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E Padlan

Publications and source records attributed to E Padlan.

6 recordsLinked to original sources

Structural correlates of an anticarcinoma antibody: identification of specificity-determining residues (SDRs) and development of a minimally immunogenic antibody variant by retention of SDRs only.

Clinical utility of murine mAbs is limited because many elicit Abs to murine Ig constant and variable regions in patients. An Ab humanized by the current procedure of grafting all the complementarity determining regions (CDRs) of a murine Ab onto the human Ab frameworks is likely to be less immunogenic, except that its murine CDRs could still evoke an anti-variable region response. Previous studies with anticarcinoma mAb CC49 showed that light chain LCDR1 and LCDR2 of humanized CC49 could be replaced with the corresponding CDRs of a human Ab with minimal loss of Ag-binding activity. The studies reported in this paper were undertaken to dissect the CC49 Ag-binding site to identify 1) specificity determining residues (SDRs), the residues of the hypervariable region that are most critical in Ag-Ab interaction, and 2) those residues that contribute to the idiotopes that are potential targets of patients' immune responses. A panel of variants generated by genetic manipulation of the murine CC49 hypervariable regions were evaluated for their relative Ag-binding affinity and reactivity to sera from several patients who had been immunized with murine CC49. One variant, designated HuCC49V10, retained only the SDRs of CC49 and does not react with the anti-variable region Abs of the sera from the murine CC49-treated patients. These studies thus demonstrate that the genetic manipulation of Ab variable regions can be accomplished by grafting only the SDRs of a xenogeneic Ab onto human Ab frameworks. This approach may reduce the immunogenicity of Abs to a minimum.

Amino Acid Sequence↗

The B-cell binding site on human immunoglobulin E.

Immunoglobulin E comprises the main immunoglobulin class associated with allergy. Its multifarious activities are mediated by two types of Fc receptors found on different cell populations, Fc epsilon R1 on mast cells and basophils, and Fc epsilon R2 on inflammatory cells (monocytes, eosinophils and platelets) and B lymphocytes. Recombinant epsilon-chain fragments synthesized in Escherichia coli have provided the means of mapping the receptor-binding sites on human IgE, and blocking IgE-receptor interactions. We have previously shown that the Fc epsilon R1 binding site is contained within a sequence (Gln 301-Arg 376) spanning the C epsilon 2 and C epsilon 3 domains. Here we show that Fc epsilon R2 can recognize a motif in the C epsilon 3 domain that is formed on dimerization of one or both of the flanking (C epsilon 2 and C epsilon 4) domains. Glycosylation of IgE is not required for the activity of either receptor.

Antibodies, Monoclonal↗

The mast cell binding site on human immunoglobulin E.

Antibodies of the immunoglobulin E isotype sensitize mast cells and basophils for antigen-induced mediator release by binding through the Fc portion to a high-affinity receptor (Fc epsilon R1, Ka = 10(9)M-1) on the cell surface causing the clinical manifestations of type I hypersensitivity. As the amino acid sequence of the human epsilon chain is now known, attempts have been made to map the Fc epsilon R1 binding site on IgE to a fragment smaller than Fc epsilon using proteolytic cleavage products, none of which proved to be active. Cleavage between the C epsilon 2 and C epsilon 3 domains released two inactive fragments, suggesting that the junction between these segments could be important in receptor binding. This region is protected against protease digestion in the rat IgE complex with the receptor of rat basophilic leukaemia cells. Here we report the mapping of the mast cell receptor binding site on human IgE to a sequence of 76 amino acids at the C epsilon 2/C epsilon 3 junction. Recombinant peptides containing this sequence inhibit passive sensitization of skin mast cells in vivo and sensitize mast cells to degranulation by anti-IgE in vitro almost as efficiently as a myeloma IgE. Fragments containing the separate domains are inactive. Additional sequences are required for rapid assembly of fragments into disulphide-linked dimers, suggesting that a single chain can form the active site. In a three-dimensional model of the human Fc epsilon, the two identical segments are far apart. Each folds to generate a cleft between the C epsilon 2 and C epsilon 3 domains on the surface of the Fc epsilon. The docking of IgE on to mast cells could take place within this cleft.

Amino Acid Sequence↗

Localized deletion-insertion mutations: a major factor in the evolution of immunoglobulin structural variability.

New and previously published amino acid sequences of mouse Vk chains completed to Trp35 were examined. This sequence includes a framework loop from NH2 to Cys23 and an antigen contacting complementarity region L1 which lies between Cys23 and Trp35. There are many different sequence variations from NH2 to Cys23 among BALB/c mouse Vk chains indicating multigenic control. Coordinately there is a remarkable structural heterogeneity of L1 size and sequence. Thus far chains with the same NH2-Cys23 sequence have similar sized L1, which suggests a close relationship between L1 size and characteristic NH2-Cys23 sequence. In this multigenic system selection for chains with size variations in L1 appears to have occurred. The mutational process that inserts or deletes triplets in this region is thought to be exploited in the derivation of new useful structural genes.

Amino Acid Sequence↗