Journal
CLINICAL IMMUNOLOGY
Volume 136, Issue 1, Pages 130-138Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.clim.2010.02.014
Keywords
Type 1 interferons; Systemic lupus erythematosus; Myositis; Plasmacytoid dendritic cells
Categories
Funding
- NIH NINDS [R21NS057225]
- Muscular Dystrophy Association [MDA3523]
- MedImmune, LLC
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To determine the potential consequences of plasmacytoid dendritic cell (pDC) accumulation in tissue sites observed in several autoimmune diseases, we measured type 1 interferon production from circulating human pDCs as a function of pDC concentration. The effects of interferon-alpha and blockade of the type 1 interferon receptor (IFNAR) on human pDC type 1 interferon and interferon-inducible transcription and protein production were measured. Human pDCs became far more efficient producers of interferon-alpha at concentrations beyond those normally present in blood, through an IFNAR-dependent mechanism. Extracellular interferon-alpha increased pDC production of type 1 interferons. The accumulation of pDCs in diseased tissue sites allows marked non-linear amplification of type 1 interferon production locally. The role of the IFNAR-dependent mechanism of interferon production by human pDCs is greater than previously suggested. IFNAR blockade has potential for diminishing type 1 interferon production by all human cells. (C) 2010 Elsevier Inc. All rights reserved.
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