Disease relevance of p-AZOBENZENEARSONATE

• Mice of 10 inbred strains were immunized with a protein conjugate of a hapten of p-azobenzenearsonate coupled to the carbon atom 5 of hydroxphenylacetic acid (ABA-HOP), and anti-ABA-HOP titers were determined by the haptenated phage inactivation [1].
• Serum samples and hybridoma cell lines derived from non-immune as well as Ars-keyhole limpet haemocyanin (KLH)-immunized Id/lpr mice were monitored for idiotype expression as well as Ars and ssDNA reactivity at various stages of disease progression [2].

Psychiatry related information on p-AZOBENZENEARSONATE

• Using two polyclonal (rabbit) and two monoclonal anti-idiotype (anti-Id) reagents, we investigated structural correlates of the Id of mAb 36-71, a somatically mutated member of the CRIA Id family that has an exceptionally high affinity for the p-azobenzenearsonate (Ars) hapten [3].

High impact information on p-AZOBENZENEARSONATE

• The T cell receptor V alpha 3 gene segment is associated with reactivity to p-azobenzenearsonate [4].
• We have tested several structurally related haptens, conjugated to ovalbumin, for their effect on activation of an inducer T-cell clone reactive to the p-azobenzenearsonate (arsonate) hapten [5].
• The heavy-chain gene is derived from an A/J mouse hybridoma cell line 36-65 whose antibody product (gamma 1, kappa) is specific for the hapten azophenylarsonate [6].
• Expression of a heavy chain variable region (VH) gene segment that partially encodes a V region structure that dominates the immune response to para-azophenylarsonate (Ars) in strain A mice was examined in the B cell population of Ars nonimmune mice [7].
• At day 13, a significant fraction of E4+ cells had mutations known to increase antibody affinity for Ars, suggesting they were products of at least one cycle of post-mutational antigen-driven selection [8].

Biological context of p-AZOBENZENEARSONATE

• Inducer T-cell clones reactive to the p-azobenzenearsonate (arsonate) hapten possess binding sites for radioactive arsanylated proteins, which are not present on clones with other antigen specificities [9].
• In vivo challenge of dHGG-treated adult animals with hapten-coupled HGG (p-azophenylarsonate [ARS]-HGG) induced a significant ARS-specific antibody response, suggesting that tolerance induction in this model does not completely abrogate tolerogen-specific Th activity in vivo [10].
• To characterize the light chain gene segments involved in the murine immune response to keyhole limpet hemocyanin p-azophenylarsonate (Ars), we have determined the amino acid and/or nucleotide sequences of several anti-arsonate antibodies of the Ars-A family in the A/J, C.AL-20, and BALB/c strains [11].
• These mutants both contained amino acid substitutions from Asn to Ser or Thr at VH CDR1 position 35, a putative Ars contact residue [12].
• In an effort to address this issue directly, we "randomly" introduced point mutations throughout the length of the VH region of an anti-p-azophenylarsonate (Ars) Ab expressed as an Fab in the phage display format [12].

Anatomical context of p-AZOBENZENEARSONATE

• The V regions expressed by hybridomas in both of these groups had 2- to 30-fold greater affinity for Ars than their unmutated precursors, despite the fact that the transgene-encoded precursors had 100-fold higher affinity than their endogenous counterparts [13].
• Ubiquitous nonimmunoglobulin p-azobenzenearsonate-binding molecules from lymphoid cells [14].
• We describe clones of hapten-specific inducer T cells from (BALB/c X A/J)F1 mice that respond to the p-azobenzenearsonate hapten conjugated to carrier proteins or directly conjugated to antigen-presenting cells [15].
• Idiotype connectance in the immune system. II. A heavy chain variable region idiotope that dominates the antibody response to the p-azobenzenearsonate group is a minor idiotope in the response to trinitrophenyl group [16].
• Antigen- and receptor-driven regulatory mechanisms. VIII. Suppression of idiotype-negative, p-azobenzenearsonate-specific T cells results from the interaction of an anti-idiotypic second-order T suppressor cell with a cross-reactive-idiotype-positive, p-azobenzenearsonate-primed T cell target [17].

Gene context of p-AZOBENZENEARSONATE

• VHIdCR-expressing hybridomas were derived from the Ars-primed, Sulf-boosted original antigenic sin response of A/J mice at various times after Ars priming, and the properties of the antibodies they express and the structure of the genes encoding these antibodies were characterized [18].
• One subpopulation occurs naturally in normal sera from strain A mice, is found mainly on IgG2 and IgG3 subclasses, does not bind p-azobenzenearsonate (ABA)+, does not express CRI5Ci, and can be selectively stimulated by low doses of antiidiotype antibody (AD8) [19].
• Immune response to the p-azobenzenearsonate (ABA)-GAT conjugate. II. Hapten-specific T cells induced with ABA-GAT in GAT responder X nonresponder F1 hybrids are restricted to the nonresponder haplotype [20].
• The T cell repertoire of BALB/c mice contains clones capable of recognizing p-azobenzenearsonate (ABA)-tyrosine (Tyr) in association with both I-A and I-E-encoded class II molecules [21].
• As expected, the expressed IgG2b anti-Ars antibodies with selected V region gene pairs were shown to have V region sequences and Ars-binding characteristics similar to those of anti-Ars hybridoma antibodies [22].

References