Overview
Nikki's Primary role is as PA to Professor Noel Morgan Vice-Dean: Research (Interim), Professor of Endocrine Pharmacology; Director - Institute of Biomedical & Clinical Science. She provides support through diary management, arrangement of meetings and minute-taking, event management, dealing with correspondence and coordination of all travel and hotel bookings, as well as the management of the Islet Biology Exeter web pages and Twitter account. Her secondary role is to provide administrative support to Professor Andrew Crosby (Professor of Human Genetics) and Professor Jonathan Mill (Professor of Epigenetics). Nikki is also an active member on several committees within the Medical School.
Career
After an 11 year career working for the RAF Nikki relocated from South Wales to Exeter where she joined the University of Exeter in 2005. After a diversity of PA and office manager roles within Campus Services and Academic Services she joined the Medical School 2014 as her current role as PA to the Vice-Dean: Research (Interim), Professor of Endocrine Pharmacology; Director - Institute of Biomedical & Clinical Science.
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Publications
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Journal articles
Dunne JL, Richardson SJ, Atkinson MA, Craig ME, Dahl-Jørgensen K, Flodström-Tullberg M, Hyöty H, Insel RA, Lernmark Å, Lloyd RE, et al (2019). Rationale for enteroviral vaccination and antiviral therapies in human type 1 diabetes.
Diabetologia,
62(5), 744-753.
Abstract:
Rationale for enteroviral vaccination and antiviral therapies in human type 1 diabetes.
In type 1 diabetes, pancreatic beta cells are destroyed by chronic autoimmune responses. The disease develops in genetically susceptible individuals, but a role for environmental factors has been postulated. Viral infections have long been considered as candidates for environmental triggers but, given the lack of evidence for an acute, widespread, cytopathic effect in the pancreas in type 1 diabetes or for a closely related temporal association of diabetes onset with such infections, a role for viruses in type 1 diabetes remains unproven. Moreover, viruses have rarely been isolated from the pancreas of individuals with type 1 diabetes, mainly (but not solely) due to the inaccessibility of the organ. Here, we review past and recent literature to evaluate the proposals that chronic, recurrent and, possibly, persistent enteroviral infections occur in pancreatic beta cells in type 1 diabetes. We also explore whether these infections may be sustained by different virus strains over time and whether multiple viral hits can occur during the natural history of type 1 diabetes. We emphasise that only a minority of beta cells appear to be infected at any given time and that enteroviruses may become replication defective, which could explain why they have been isolated from the pancreas only rarely. We argue that enteroviral infection of beta cells largely depends on the host innate and adaptive immune responses, including innate responses mounted by beta cells. Thus, we propose that viruses could play a role in type 1 diabetes on multiple levels, including in the triggering and chronic stimulation of autoimmunity and in the generation of inflammation and the promotion of beta cell dysfunction and stress, each of which might then contribute to autoimmunity, as part of a vicious circle. We conclude that studies into the effects of vaccinations and/or antiviral drugs (some of which are currently on-going) is the only means by which the role of viruses in type 1 diabetes can be finally proven or disproven.
Abstract.
Author URL.
Full text.
Publications by year
2019
Dunne JL, Richardson SJ, Atkinson MA, Craig ME, Dahl-Jørgensen K, Flodström-Tullberg M, Hyöty H, Insel RA, Lernmark Å, Lloyd RE, et al (2019). Rationale for enteroviral vaccination and antiviral therapies in human type 1 diabetes.
Diabetologia,
62(5), 744-753.
Abstract:
Rationale for enteroviral vaccination and antiviral therapies in human type 1 diabetes.
In type 1 diabetes, pancreatic beta cells are destroyed by chronic autoimmune responses. The disease develops in genetically susceptible individuals, but a role for environmental factors has been postulated. Viral infections have long been considered as candidates for environmental triggers but, given the lack of evidence for an acute, widespread, cytopathic effect in the pancreas in type 1 diabetes or for a closely related temporal association of diabetes onset with such infections, a role for viruses in type 1 diabetes remains unproven. Moreover, viruses have rarely been isolated from the pancreas of individuals with type 1 diabetes, mainly (but not solely) due to the inaccessibility of the organ. Here, we review past and recent literature to evaluate the proposals that chronic, recurrent and, possibly, persistent enteroviral infections occur in pancreatic beta cells in type 1 diabetes. We also explore whether these infections may be sustained by different virus strains over time and whether multiple viral hits can occur during the natural history of type 1 diabetes. We emphasise that only a minority of beta cells appear to be infected at any given time and that enteroviruses may become replication defective, which could explain why they have been isolated from the pancreas only rarely. We argue that enteroviral infection of beta cells largely depends on the host innate and adaptive immune responses, including innate responses mounted by beta cells. Thus, we propose that viruses could play a role in type 1 diabetes on multiple levels, including in the triggering and chronic stimulation of autoimmunity and in the generation of inflammation and the promotion of beta cell dysfunction and stress, each of which might then contribute to autoimmunity, as part of a vicious circle. We conclude that studies into the effects of vaccinations and/or antiviral drugs (some of which are currently on-going) is the only means by which the role of viruses in type 1 diabetes can be finally proven or disproven.
Abstract.
Author URL.
Full text.
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