PMID- 24632583
OWN - NLM
STAT- MEDLINE
DCOM- 20141203
LR  - 20220317
IS  - 1735-367X (Electronic)
IS  - 1735-1383 (Linking)
VI  - 11
IP  - 1
DP  - 2014 Mar
TI  - Islet amyloid polypeptide is not a target antigen for CD8+ T-cells in type 2 
      diabetes.
PG  - 1-12
AB  - BACKGROUND: Type 2 diabetes (T2D) is a chronic metabolic disorder in which 
      beta-cells are destroyed. The islet amyloid polypeptide (IAPP) produced by 
      beta-cells has been reported to influence beta-cell destruction. OBJECTIVE: To 
      evaluate if IAPP can act as an autoantigen and therefore, to see if CD8+ T-cells 
      specific for this protein might be present in T2D patients. METHODS: Peripheral 
      blood mononuclear cells (PBMC) were obtained from human leukocyte antigen 
      (HLA)-A2+ T2D patients and non-diabetic healthy subjects. Cells were then 
      screened for peptide recognition using ELISPOT assay for the presence of IFN-gamma 
      producing CD8+ T-cells against two HLA Class I-restricted epitopes derived from 
      IAPP (IAPP5-13 and IAPP9-17) and common viral antigenic minimal epitopes Flu MP 
      58-66, CMV495-503, EBV280-288 and HIV77-85 as controls. RESULTS: A total of 36.4% 
      of patients and 56.2% of healthy subjects showed a response against IAPP5-13 
      peptide. No significant difference in response against this peptide was noted 
      between the patients and the healthy donors. With respect to peptide IAPP9-17, 
      although healthy subjects showed a higher mean number of spot forming cells than 
      the patients, the difference was not significant; 36.4% of patients and 37.5% of 
      controls responded to this peptide. The response of healthy subjects to the 
      common viral peptides was stronger than that of the patients, though the result 
      was not significant. CONCLUSIONS: It is unlikely that IAPP would be a target for 
      CD8+ T-cells in diabetic patients; however, the trend observed toward a lower 
      response of T2D patients against IAPP and common viral peptides may imply a 
      decreased immune response in these patients.
FAU - Kalantar, Fathollah
AU  - Kalantar F
AD  - Department of Immunology, Shiraz University of Medical Sciences, Shiraz, Iran.
FAU - Dabbaghmanesh, Mohammad Hossein
AU  - Dabbaghmanesh MH
FAU - Martinuzzi, Emanuela
AU  - Martinuzzi E
FAU - Moghadami, Mohsen
AU  - Moghadami M
FAU - Amirghofran, Zahra
AU  - Amirghofran Z
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Iran
TA  - Iran J Immunol
JT  - Iranian journal of immunology : IJI
JID - 101282932
RN  - 0 (Autoantigens)
RN  - 0 (Epitopes, T-Lymphocyte)
RN  - 0 (HLA-A2 Antigen)
RN  - 0 (Islet Amyloid Polypeptide)
RN  - 0 (Peptide Fragments)
RN  - 82115-62-6 (Interferon-gamma)
SB  - IM
MH  - Adult
MH  - Autoantigens/immunology
MH  - CD8-Positive T-Lymphocytes/*immunology/metabolism
MH  - Case-Control Studies
MH  - Diabetes Mellitus, Type 2/*immunology/metabolism
MH  - Epitopes, T-Lymphocyte/chemistry/immunology
MH  - Female
MH  - HLA-A2 Antigen/immunology
MH  - Humans
MH  - Immunophenotyping
MH  - Interferon-gamma/biosynthesis
MH  - Islet Amyloid Polypeptide/chemistry/*immunology
MH  - Leukocytes, Mononuclear/immunology/metabolism
MH  - Male
MH  - Peptide Fragments/chemistry/immunology
EDAT- 2014/03/19 06:00
MHDA- 2014/12/15 06:00
CRDT- 2014/03/18 06:00
PHST- 2014/03/18 06:00 [entrez]
PHST- 2014/03/19 06:00 [pubmed]
PHST- 2014/12/15 06:00 [medline]
AID - 01 [pii]
PST - ppublish
SO  - Iran J Immunol. 2014 Mar;11(1):1-12.