No abstract

ChemBank (http://chembank.broad.harvard.edu/) is a public, web-based informatics environment developed through a collaboration between the Chemical Biology Program and Platform at the Broad Institute of Harvard and MIT. This knowledge environment includes freely available data derived from small molecules and small-molecule screens and resources for studying these data. ChemBank is unique among small-molecule databases in its dedication to the storage of raw screening data, its rigorous definition of screening experiments in terms of statistical hypothesis testing, and its metadata-based organization of screening experiments into projects involving collections of related assays. ChemBank stores an increasingly varied set of measurements derived from cells and other biological assay systems treated with small molecules. Analysis tools are available and are continuously being developed that allow the relationships between small molecules, cell measurements, and cell states to be studied. Currently, ChemBank stores information on hundreds of thousands of small molecules and hundreds of biomedically relevant assays that have been performed at the Broad Institute by collaborators from the worldwide research community. The goal of ChemBank is to provide life scientists unfettered access to biomedically relevant data and tools heretofore available primarily in the private sector.

No abstract

T cells that express the T cell receptor V beta 5.2 domain react with the class II major histocompatibility complex (MHC) molecule I-E, and V beta 5.2+ T cells are deleted in mouse strains that express I-E glycoproteins. By examination of genetically defined recombinant inbred (RI) mouse strains, it was found that the deletion was dependent on the expression of I-E and one of a limited number of non-MHC gene products (cotolerogens). The gene encoding one of these cotolerogens maps to chromosome 12 and is linked to the endogenous provirus Mtv-9. These observations suggest that the I-E-mediated and minor lymphocyte-stimulating antigen (Mls)-mediated deletions of alpha beta T cells from the repertoire are similar; both require the expression of a class II MHC glycoprotein and a second non-MHC gene product.

A special class of self-antigens (endogenous superantigens) is capable of deleting many murine T cells on the basis of their expression of particular T-cell receptor V beta gene segments. In mice that endogenously express these antigens, tolerance is mediated in part by the clonal deletion of the relevant V beta-bearing T cells. The deletion of I-E-reactive V beta 5.2-bearing T cells is dependent on the coexpression of an I-E tolerogenic coligand (Etc)14 and the gene for one of these coligands, Etc-1, maps to chromosome 12, near the mouse mammary tumour viral integrant, Mtv-9. Here we report a perfect genetic linkage between Etc-1 and Mtv-9 and show that Etc-1 is also involved in the I-E-dependent deletion of T cells bearing V beta 5.1 and V beta 11 domains. We also demonstrate that Mtv-9 transcripts are present in B cells expressing Etc-1 and suggest that the coligand recognized by roughly 15% of all T lymphocytes is encoded by the Mtv-9 genome.