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Τρίτη 25 Ιουνίου 2019


Ultraviolet light induces increased T cell activation in lupus-prone mice via type I IFN-dependent inhibition of T regulatory cells
Publication date: Available online 24 June 2019Source: Journal of AutoimmunityAuthor(s): Sonya J. Wolf, Shannon N. Estadt, Jonathan Theros, Tyson Moore, Jason Ellis, Jianhua Liu, Tamra J. Reed, Chaim O. Jacob, Johann E. Gudjonsson, J. Michelle KahlenbergAbstractUltraviolet (UV) light is a known trigger of skin and possibly systemic inflammation in systemic lupus erythematosus (SLE) patients. Although type I interferons (IFN) are upregulated in SLE skin after UV exposure, the mechanisms to explain...
ScienceDirect Publication: Journal of Autoimmunity
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Ultraviolet light induces increased T cell activation in lupus-prone mice via type I IFN-dependent inhibition of T regulatory cells 15h
via ScienceDirect Publication: Journal of Autoimmunity
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Publication date: Available online 24 June 2019

Source: Journal of Autoimmunity

Author(s): Sonya J. Wolf, Shannon N. Estadt, Jonathan Theros, Tyson Moore, Jason Ellis, Jianhua Liu, Tamra J. Reed, Chaim O. Jacob, Johann E. Gudjonsson, J. Michelle Kahlenberg

Abstract
Ultraviolet (UV) light is a known trigger of skin and possibly systemic inflammation in systemic lupus erythematosus (SLE) patients. Although type I interferons (IFN) are upregulated in SLE skin after UV exposure, the mechanisms to explain increased UVB-induced inflammation remain unclear. This paper compares the role of type I IFNs in regulating immune cell activation between wild-type and lupus-prone mice following UVB exposure. 10-week old female lupus-prone (NZM2328), wild-type (BALB/c) and iNZM mice (lack a functional type I IFN receptor on NZM2328 background) were treated on their dorsal skin with 100 mJ/cm2 of UVB for 5 consecutive days. Following UVB treatment, draining lymph node cell populations were characterized via flow cytometry and suppression assays; treated skin was examined for changes in expression of type I IFN genes. Only NZM2328 mice showed an increase in T cell numbers and activation 2 weeks post UVB exposure. This was preceded by a significant increase in UVB-induced type I IFN expression in NZM2328 mice compared to BALB/c mice. Following UVB exposure, both BALB/c and iNZM mice demonstrated an increase in functional T regulatory (TReg) cells; however, this was not seen in NZM2328 mice. These data suggest a skewed UVB-mediated T cell response in lupus-prone mice where activation of T cells is enhanced secondary to a type I IFN-dependent suppression of TReg cells. Thus, we propose type I IFNs are important for UVB-induced inflammation in lupus-prone mice and may be an effective target for prevention of UVB-mediated flares.

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