In lupus, anti double strand DNA and anti Sm distinguishes it from scleroderma, where the profile is anti DNA topoisomerase 1 and anti centromere proteins. The autoantigensare cell components involved in universal and basic GSK-3 inhibition gene expression pathways, such as Sm in precursor mRNA splicing and DNA topoisomerase 1 in DNA replication and transcription. Features of autoantibodies in cancer: Autoantibodies in cancer target intracellular molecules referred to as TAAs. As in rheumatic disorders, no individual autoantibody antigen system has sensitivity and specificity to serve as a stand alone diagnostic marker. Most tumors show multiple antibody specificities and with panels of TAA anti TAAs the cumulative sensitivity and specificity reaches diagnostic significance.
Different tumorigenesis pathways are activated in similar cell type tumors from the same organ and are the driving mechanisms IEM 1754 697221-65-1 behind the autoantibody response. The immune responses are directed to products of oncogenes and tumor suppressor genes such as p53 and other proteins that regulate and modulate the functions of p53. Protein phosphatase 2A is an important tumor suppressor protein. It is a serine/threonine phosphatase and is a trimeric complex. The B subunit is recruited from several intracellular proteins and the type of B subunit determines the substrate of its tumor suppressor activity. One of the B subunits, p90, was identified in our laboratory with autoantibody from a patient with hepatocellular carcinoma. It was found to co immunoprecipitate with other subunits of PP2A and was shown to function as an inhibitor of the tumor suppressor activity of PP2A.
The immune system is capable of sensing dysregulation of tumorigenesis pathways. The goal of continuing research is in developingTAA anti TAAs for detecting cancer in individual patients and profiles which are common to specific types of tumors. Understanding etiology and molecular pathogenesis of rheumatoid arthritis is key Meristem to the development of precise prevention and curative therapy for this disease. Recent progress on how genes and environment interact in causing immune reactions that may induce arthritis in humans as well as in mice, have provided a conceptual basis for the development of new prevention and treatment strategies which need to be different for different subsets of RA.
In order to bring this emerging knowledge to chemical catalogs the level where basic and clinical academic science can collaboratewitj industry for rapid development of the potential new therapies, there is a need for closer collaboration between basic and clinical scientists from many centers, and for increased collaboration between industry and academia in translational medicine. In Europe, both the EU funded framework programs and the EU and industry funder Innovative Medicine Initiative funder programs in rheumatology are geared to accomplishing these goals.