Reduced IFN-α secretion by blood dendritic cells in human diabetes

Summers, Kelly L.; Marleau, Annette M.; Mahon, Jeffrey L.; McManus, Ruth; Hramiak, Irene; Singh, Bhagirath

doi:10.1016/j.clim.2006.05.015

Cited by 57 publications

(50 citation statements)

References 45 publications

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“…This group also found a higher proportion of plasmacytoid dendritic cells in type 1 diabetes, although specific results are not reported, limiting the opportunity for direct comparison. A more recent report focuses on patients with type 1 diabetes of at least 5 years duration and finds no abnormality of blood dendritic cell balance, similar to our own analysis of longstanding patients (21). In contrast, Vuckovic et al (22) have reported decreased dendritic cell numbers in children with new-onset type 1 diabetes.…”

Section: Discussionmentioning

confidence: 63%

Plasmacytoid Dendritic Cells Are Proportionally Expanded at Diagnosis of Type 1 Diabetes and Enhance Islet Autoantigen Presentation to T-Cells Through Immune Complex Capture

et al. 2009

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OBJECTIVE-Immune-mediated destruction of ␤-cells resulting in type 1 diabetes involves activation of proinflammatory, islet autoreactive T-cells, a process under the control of dendritic cells of the innate immune system. We tested the hypothesis that type 1 diabetes development is associated with disturbance of blood dendritic cell subsets that could enhance islet-specific autoimmunity. RESEARCH DESIGN AND METHODS-We examined blood dendritic cells (plasmacytoid and myeloid) in 40 patients with recent-onset diabetes (median duration 28 days) and matched control subjects. We also examined the relative ability of different dendritic cell subsets to process and present soluble or immune complexed islet cell autoantigen (the islet tyrosine phosphatase IA-2) to responder CD4 T-cells.

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Section: Discussionmentioning

confidence: 63%

Plasmacytoid Dendritic Cells Are Proportionally Expanded at Diagnosis of Type 1 Diabetes and Enhance Islet Autoantigen Presentation to T-Cells Through Immune Complex Capture

et al. 2009

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“…However, such studies have produced discrepant results. In recent-onset T1D patients, increased blood MDC and PDC numbers have been reported relative to established T1D patients and controls [7], whereas other studies have shown no difference in the numbers of blood MDC and PDC between adult subjects with established T1D and age-matched controls [8]. We have previously reported that diabetic children, aged 2-10 years, exhibit a marked decrease in blood MDC and PDC numbers whereas this difference was less obvious when comparing older cohorts [3].…”

Section: Introductionmentioning

confidence: 86%

“…These differences between the reported blood DC and T Reg numbers may result from different experimental conditions (e.g. study of erythrocyte-lysed fresh blood samples [3,13] versus Ficoll-density gradient isolated blood mononuclear cells [7][8][9][10][11][12] or superficial analyses (e.g. restricted surface markers for identifying DC and T Reg cells, constraints of three-to four-color flow cytometry).…”

Section: Introductionmentioning

confidence: 99%

Type 1 Diabetic Children and Siblings Share a Decrease in Dendritic Cell and Monocyte Numbers but are Differentiated by Expansion of CD4+T Cells Expressing IL-17

Wilkinson¹,

Bian²,

Khalil³

et al. 2011

J Clin Cell Immunol

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Type 1 diabetes (T1D) is an autoimmune disease characterised by multiple defects of immune cells which allow the expansion of pathogenic β cell-specific T effector cells and subsequent T1D development. We performed immunomonitoring assays on blood immune cells in T1D children, their siblings and controls with the supposition that the results would elucidate the sequence of abnormalities in peripheral immune cells leading to the progression of autoimmunity from non-diabetic siblings to diabetic children. We assessed myeloid dendritic cell (MDC), plasmacytoid (P)DC, monocyte, CD4 + monocytes that may result from shared genetic or environmental factors. However, this reduction of blood immune cells requires combination with the proinflammatory cytokine IL-17 to allow disease expression in diabetic children.

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“…An abnormal cytokine response by DC from T1D patients upon antigenic [305] or nonantigenic stimulation was proposed [306] but has not been confirmed by other studies [307]. More robustly, phenotypic characterization suggests that DC from recent-onset T1D patients exhibit an immature phenotype and may have a decreased T-cell stimulatory capacity, compared to controls [308].…”

Section: Apcmentioning

confidence: 82%