, D. C. 20012
Department of Immunology, Walter Reed Army Institute of Research, Washington, D. C. 20012
Department of Gastroenterology, Walter Reed Army Institute of Research, Washington, D. C. 20012
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Published August 1, 1980 - More info
We have compared the abilities of immunoglobulin (Ig)G, IgM, and IgA to induce either mononuclear cell-mediated (complement-independent) or complement-mediated (cell-free) antibacterial activity against group C meningococci. In each of these assays, immunoglobulins purified from the sera of individuals immunized with meningococcal group C polysaccharide were compared with those purified from sera of patients convalescing from disseminated meningococcal disease. Our data support three conclusions. First, although nonbactericidal in cooperation with complement, IgA can induce cell-mediated antibacterial activity as well as IgG. Second, the amount of IgG required to induce cell-mediated antibacterial activity is similar to the amount required for complement-mediated killing. Third, although the amount of either postimmunization or convalescent IgM required to induce complement-mediated killing is 16- to 20-fold less than the amount of respective IgG required, IgM is inferior to IgG in its ability to induce cell-mediated antibacterial activity because in the cell-mediated system (a) postimmunization IgM is ineffective; (b) the amount of convalescent IgM required for minimal activity is eightfold more than the amount of convalescent IgG required; and (c) the maximal antibacterial index induced by convalescent IgM is 50% less than that which can be induced by IgG. These data suggest that IgG and IgA may play a greater role than IgM in mononuclear cell-mediated antibacterial host immune defense.