John David Pollard

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Hereditary neuropathy with liability to pressure palsies (HNPP) has been a associated with a deletion of 1.5 megabases of chromosome 17p. One of four biopsy proven HNPP families that we have studied did not possess this deletion. As the deleted DNA region includes the coding region for a peripheral myelin gene (PMP22), we used single strand conformation(More)
Tumor necrosis factor (TNF)-dependent sites of action in the generation of autoimmune inflammation have been defined by targeted disruption of TNF in the C57BL/6 mouse strain. C57BL/6 mice are susceptible to an inflammatory, demyelinating form of experimental autoimmune encephalomyelitis (EAE) induced by the 35-55 peptide of myelin oligodendrocyte(More)
The etiology of the Guillain-Barré syndrome (GBS) still remains elusive. Recent years have witnessed important advances in the delineation of the mechanisms that may operate to produce nerve damage. Evidence gathered from cell biology, immunology, and immunopathology studies in patients with GBS and animals with experimental autoimmune neuritis (EAN)(More)
Neuropathologic abnormalities can be sufficiently characteristic to suggest the genetic basis of some hereditary neuropathies such as those associated with mutations in MPZ, GJB1, GDAP1, MTMR2, SH3TC2, PRX, FGD4, and LMNA. We analyzed the morphologic features of 9 sural nerve biopsies from 6 patients with mutations of mitofusin 2. All patients presented in(More)
The role of cyclosporin A (CsA) in the treatment of resistant chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) was retrospectively reviewed in 19 patients who had failed to respond adequately to corticosteroids, plasmapheresis, intravenous immunoglobulin, and in some cases other immunosuppressive agents. Patients were subdivided into(More)
A prevalence study of chronic inflammatory demyelinating polyneuropathy (CIDP) was performed in New South Wales (NSW), Australia, with a prevalence day of August 6, 1996, which coincided with a national census. The population of NSW was 5,995,544, and the crude prevalence of CIDP was 1.9 per 100,000 population. It was higher in male patients than in female(More)
Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is an inflammatory neuropathy, classically characterised by a slowly progressive onset and symmetrical, sensorimotor involvement. However, there are many phenotypic variants, suggesting that CIDP may not be a discrete disease entity but rather a spectrum of related conditions. While the(More)
Studies were conducted in experimental allergic neuritis (EAN) to evaluate the possible interaction of cellular and humoral immune mechanisms in the demyelinating process. EAN was induced in Lewis rats by passive transfer of T cells reactive to P2 myelin protein or by active immunisation with whole myelin. Animals were then given systemic antimyelin(More)
Prompted by observations in experimental autoimmune neuritis we reanalyzed immunohistochemically the inflammatory infiltrates in sural nerve biopsies of 22 cases with Guillain-Barre syndrome (GBS) and 13 cases with chronic inflammatory demyelinating polyneuropathy (CIDP). Endoneurial infiltration of CD3+ T cells was found in 20 cases of GBS (median 5.5(More)
Proinflammatory cytokines contribute to the regulation of the disease process in inflammatory neuropathies. Cellular localisation of cytokine expression in CIDP nerve biopsies should provide further insight into the pathogenic mechanisms of the disease and the individual cells involved. In this study in situ hybridisation was used to determine the exact(More)