| Autor: |
Kreuzer, D., Nikoopour, E., Au, B. C. Y., Krougly, O., Lee‐Chan, E., Summers, K. L., Haeryfar, S. M. M., Singh, B. |
| Předmět: |
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| Zdroj: |
Clinical & Experimental Immunology; Feb2015, Vol. 179 Issue 2, p245-255, 11p |
| Abstrakt: |
The increased risk and persistence of infections in diabetic condition is probably associated with defects in the cellular immune responses. We have previously shown a decrease in the production of interferon ( IFN)-α by dendritic cells ( DCs) in diabetic subjects. The basal level of IFN-α in splenic plasmacytoid DCs (p DCs) is also lower in non-obese diabetic ( NOD) mice compared to prediabetic mice. The objective of this study was to analyse the ability of diabetic mice to mobilize innate and CD8+ T cell-mediated immune response to influenza A virus ( IAV) with the live influenza A/ Puerto Rico/8/1934 H1 N1 ( PR8) strain or with its immunodominant CD8+ T cell epitopes. We found that following immunization with IAV, the level of IFN-α in diabetic mice was increased to the level in prediabetic mice. Immunization of NOD mice with the immunodominant IAV PR8 peptide induced clonal expansion of IFN-γ-producing CD8+ T cells similar to the response observed in prediabetic mice. Thus, diabetic and prediabetic NOD mice have a similar capacity for IFN-α and IFN-γ production by p DCs and CD8+ T cells, respectively. Therefore, the DC-related immune defect in diabetic NOD mice does not impair their capacity to develop an effective immune response to IAV. Our results suggest that reduced IFN-α production by diabetic human and mouse DCs is not an impediment to an effective immunity to IAV in type 1 diabetic subjects vaccinated with live attenuated influenza vaccine. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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