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Updated: Aug 10, 2026

Humanized NOD/SCID/IL2rγnull (hu-NSG) Mouse Model for HIV Replication and Latency Studies
Published on: January 7, 2019
Immunoglobulin heavy-chain receptor editing is observed in the NOD/SCID model of human B-cell development
1Program in Molecular Immunogenetics, Oklahoma Medical Research Foundation, 825 NE 13th Street, Oklahoma City, OK 73003, USA.
Receptor editing and receptor revision are the two mechanisms of antibody diversity that result in either complete V-gene replacement or the formation of hybrid V genes. We do not yet understand how this process unfolds, because they are rare and difficult to study in vivo. In this study, we describe a family of VH4-34:VH4-61 hybrids isolated from a human B-cell chimeric non-obese diabetic/severe combined immunodeficient mouse. The observation of hybrid immunoglobulin sequences in human B cells that developed in this model system makes it useful for the study of this mechanism of diversification and tolerance.
Receptor editing and receptor revision are the two mechanisms of antibody diversity that result in either complete V-gene replacement or the formation of hybrid V genes. We do not yet understand how this process unfolds, because they are rare and difficult to study in vivo. In this study, we describe a family of VH4-34:VH4-61 hybrids isolated from a human B-cell chimeric non-obese diabetic/severe combined immunodeficient mouse. The observation of hybrid immunoglobulin sequences in human B cells that developed in this model system makes it useful for the study of this mechanism of diversification and tolerance.
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