Disease relevance of Scl22

• It was concluded that the rIL-4 effect was probably by inhibition of Tc1 cells, which normally mediate the glomerular injury that results in proteinuria [1].
• In this work, we report the cloning and characterization of the first cell surface casein kinase II (CKII) substrate (Tc-1) of Trypanosoma cruzi, the causative agent of Chagas' disease [2].
• Neonatal tolerance to a Th2-mediated autoimmune disease generates CD8+ Tc1 regulatory cells [3].
• Immunochemical analysis of solubilized cell membranes of the lymphoma G1-Tc1 demonstrates that the 1F2 antibody recognizes an epitope on a retroviral gp 70 envelope protein [4].
• A Gross virus induced rat T cell lymphoma G1-Tc1 and a Moloney virus induced mouse T cell lymphoma YAC-1 are shown to exert a strong cytotoxic activity against rat yolk sac tumours but not to various types of rat, mouse or human normal cells or tumour cell lines including carcinomas, sarcomas, lymphomas and gliomas [4].

High impact information on Scl22

• Il-4 therapy prevents the development of proteinuria in active Heymann nephritis by inhibition of Tc1 cells [1].
• Analysis of the translated amino acid sequence indicates that the Tc-1 gene has a putative transmembrane domain with multiple cytoplasmic and extracellular CKII phosphosites [2].
• Exogenous human CKII was able to phosphorylate serine residues on both recombinant Tc-1 and Tc-1 of intact trypomastigotes [2].
• At the amino acid level, Tc-1 displayed 95% and 99% identity to two hypothetical proteins recently reported by the T. cruzi genome project [2].
• Upon mercury recall, CD8+ CD45RC(high) T cells, that represent the Tc1 subset in the rat, expanded and were polarized towards IFNgamma production [3].

Biological context of Scl22

• We report here that resistance to mercury disease is long lasting and not mercury-specific, suggesting that different CD8+ T cells are involved in resistance and neonatal tolerance, and that regulatory CD8+ Tc1 cells generated in tolerance are required to control the CD8- cell population from developing Th2-mediated autoimmunity [3].
• Tc maintained bone formation indices almost at Ova level, and only decreased mineral apposition rate (MAR) in Tc1 group, and declined bone resorption perimeter [5].

Anatomical context of Scl22

• A rat B cell hybridoma was established from a Wistar/Furth (WF) rat immunized with the syngeneic lymphoma G1-Tc1 producing an immunoglobulin (Ig)G2c monoclonal antibody (MoAb) 1F2 [4].

Associations of Scl22 with chemical compounds

• METHODS: Forty 3-month-old rats were randomly divided into 5 groups: sham group, Ova group, Tc1 group (1.2 mg/kg/d), Tc2 group (4.8 mg/kg/d), and estrone group (1.48 mg/kg/d), oral fed for 3 months [5].

Analytical, diagnostic and therapeutic context of Scl22

• Southern blot analysis indicates that Tc-1 is a single-copy gene [2].
• Molecular cloning of a Trypanosoma cruzi cell surface casein kinase II substrate, Tc-1, involved in cellular infection [2].

References