Th1 and Th2 cell responses of type 1 diabetes patients and healthy controls to human heat-shock protein 60 peptides AA437-460 and AA394-408
Type 1 diabetes mellitus (T1) is considered to be an immune mediated disease. Based on previous findings it might be suggested that heat shock protein 60 (Hsp60) could be involved in the mediation of the development of the disease. Furthermore a bias toward Th1 immune response was observed in T1D pa...
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Published in | Inflammation research Vol. 54; no. 10; pp. 415 - 419 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Switzerland
Springer Nature B.V
01.10.2005
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Subjects | |
Online Access | Get full text |
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Summary: | Type 1 diabetes mellitus (T1) is considered to be an immune mediated disease. Based on previous findings it might be suggested that heat shock protein 60 (Hsp60) could be involved in the mediation of the development of the disease. Furthermore a bias toward Th1 immune response was observed in T1D patients where the level of Th1 cytokines was elevated, while the level of Th2 was decreased.
To determine Th1 (IFN-gamma) and Th2 (IL-13) cytokine levels in T1 diabetic and control subjects as well as to determine whether there is a shift towards Th1 or Th2 immune response.
ELISPOT (Enzyme-linked ImmunoSPOT) analysis was employed to differentiate antigen specific T-cell responses of a Th1 (IFN-gamma) or Th2 (IL-13) type. 11 T1 diabetic patients and 9 healthy controls were investigated. For T-cell stimulation, we used a polyclonal mitogen or Tetanus toxoid (TT) as positive controls and two peptide antigens Hsp60 AA394-408 and Hsp60 AA437-460.
In case of Hsp60 AA437-460 we found significantly decreased Th2 response in patients, although there was no significant difference in Th1 response. In case of Hsp60 AA394-408 and positive controls there was no significant difference.
Comparing the control and diabetic subjects a significant shift towards Th1 response in T1 diabetes mellitus for Hsp60 AA437-460 was observed. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1023-3830 1420-908X |
DOI: | 10.1007/s00011-005-1362-9 |