Dorothy Hodgkin Lecture 2017: Bringing the human pancreas into focus: new paradigms for the understanding of Type 1 diabetes.

2.50
Hdl Handle:
http://hdl.handle.net/11287/620351
Title:
Dorothy Hodgkin Lecture 2017: Bringing the human pancreas into focus: new paradigms for the understanding of Type 1 diabetes.
Authors:
Morgan, Noel
Other Titles:
Bringing the human pancreas into focus: new paradigms for the understanding of Type 1 diabetes
Abstract:
Type 1 diabetes affects increasingly large numbers of people globally (including at least half a million children under the age of 14 years) and it remains an illness with life-long and often devastating consequences. It is surprising, therefore, that the underlying aetiology of Type 1 diabetes remains poorly understood. This is largely because the cellular and molecular processes leading to the loss of β cells in the pancreas have rarely been studied at, or soon after, the onset of disease. Where such studies have been undertaken, a number of surprises have emerged which serve to challenge conventional wisdom. In particular, it is increasingly understood that the process of islet inflammation (insulitis) is much less florid in humans than in certain animal models. Moreover, the profile of immune cells involved in the inflammatory attack on β cells is variable and this variation occurs at the level of individual patients. As a result, two distinct profiles of insulitis have now been defined that are differentially aggressive and that might, therefore, require specifically tailored therapeutic approaches to slow the progression of disease. In addition, the outcomes are also different in that the more aggressive form (termed 'CD20Hi') is associated with extensive β-cell loss and an early age of disease onset (<7 years), while the less aggressive profile (known as 'CD20Lo') is associated with later onset (>13 years) and the retention of a higher proportion of residual β cells. In the present review, these new findings are explained and their implications evaluated in terms of future therapies.
Citation:
Dorothy Hodgkin Lecture 2017: Bringing the human pancreas into focus: new paradigms for the understanding of Type 1 diabetes. 2017 Diabet. Med.
Publisher:
Wiley
Journal:
Diabetic medicine : a journal of the British Diabetic Association
Issue Date:
20-Apr-2017
URI:
http://hdl.handle.net/11287/620351
DOI:
10.1111/dme.13365
PubMed ID:
28429491
Additional Links:
http://dx.doi.org/10.1111/dme.13365
Type:
Journal Article
Language:
en
ISSN:
1464-5491
Appears in Collections:
Honorary contracts publications; 2017 RD&E publications

Full metadata record

DC FieldValue Language
dc.contributor.authorMorgan, Noelen
dc.date.accessioned2017-06-05T14:07:30Z-
dc.date.available2017-06-05T14:07:30Z-
dc.date.issued2017-04-20-
dc.identifier.citationDorothy Hodgkin Lecture 2017: Bringing the human pancreas into focus: new paradigms for the understanding of Type 1 diabetes. 2017 Diabet. Med.en
dc.identifier.issn1464-5491-
dc.identifier.pmid28429491-
dc.identifier.doi10.1111/dme.13365-
dc.identifier.urihttp://hdl.handle.net/11287/620351-
dc.description.abstractType 1 diabetes affects increasingly large numbers of people globally (including at least half a million children under the age of 14 years) and it remains an illness with life-long and often devastating consequences. It is surprising, therefore, that the underlying aetiology of Type 1 diabetes remains poorly understood. This is largely because the cellular and molecular processes leading to the loss of β cells in the pancreas have rarely been studied at, or soon after, the onset of disease. Where such studies have been undertaken, a number of surprises have emerged which serve to challenge conventional wisdom. In particular, it is increasingly understood that the process of islet inflammation (insulitis) is much less florid in humans than in certain animal models. Moreover, the profile of immune cells involved in the inflammatory attack on β cells is variable and this variation occurs at the level of individual patients. As a result, two distinct profiles of insulitis have now been defined that are differentially aggressive and that might, therefore, require specifically tailored therapeutic approaches to slow the progression of disease. In addition, the outcomes are also different in that the more aggressive form (termed 'CD20Hi') is associated with extensive β-cell loss and an early age of disease onset (<7 years), while the less aggressive profile (known as 'CD20Lo') is associated with later onset (>13 years) and the retention of a higher proportion of residual β cells. In the present review, these new findings are explained and their implications evaluated in terms of future therapies.en
dc.language.isoenen
dc.publisherWileyen
dc.relation.urlhttp://dx.doi.org/10.1111/dme.13365en
dc.rightsArchived with thanks to Diabetic medicine : a journal of the British Diabetic Associationen
dc.subjectWessex Classification Subject Headings::Endocrinology::Diabetesen
dc.titleDorothy Hodgkin Lecture 2017: Bringing the human pancreas into focus: new paradigms for the understanding of Type 1 diabetes.en
dc.title.alternativeBringing the human pancreas into focus: new paradigms for the understanding of Type 1 diabetesen
dc.typeJournal Articleen
dc.identifier.journalDiabetic medicine : a journal of the British Diabetic Associationen
dc.type.versionIn press (epub ahead of print)en

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