Disease relevance of Igh-V

• Tubular antigen-derivatized cells induce a disease-protective, antigen-specific, and idiotype-specific suppressor T cell network restricted by I-J and Igh-V in mice with experimental interstitial nephritis [1].
• B cell hyperactivity, hypergammaglobulinemia, and autoantibody expression, the hallmarks of systemic lupus erythematosus, might be associated with structural abnormalities within the Ig heavy chain variable region (Igh-V) gene complex [2].
• Our study showed that the Igh-V loci from lupus and haplotype-matched nonlupus mice resulted in essentially identical restriction fragment patterns, a finding which suggests that the Igh-V gene complex does not carry a primary defect responsible for autoimmune disease [2].
• Investigations into the nature of Igh-V region-restricted T cell interactions by using antibodies to antigens on methylcholanthrene-induced sarcomas. I. Analysis of an Igh-V-restricted suppressor-inducer factor [3].
• Fine specificity of the immune response to oxazolones III. Antibodies but not contact sensitivity specific for 2-furyloxazolone are controlled by an Igh-V gene in the mouse [4].

Psychiatry related information on Igh-V

• We therefore evaluated the role of two possible Igh-V region-linked gene products in BCL1 growth inhibition; namely, an Igh-V region-linked minor H antigen or alternatively the BCL1 IgM idiotype (Id) [5].

High impact information on Igh-V

• Igh-V or closely linked gene(s) control immunological memory to a thymus-independent antigen [6].
• Contribution of immunoglobulin heavy-chain variable-region genes to antibody diversity [7].
• Receptor revision of immunoglobulin heavy chain variable region genes in normal human B lymphocytes [8].
• The Ts-2 cell is functionally restricted in its suppressive effect by I-J and Igh-V gene products, and acts on the effector limb of the cell-mediated anti-tubular basement membrane immune response [1].
• We have previously described an idiotype (Id460) that transiently dominates anti-2,4-dinitrophenyl (DNP) antibody responses of mice that possess the appropriate Igh-V and V kappa genotypes [9].

Biological context of Igh-V

• These results suggest that the MRL substrains and their LG parent are haplotype j at the Igh-V locus [10].
• The Igh-V locus of MRL mice: restriction fragment length polymorphism in eleven strains of mice as determined with VH and D gene probes [10].
• This map confirms genetically the localization of the Igh-V gene complex distal to Igh-C on the chromosome [11].
• The major determinant for the antibody production was encoded in Igh-C, but not in Igh-V [12].
• This determinant specific immunodeficiency suggests the existence of as yet unknown regulatory influences on Igh-V gene expression or B cell activation [13].

Anatomical context of Igh-V

• Therefore, it can be suggested that the two genes coding for the T cell allodeterminants (distinct from those of the B cell Igh) are located in the right side of the B cell Igh-V on the 12th chromosome, and that both encode the antigen-recognition units of the functionally distinct T cell factors [14].
• Detection of one site, HS1, is restricted to pro-B cell lines and HS1 is accessible to restriction enzyme digestion exclusively in normal pro-B cells, the stage defined by actively rearranging Igh-V loci [15].
• These results demonstrate clearly that the Ly-1 TsiF from allogeneic bone marrow chimeras are donor Igh-V-restricted and are not influenced by the recipient micro-environment, presumably that provided by the thymuses of the recipient mice [16].
• It may be considered surprising to find a structure in the thymus that acts to select MHC-positive molecules that see Igh-V-linked structures as self [17].
• T suppressor cells activated by anti-Tsud serum are Igh-V-restricted [18].

Associations of Igh-V with chemical compounds

• Homologies between cell interaction molecular controlled by major histocompatibility complex- and Igh-V-linked genes that T cells use for communication. Tandem "adaptive" differentiation of producer and acceptor cells [19].
• The antibody did not bind to the human blood group B glycolipid, Gal alpha 1-3(Fuc alpha 1-2)Gal beta 1-4GlcNAc beta 1-3Gal beta 1-4Glc1-1Cer, and, therefore, branching at the penultimate galactose blocks Gal-13 binding [20].
• To have a means for exploring this possibility and for studying the species and tissue distribution of this epitope we have raised a monoclonal antibody (Gal-13) which specifically binds to glycoconjugates with a nonreducing terminal Gal alpha 1-3Gal disaccharide [20].
• Gal-13 has been used to demonstrate that the Gal alpha 1-3Gal ceramide pentahexoside has been evolutionarily conserved in red cells of animals up to the stage of New World monkeys but is not found in Old World monkey red cells.(ABSTRACT TRUNCATED AT 400 WORDS)[20]
• Other Gal alpha 1-3Gal glycosphingolipids with an isogloboside or globoside core structure were not recognized by Gal-13 suggesting that the antibody binds to Gal alpha 1-3Gal carried by a lactosamine core structure [20].

Other interactions of Igh-V

• On the basis of these results the Igh-Ox marker is tentatively placed between Igh-C and the rest of the Igh-V markers [21].
• Deletion mapping of the mouse ornithine decarboxylase-related locus Odc-rs8 within Igh-V [22].
• There is extensive restriction fragment length polymorphism among the strains analyzed allowing the assignment of complete (Igh-V + Igh-C) Igh haplotypes for eighteen inbred mouse strains [23].
• The patterns of inheritance of these markers in backcross progeny and recombinant inbred mouse strains allowed their localization with respect to previously mapped genes to yield the linkage map: Aat-15.8 cM-Ck-3-0.9 cM-(Crip, Akt, Igh-C)-0.3 cM-(D12N1, Igh-V) [11].
• The restriction fragment length polymorphism of probes derived from the Igh-V, Igk-V, Tcr alpha-C loci and of the long terminal repeat of the mouse mammary tumour virus revealed that NZB/BlLwPtIbm were grossly different from NZB/BlNJ and NZB/BlOla [24].

Analytical, diagnostic and therapeutic context of Igh-V

• Seven families of Igh-V genes have been defined by Southern blot analysis of genomic DNA from eighteen inbred strains of mice [23].
• Adoptive transfer experiments between major histocompatibility complex and allotype congenic strains of mice allowed demonstration of both Igh-V and I-A restrictions in the transfer of this cell population [25].
• The extent of a-gal epitope expression on cells correlates with the subsequent inhibition of M86 binding in ELISA [26].
• The mouse IgM M86 monoclonal antibody, which was highly specific for alpha-Gal epitopes, was used to document alpha-Gal epitope expression by immunostaining of tissues and immunofluorescence [27].
• Three different anti-I-Jk mAbs (1G8, 4B11, and KN34) showed different inhibitory patterns in allogeneic mixed lymphocyte reactions of individual H-2k strains, depending on the H-2 and immunoglobulin heavy chain variable region (IgVH) genes possessed by the stimulator strains [28].

References