ArticleJournal of immunological methods2006
Forced expression of AID facilitates the isolation of class switch variants from hybridoma cells.
Article in Journal of immunological methods, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- Development of functional antibodies against influenza B virus by activation-induced cytidine deaminase in hybridoma cells.Virologica Sinica · 2022Article
- The constant region contributes to the antigenic specificity and renal pathogenicity of murine anti-DNA antibodies.Journal of autoimmunity · 2012Article
- Molecular characterization of hybridoma subclones spontaneously switching at high frequencies in vitro.Journal of immunological methods · 2009Article
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5 authors at 1 institution in 1 country.
Funding
Abstract
Monoclonal antibodies are used in the treatment and diagnosis of diseases and to study the protective and adverse functions of antibodies in vitro and in vivo. Since the isotype determines the effector function, half-life in the serum and distribution throughout the body, it would be useful to have a battery of antibodies with the same binding site associated with different isotypes. However, since hybridomas switch isotypes at very low frequencies in tissue culture, it has been difficult and very labor intensive to isolate panels of class switch variants. We show here that stable transfection of activation-induced cytidine deaminase (AID) in hybridomas increased their frequency of switching to a level that greatly facilitated the isolation of subclones expressing monoclonal antibodies of different isotypes. Although forced expression of AID also increased the frequency of somatic hypermutation in the immunoglobulin variable regions that encode the antigen binding site, antigen recognition was retained in the isotype switched antibodies.
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