Analyze natively paired murine Heavy and Light chain variable domains from single-cell B-cell RNA-seq (10x Genomics scVDJ), well-indexed hybridoma plate assays, or paired antibody tables. Computes paired V(D)J germline calls, paired VH family × VL family pairing matrix, paired CDR3 lengths, and somatic hypermutation across both chains simultaneously.
Execute high-throughput repertoire profiling across large multi-FASTA, AIRR TSV, or mouse SRA/ERR datasets. Computes global Dildrop VH and J family usage distributions, CDR3 length histograms, somatic hypermutation divergence, and kappa-to-lambda ratios.
| Gene ID | Chain / Locus | Family | IMGT Ref | Kabat Name | Class | CDR1 / CDR2 | Actions |
|---|
Curated collection of the most consequential hybridomas and antibodies in the history of immunology. Includes the foundational B1-8 anti-NP model (Bothwell & Rajewsky), the original MOPC-21 myeloma (Köhler & Milstein), the 17.2.25 quasi-monoclonal mouse (Cascalho & Wabl), the 2B8 parent of Rituximab, OKT3 (Muromonab-CD3), and the classic S107 / TEPC-15 antiphosphorylcholine T15 idiotype.
| Accession | Clone Name | Strain | Isotype | Mapped V | Mapped J | SHM Identity | Boundary | Target Antigen | Scientific Significance |
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In 1975, Georges Köhler and César Milstein published their landmark paper in Nature describing continuous cultures of fused cells secreting antibody of predefined specificity. By fusing sheep red blood cell-primed BALB/c splenocytes with the P3-X63-Ag8 myeloma line (derived from MOPC-21), they founded hybridoma technology, transforming immunology, molecular biology, and modern biotherapeutics.
Renate Dildrop's seminal 1984 classification established the canonical murine VH gene family nomenclature: J558 (VH1, Clan I), 7183 (VH5, Clan III), Q52 (VH2, Clan II), S107 (VH7), 36-60 (VH9), 3609 (VH3), and X24 (VH10). This framework provided the structural taxonomy for all subsequent murine immunoglobulin genetics and remains the gold standard in comparative immunology.
The B1-8 murine hybridoma (specific for the (4-hydroxy-3-nitrophenyl)acetyl [NP] hapten) and its V186.2 variable gene provided the experimental foundation for elucidating somatic hypermutation and affinity maturation in B-cells. The single amino acid replacement Trp33Leu (W33L) in CDR1 demonstrated how somatic point mutations drive ten-fold increases in antigen binding affinity during the germinal center reaction.
Created the quasi-monoclonal (QM) mouse from the rearranged 17.2.25 anti-NP heavy chain gene, demonstrating how targeted gene replacement and receptor editing maintain immunological tolerance and diversify primary B-cell repertoires in vivo.
From the pioneering 1970 variability metric and first antibody databases of Wu & Kabat, to the rigorous standardized immunogenetic numbering of Marie-Paule Lefranc (IMGT), and the automated alignment and somatic hypermutation analysis developed by Werner Müller (DNAPLOT) and Ida Retter (VBASE2), VBASE3 stands upon five decades of open comparative immunoinformatics.