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Gene Review

Ts  -  tail-short

Mus musculus

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Disease relevance of Ts

 

Psychiatry related information on Ts

  • Being able to identify the pathogenic idiotype allowed us to generate T suppressor (Ts) cells specific for the 16/6 Id [5].
 

High impact information on Ts

  • The mouse mutant tail-short (Ts) which maps to the homologous syntenic region on mouse chromosome 11, displays some of the features of CMPD1 [6].
  • Conversely, as T-suppressor (Ts) and T-proliferative (Tp) cells almost invariably seem to recognize distinct, non-overlapping determinants on protein antigens, suppressor-mediated tolerance should not be affected by substitutions in the proliferative T-cell epitope [7].
  • These T suppressor cells (Ts) inhibit various lymphoid functions-this either reflects their polyclonal origin or indicates that the structures recognized by the Ts receptors must be common for many cell types [8].
  • The dominant determinant seems to exist on the peptide CB-2-3 (residues 3-187), and presumably is destroyed by its cleavage at Met 92; the Th cells that it induces are suppressible by each of the Ts-inducing peptides [2].
  • A final implication of these results is that, not only does the existence of a Th-inducing determinant depend on its being an appropriate distance from a B cell epitope, but the existence of Ts-inducing determinants likewise depends on the existence of a neighboring Th-B cell association [2].
 

Chemical compound and disease context of Ts

 

Biological context of Ts

  • In addition, the Rbt mutant displays strong similarities to the phenotype observed in Ts (Tail-short), indicating also a homeotically transformed phenotype in these mice [13].
  • Six microsatellite markers were co-localized to the Ts locus, providing reagents for positional cloning of Ts [14].
  • Fetal erythropoiesis and hemoglobin ontogeny in tail-short (Ts/+) mutant mice [1].
  • Changes in proportions of embryonic hemoglobins during fetal development are similar in Ts/+ and +/+ fetuses at day 12 and later of gestation [1].
  • We planned to map the gene(s) that controls strain differences in the viability of the Ts heterozygotes [15].
 

Anatomical context of Ts

  • Mutant Ts/+ fetuses are developmentally retarded as compared to normal +/+ littermates [1].
  • Moreover, adult hemoglobin is detected in circulating primitive nucleated erythrocytes in the developmentally retarded Ts/+ mutant fetuses at about the same chronologic age as their +/+ normal littermates [1].
  • In both the Patch and Tail-short embryos the notochord was also deflected from its medial position [16].
  • The Ts hybridomas were I-A restricted, as are many T helper cells [17].
  • Both the Ts hybridoma cells and a suppressor factor (TsF) inhibited in an antigen-specific and I-Ak-restricted fashion the in vitro proliferative response of BSA-immunized lymph node cells [17].
 

Associations of Ts with chemical compounds

  • These results indicate that oral administration of a thymic-dependent antigen (SRBC) to LPS-responsive mice induced a Ts cell population in PP, which, after migration to peripheral lymphoid tissue (e.g., spleen), suppressed responses to systemically administered antigen [18].
  • Treatment of mice with i.p. administration of 20 mg/kg of cyclophosphamide 2 days before EC harvesting abrogates the ability of HD-EC from these mice to induce Ts cell formation [19].
  • There was no inhibitory effect of the sterol on Ts or B cell activity [20].
  • These experiments illustrate the contribution of external (HA and NA) as well as internal (M + NP) viral proteins to Ts cell generation and function [21].
  • The addition of IL 1 to cultures of DNBS-tolerant cells and glutaraldehyde fixed DNP-SC restored the ability of the Ts to release the synthesized factor [9].
 

Regulatory relationships of Ts

  • Exposure to either anti-CD8 or anti-CD4 mAb in vitro or in vivo leads to loss of the capacity of Ts to induce Igh-1b allotypic suppression [22].
  • IL-2 but not IL-1 was able to stimulate the Ts to release synthesized SSF in the absence of L3T4+ TH activity [23].
  • One factor (TsF-A) shares Mhc determinants with the A alpha A beta molecule and suppresses proliferating Th cells; the other (TsF-E) shares determinants with the E alpha E beta molecule and it inhibits the maturation of the T suppressor (Ts) cells [24].
 

Other interactions of Ts

  • This indicates that Rbt and Ts may be allelic mutations [13].
  • The Ts locus was mapped within a shorter interval of approximately 3 cM between D11Mit128 and D11Mit203 [13].
  • We present here detailed mapping of Ts locus relative to the Sox9, using an intersubspecific cross [14].
  • A further nine recombinants were detected between Ts and the polycomb-like gene M33, suggesting that these loci are separated by 1.8 +/- 0.011 cM [14].
  • A spontaneous morphological mutation characterized by a short and kinky tail (Tail-short Shionogi: Tss) was observed in a BALB/cMs mouse breeding colony [25].
 

Analytical, diagnostic and therapeutic context of Ts

  • The expression pattern and chromosomal location of Sox9 suggest that it may be the gene defective in the mouse skeletal mutant Tail-short, a potential animal model for campomelic dysplasia [26].
  • LPS-nonresponsive mice lack this Ts cell pathway and continually respond to oral administration of antigen [18].
  • Southern blot analysis with a probe specific for genes encoding the beta chain of the T cell receptor on T helper and T killer cells revealed no rearrangement of the beta genes in the Ts cells [17].
  • Normal PBM were fractionated into B, TH and T suppressor/cytotoxic (Ts) cells by fluorescence-activated cell sorting techniques [20].
  • Intravenous administration of hapten-coupled, high-density (density greater than 1.077) epidermal cells (HD-EC) to mice results in the appearance of transferable splenic T suppressor (Ts) cells as assayed in adoptive transfer experiments [19].

References

  1. Fetal erythropoiesis and hemoglobin ontogeny in tail-short (Ts/+) mutant mice. Brotherton, T.W., Chui, D.H., McFarland, E.C., Russell, E.S. Blood (1979) [Pubmed]
  2. Repertoires of T cells directed against a large protein antigen, beta-galactosidase. II. Only certain T helper or T suppressor cells are relevant in particular regulatory interactions. Krzych, U., Fowler, A.V., Sercarz, E.E. J. Exp. Med. (1985) [Pubmed]
  3. Selective inhibition of the generation of T suppressor cells of contact sensitivity in vitro by interferon. Knop, J., Taborski, B., DeMaeyer-Guignard, J. J. Immunol. (1987) [Pubmed]
  4. Isolation and characterization of in vitro and in vivo functions of a tumor-specific T suppressor cell clone from a BALB/c mouse bearing the syngeneic ADJ-PC-5 plasmacytoma. Haubeck, H.D., Kölsch, E. J. Immunol. (1985) [Pubmed]
  5. Pathogenic idiotypes of autoantibodies in autoimmunity: lessons from new experimental models of SLE. Shoenfeld, Y., Mozes, E. FASEB J. (1990) [Pubmed]
  6. Assignment of an autosomal sex reversal locus (SRA1) and campomelic dysplasia (CMPD1) to 17q24.3-q25.1. Tommerup, N., Schempp, W., Meinecke, P., Pedersen, S., Bolund, L., Brandt, C., Goodpasture, C., Guldberg, P., Held, K.R., Reinwein, H. Nat. Genet. (1993) [Pubmed]
  7. Neonatal T-cell tolerance to minimal immunogenic peptides is caused by clonal inactivation. Gammon, G., Dunn, K., Shastri, N., Oki, A., Wilbur, S., Sercarz, E.E. Nature (1986) [Pubmed]
  8. Selective inhibition of T suppressor-cell function by a monosaccharide. Koszinowski, U.H., Kramer, M. Nature (1981) [Pubmed]
  9. Soluble factors in tolerance and contact sensitivity to DNFB in mice. VI. Cellular and lymphokine requirements for stimulating suppressor factor production in vitro. Fairchild, R.L., Moorhead, J.W. J. Immunol. (1986) [Pubmed]
  10. Effect of methanol extraction residue tubercle bacillus fraction treatment in vivo and in vitro on the release and activity of suppressor factor inhibiting the efferent phase of contact sensitivity in mice. Zimber, C., Ben-Efraim, S., Weiss, D.W. Cell. Immunol. (1985) [Pubmed]
  11. Soluble factors in tolerance and contact sensitivity to DNFB in mice. VIII. Regulation of T suppressor cell function by autoreactive T helper cells. Fairchild, R.L., Moorhead, J.W. Cell. Immunol. (1988) [Pubmed]
  12. Maternal treatment with teratogen causes congenital malformations in mouse embryos. Matta, C.A. Folia morphologica. (1990) [Pubmed]
  13. Rbt (Rabo torcido), a new mouse skeletal mutation involved in anteroposterior patterning of the axial skeleton, maps close to the Ts (tail-short) locus and distal to the Sox9 locus on chromosome 11. Hustert, E., Scherer, G., Olowson, M., Guénet, J.L., Balling, R. Mamm. Genome (1996) [Pubmed]
  14. Exclusion of Sox9 as a candidate for the mouse mutant tail-short. Uchida, K., Koopman, P., Mita, A., Wakana, S., Wright, E., Kikkawa, Y., Yonekawa, H., Moriwaki, K., Shiroishi, T. Mamm. Genome (1996) [Pubmed]
  15. Dominant lethality of the mouse skeletal mutation tail-short (Ts) is determined by the Ts allele from mating partners. Ishijima, J., Yasui, H., Morishima, M., Shiroishi, T. Genomics (1998) [Pubmed]
  16. Abnormal development of the notochord and perinotochordal sheath in duplicitas posterior, patch and tail-short mice. Center, E.M., Marcus, N.M., Wilson, D.B. Histol. Histopathol. (1988) [Pubmed]
  17. Antigen-specific, I-A-restricted suppressor hybridomas with spontaneous cytolytic activity. Functional properties and lack of rearrangement of the T cell receptor beta chain genes. Blanckmeister, C.A., Yamamoto, K., Davis, M.M., Hämmerling, G.J. J. Exp. Med. (1985) [Pubmed]
  18. Lack of oral tolerance in C3H/HeJ mice. Kiyono, H., McGhee, J.R., Wannemuehler, M.J., Michalek, S.M. J. Exp. Med. (1982) [Pubmed]
  19. Epidermal cells in activation of suppressor lymphocytes: further characterization. Granstein, R.D., Askari, M., Whitaker, D., Murphy, G.F. J. Immunol. (1987) [Pubmed]
  20. 1,25-Dihydroxyvitamin D3 suppresses human T helper/inducer lymphocyte activity in vitro. Lemire, J.M., Adams, J.S., Kermani-Arab, V., Bakke, A.C., Sakai, R., Jordan, S.C. J. Immunol. (1985) [Pubmed]
  21. Influenza-specific suppression: contribution of major viral proteins to the generation and function of T suppressor cells. Hurwitz, J.L., Hackett, C.J. J. Immunol. (1985) [Pubmed]
  22. T cell-induced Ig allotypic suppression in mice. II. Both CD4+ CD8- and CD4- CD8+ T cell subsets from sensitized Igha mice are required to induce suppression of Igh-1b allotype expression. Benaroch, P., Bordenave, G. J. Immunol. (1989) [Pubmed]
  23. Soluble factors in tolerance and contact sensitivity to DNFB in mice. X. IL-2 is the activation signal mediating release of synthesized suppressor factor. Fairchild, R.L., Moorhead, J.W. Cell. Immunol. (1991) [Pubmed]
  24. Manipulation of anti-LDH-B response by T suppressor factors. Ikezawa, Z., Nagy, Z.A., Klein, J. J. Immunol. (1984) [Pubmed]
  25. Tss (Tail-short Shionogi), a new short tail mutation found in the BALB/cMs strain, maps quite closely to the Tail-short (Ts) locus on mouse chromosome 11. Tsukahara, K., Hirasawa, T., Makino, S. Exp. Anim. (2000) [Pubmed]
  26. The Sry-related gene Sox9 is expressed during chondrogenesis in mouse embryos. Wright, E., Hargrave, M.R., Christiansen, J., Cooper, L., Kun, J., Evans, T., Gangadharan, U., Greenfield, A., Koopman, P. Nat. Genet. (1995) [Pubmed]
 
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