Bernard J. Morley

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Human autoimmune diseases thought to arise from the combined effects of multiple susceptibility genes include systemic lupus erythematosus (SLE) and autoimmune diabetes. Well-characterised polygenic mouse models closely resembling each of these diseases exist, and genetic evidence links receptors for the Fc portion of immunoglobulin G (FcR) with their(More)
The TCR recognizes antigens associated with MHC molecules (1). This recognition event is then transduced across the plasma membrane to initiate intracellular biochemical events that include phosphatidylinositol hydrolysis and tyrosine kinase activation (2). The remarkable complexity of the TCR is likely to have evolved to carry out efficiently both its(More)
The human complement protein Factor B is encoded by a single gene in the major histocompatibility complex and is closely linked to the gene encoding the second component of complement C2. DNA sequencing, S1 mapping, and primer extension experiments have established that the transcription initiation site of the Factor B gene lies only 421 bp from the poly(A)(More)
The 5'-sequences flanking the human complement component C4 genes (C4A and C4B) have been analyzed for their ability to direct expression of a reporter gene in cell lines that constitutively express or do not express C4. No difference in the level of reporter gene expression was detected in cells transfected with C4A- or C4B-specific constructs. A series of(More)
Lupus-prone New Zealand Black and New Zealand White mice produce high serum levels of the endogenous retroviral envelope protein gp70 and develop an Ab response to this autoantigen as part of their autoimmune disease. Linkage analysis of two crosses involving New Zealand and BALB/c mice mapped these traits to a group of overlapping loci, including a novel(More)
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