Apportioning Blame: Autoreactive CD4+ and CD8+ T Cells in Type 1 Diabetes
Type 1 diabetes (T1D) is one of the most studied archetypal organ-specific autoimmune diseases. Although many clinical, epidemiological, and pathological characteristics have been described, there are still important issues which need to be resolved as these will have a major impact on the developme...
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Published in | Archivum Immunologiae et Therapiae Experimentalis Vol. 65; no. 4; pp. 275 - 284 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Cham
Springer International Publishing
01.08.2017
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Subjects | |
Online Access | Get full text |
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Summary: | Type 1 diabetes (T1D) is one of the most studied archetypal organ-specific autoimmune diseases. Although many clinical, epidemiological, and pathological characteristics have been described, there are still important issues which need to be resolved as these will have a major impact on the development of future antigen-specific immunotherapies. An important question relates to T lymphocytes in the development of the disease, in particular their role in the destruction of insulin-producing beta cells. Since the discovery that certain class II histocompatibility complex molecules (HLA) are linked to the development of T1D, much research has focused on CD4
+
helper T lymphocytes; however, recent studies highlight class I HLA molecules as an independent risk factor; hence, research into the role played by CD8
+
cytotoxic T lymphocytes has gained momentum. In this review, we summarize recent studies clarifying the role played by both sets of autoreactive T lymphocytes in T1D, discuss the targets recognized by these cells and their phenotype in T1D patients. Finally, we will examine the possible generation of regulatory CD8
+
T lymphocytes upon different immuno-intervention strategies. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 |
ISSN: | 0004-069X 1661-4917 |
DOI: | 10.1007/s00005-016-0452-4 |