Human Monoclonal Antibodies against an Epitope on the Class 5c Outer Membrane Protein Common to Many Pathogenic Strains of Neisseria meningitidis

Neisseria meningitidis is a causative agent of meningitis. Despite vaccination programs, it still causes a large number of deaths in youngchildren. Early diagnosis followedbypassiveimmunization with human monoclonal antibodies could be an approach to effective therapy. Peripheral blood lymphocytes f...

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Published inThe Journal of infectious diseases Vol. 166; no. 6; pp. 1322 - 1328
Main Authors Fernández de Cossío, Maria E., Ohlin, Mats, Llano, Manual, Selander, Barbro, Cruz, Silian, del Valle, Jesus, Borrebaeck, Carl A. K.
Format Journal Article
LanguageEnglish
Published United States The University of Chicago Press 01.12.1992
University of Chicago Press
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Summary:Neisseria meningitidis is a causative agent of meningitis. Despite vaccination programs, it still causes a large number of deaths in youngchildren. Early diagnosis followedbypassiveimmunization with human monoclonal antibodies could be an approach to effective therapy. Peripheral blood lymphocytes from normal, healthy blood donors and from vaccinated individuals were immunized in vitro, using outer membrane proteins purified from N. meningitidis B:4:P1.15. The immunized human B cells were Epstein-Barr virus transformed and fused to a heteromyelorna. Several stable human hybridoma cell lines were established and two, secreting antibodies against the 31-kDa class Sc outer membrane protein, were characterized further. The human antibodies were of IgGl and IgG3 isotypes, with K light chains. The recognized epitope was commonly found among pathogenic strains of N. meningitidis; thus, these human monoclonal antibodies may be important in the evaluation of N. meningitidis infections.
Bibliography:istex:A2CC7FCDD7BAA82EE76DBA89AA7B4E01FBFFAD43
Reprints or correspondence: Dr. Carl Borrebaeck, Department of Immunotechnology. Lund University. P. O. Box 7031. S-220 07 Lund, Sweden.
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ISSN:0022-1899
1537-6613
DOI:10.1093/infdis/166.6.1322