Disease relevance of Tcrb

• For this purpose, various genetically engineered immunodeficient mice were employed, including RAG-2 SCID, Igh-6 (B-cell deficient), Tcrb Tcrd (T-cell deficient) and Hc(0) (C5 deficient) [1].
• Using an in vitro coculture system, Vgamma1 T cells from Tcrb(-/- )mice were found to be activated by DC infected in vitro with BCG, as indicated by the elevated CD69 expression, IFN-gamma secretion and cytotoxic activity [2].
• Establishment of a Tcrb and Trp53 genes deficient mouse strain as an animal model for spontaneous colorectal cancer [3].
• Locus controlling Bordetella pertussis-induced histamine sensitization (Bphs), an autoimmune disease-susceptibility gene, maps distal to T-cell receptor beta-chain gene on mouse chromosome 6 [4].
• This deletion of T-cell receptor beta-chain segments occurs in a strain known to contribute to lupus-like autoimmune disease [5].

High impact information on Tcrb

• Molecular genetics of the T cell-receptor beta chain [6].
• A novel disulfide-linked heterodimer on pre-T cells consists of the T cell receptor beta chain and a 33 kd glycoprotein [7].
• Short sequences similar to those implicated in immunoglobulin gene and T cell receptor beta chain gene rearrangement flank the V and J segments of this family [8].
• The T cell receptor beta chain genes are located on chromosome 6 in mice and chromosome 7 in humans [9].
• Here we describe a CD3epsilon-associated complex on the facilitating cell surface that consists of the T-cell receptor beta-chain disulfide-linked to a previously unknown 33-kilodalton glycoprotein [10].

Biological context of Tcrb

• Synteny has been observed between a region of mouse chromosome 6 and the long arm of human chromosome 7 encompassing the markers Cpa, Tcrb and Try-1 [11].
• Consistent with previous reports, we show that the Raf-CAAX transgene does not inhibit Tcrb recombination in DN thymocytes [12].
• Transgenic mice were generated by co-injection of the human gene together with the mouse Tcrb enhancer [13].
• However, there was no evidence for Tcrb gene rearrangements in this organ [14].
• No polymorphism of the Tcrb haplotype was detected between H and L mice in all selections which were all found to be of the BALB/c type [15].

Anatomical context of Tcrb

• The Tcrb locus is also implicated, although there is no proof that the susceptibility gene in this region codes for the T-cell receptor [16].
• A functionally rearranged TCR beta (Tcrb) gene was isolated from a cloned human T helper cell recognizing the CS.T3 epitope of Plasmodium falciparum with HLA-DR2 [13].
• Cytolytic and IFN-gamma-producing activities of gamma delta T cells in the mouse intestinal epithelium are T cell receptor-beta-chain dependent [17].
• Intestinal microflora are necessary for development of spontaneous adenocarcinoma of the large intestine in T-cell receptor beta chain and p53 double-knockout mice [18].
• Pro-T cells in fetal thymus express c-kit and RAG-2 but do not rearrange the gene encoding the T cell receptor beta chain [19].

Associations of Tcrb with chemical compounds

• Protein tyrosine kinase p56lck controls allelic exclusion of T-cell receptor beta-chain genes [20].
• A serine/threonine phosphorylation site in the ectodomain of a T cell receptor beta chain is required for activation by superantigen [21].
• A mutational analysis of the binding of staphylococcal enterotoxins B and C3 to the T cell receptor beta chain and major histocompatibility complex class II [22].
• Increased frequency of 2,4,6-trinitrophenyl (TNP)-specific, H-2b-restricted cytotoxic T lymphocyte precursors in transgenic mice expressing a T cell receptor beta chain gene from an H-2b-restricted, TNP-specific cytolytic T cell clone [23].
• C5 cells were phenotypically Thy 1.2+ and Lyt 2.1+ with rearrangement of the T-cell receptor beta chain gene also being identified [24].

Physical interactions of Tcrb

• We analysed a restriction-fragment-length polymorphism of major histocompatibility complex class I and class II genes and T-cell receptor beta-chain genes in infected domestic rabbits [25].

Regulatory relationships of Tcrb

• In T-cell precursors, the T-cell-receptor beta chain is expressed before the T-cell-receptor alpha chain and is sufficient to advance T-cell development in the absence of T-cell receptor alpha chains [26].
• Antibodies to CD3 molecules inhibit full rearrangement of T-cell receptor beta chain genes in organ cultures of early embryo mouse thymus [27].
• Major histocompatibility complex products and endogenous retroviral gene products have both been shown to exert powerful influences on the frequency distribution of T-cell receptor beta-chain variable region families in the mouse [28].

Other interactions of Tcrb

• Restoration of early thymocyte differentiation in T-cell receptor beta-chain-deficient mutant mice by transmembrane signaling through CD3 epsilon [29].
• One of these haplotypes (Tcre alpha) appears to arise from a recombination between the Tcrb alpha and Tcra alpha haplotypes, the latter being the most frequently found in the conventional inbred strains [30].
• Tcrb and Tcrg gene polymorphism was investigated in high (H) and low (L) responder Biozzi mice from selection I, II, and GS by Southern blot analysis with appropriate V and C probes [15].
• None of the hybrids had rearranged the Tcrb gene cluster and 13 contained DJ rearrangements at the Igh locus [14].
• The map location of this cluster between IgK and Tcrb coincides with the morphological mutation hypodactyly (Hd) [11].

Analytical, diagnostic and therapeutic context of Tcrb

• The role of gamma delta T cells was then investigated using transgenic donors (C57BL/6 x 129 background) in which a portion of the T-cell receptor-beta chain gene was deleted by gene targeting so that these mice lack alpha beta T cells [31].
• None of the alphabeta T cell-deficient recipient mice (T cell receptor beta chain knockout mice) experienced allograft rejection with follow-up ranging from 8 to 28 days [32].
• The repertoire of tissue-infiltrating T cells was assessed for the presence of dominant T cell populations by using T cell receptor beta-chain-specific PCR followed by sequencing [33].
• We applied reverse transcription-polymerase chain reaction (RT-PCR) with family specific primers for monkey T cell receptor beta chain V regions and single-strand conformation polymorphism (SSCP) analysis to analyze the expanded T cell clones in cynomolgus monkeys (Macaca fascicularis) [34].
• Expression of a transgenic T cell receptor beta chain enhances collagen-induced arthritis [35].

References