Cellular interferon-γ and interleukin-13 immune reactivity in type 1, type 2 and latent autoimmune diabetes: action LADA 6
| Author | |
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| Abstract |
OBJECTIVE: Type 1 diabetes and latent autoimmune diabetes in adults (LADA) are thought to result from immune-mediated β-cell destruction. It remains unclear why LADA is clinically less severe compared to type 1 diabetes. This study aimed to compare the pro-inflammatory (interferon-γ, IFN-γ) and anti-inflammatory (interleukin-13, IL-13) T-cell responses in humans with LADA and type 1 diabetes. RESEARCH DESIGN AND METHODS: IFN-γ and IL-13 T-cell responses to a panel of 16 (auto)-antigens were tested using an enzyme linked immune-spot technique and peripheral T-cells from 35 patients with type 1 diabetes, 59 patients with type 2 diabetes, 23 LADA patients, and 42 control subjects. RESULTS: LADA and type 1 diabetes patients did not display any statistically significant differences in the frequency of IFN-γ or IL-13 responses to auto-antigenic stimuli, positive control or mitogen. Overall very low T cell reactivity to autoantigens was detected in all groups. IL-13 responses but not IFN-γ responses to recall antigen tetanus toxoid were higher in healthy control subjects compared to patients with type 1 or type 2 diabetes or LADA (P<0.05). Diabetes, independent of type, was associated with weaker response to recall antigen tetanus toxoid. CONCLUSIONS: LADA patients are indistinguishable from type 1 diabetes patients for cellular IFN-γ and IL-13 responses upon mitogen and recall antigen stimulation. These results extend previous findings showing that systemic cytokine/chemokine and humoral responses in type 1 diabetes and LADA are similar. |
| Year of Publication |
2012
|
| Journal |
Cytokine
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| Volume |
58
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| Issue |
2
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| Number of Pages |
148-51
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| Date Published |
05/2012
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| ISSN Number |
1096-0023
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| DOI |
10.1016/j.cyto.2012.01.002
|
| Alternate Journal |
Cytokine
|
| PMID |
22305546
|
| Download citation | |
| Reactivity |
Human
|
| Category |
T cell ELISPOT
|
| Analyte | IFN-γ, IL-13
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