tetano
Editor, Senior Moderator
Clin Exp Immunol. 2014 Oct 6. doi: 10.1111/cei.12462. [Epub ahead of print]
Reduced interferon-α production by dendritic cells in type 1 diabetes does not impair immunity to Influenza Virus.
Kreuzer D1, Nikoopour E, Au BC, Krougly O, Lee-Chan E, Summers KL, Haeryfar SM, Singh B.
Author information
Abstract
Increased risk and persistence of infections in diabetic condition is likely associated with defect in the cellular immune responses. We previously showed a decrease in the production of interferon-α (IFN-α) by dendritic cells (DCs) in diabetic subjects. The basal level of IFN-α in splenic plasmacytoid DCs (pDCs) is also lower in diabetic NOD mice compared to pre-diabetic mice. The objective of this study was to analyze the ability of diabetic mice to mobilize innate and CD8+ T cell-mediated immune response to influenza A virus (IAV) with live influenza A/Puerto Rico/8/1934 H1N1 (PR8) strain or with its immunodominant CD8+ T cells epitopes. We found that following immunization with IAV, the level of IFN-α in diabetic mice was increased to the level in pre-diabetic mice. Immunization of NOD mice with the immunodominant IAV PR8 peptide induced clonal expansion of interferon-γ (IFN-γ) producing CD8+ T-cells similar to the response observed in pre-diabetic mice. Thus, diabetic and prediabetic NOD mice have a similar capacity for IFN-α and IFN-γ production by pDCs and CD8+ T-cells, respectively. Therefore, dendritic cell related immune defect in diabetic NOD mice does not impair their capacity to develop effective immune response to IAV. Our results suggest 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.
This article is protected by copyright. All rights reserved.
PMID:
25286929
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/25286929
Reduced interferon-α production by dendritic cells in type 1 diabetes does not impair immunity to Influenza Virus.
Kreuzer D1, Nikoopour E, Au BC, Krougly O, Lee-Chan E, Summers KL, Haeryfar SM, Singh B.
Author information
Abstract
Increased risk and persistence of infections in diabetic condition is likely associated with defect in the cellular immune responses. We previously showed a decrease in the production of interferon-α (IFN-α) by dendritic cells (DCs) in diabetic subjects. The basal level of IFN-α in splenic plasmacytoid DCs (pDCs) is also lower in diabetic NOD mice compared to pre-diabetic mice. The objective of this study was to analyze the ability of diabetic mice to mobilize innate and CD8+ T cell-mediated immune response to influenza A virus (IAV) with live influenza A/Puerto Rico/8/1934 H1N1 (PR8) strain or with its immunodominant CD8+ T cells epitopes. We found that following immunization with IAV, the level of IFN-α in diabetic mice was increased to the level in pre-diabetic mice. Immunization of NOD mice with the immunodominant IAV PR8 peptide induced clonal expansion of interferon-γ (IFN-γ) producing CD8+ T-cells similar to the response observed in pre-diabetic mice. Thus, diabetic and prediabetic NOD mice have a similar capacity for IFN-α and IFN-γ production by pDCs and CD8+ T-cells, respectively. Therefore, dendritic cell related immune defect in diabetic NOD mice does not impair their capacity to develop effective immune response to IAV. Our results suggest 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.
This article is protected by copyright. All rights reserved.
PMID:
25286929
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/25286929