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Radiation-Induced Dermatitis is Mediated by IL17-Expressing γδ T Cells.

Abstract Radiation dermatitis is a serious cutaneous injury caused by radiation therapy or upon accidental nuclear exposure. However, the pathogenic immune mechanisms underlying this injury are still poorly understood. We seek to discover how the dysregulated immune response after irradiation orchestrates skin inflammation. The skin on the left flank of C57BL/6J wild-type and C57BL/6J Tcrd(-/-) mice, which are deficit in γδ T cells, was exposed to a single X-ray dose of 25 Gy, and the right-flank skin was used as a sham-irradiated control. At 4 weeks postirradiation, the wild-type skin exhibited signs of depilation, erythema and desquamation. Histological analysis showed hyperproliferation of keratinocytes and acanthosis. Dramatic elevation of IL17-expressing T cells was identified from the irradiated skin, which was mainly contributed by γδ T cells and innate lymphoid cells, rather than Th17 cells. Furthermore, protein levels of critical cytokines for IL17-expressing γδ T cell activation, IL1β and IL23 were found markedly upregulated. Lastly, radiation-induced dermatitis was significantly attenuated in γδ T cell knockout mice. In vitro, normal human epidermal keratinocytes (NHEKs) could be initiator cells of inflammation by providing a great number of pro-inflammatory mediators upon radiation, and as well as effector cells of epidermal hyperplasia in response to exogenous IL17 and/or IL22 treatment. Our findings implicate a novel role of IL17-expressing γδ T cells in mediating radiation-induced skin inflammation. This study reveals the innate immune response pathway as a potential therapeutic target for radiation skin injury.
PMID
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Radiation-Induced Dermatitis is Mediated by IL17-Expressing γδ T Cells.

Authors

Mayor MeshTerms
Keywords
Journal Title radiation research
Publication Year Start




PMID- 28406748
OWN - NLM
STAT- MEDLINE
DA  - 20170413
DCOM- 20170414
LR  - 20170414
IS  - 1938-5404 (Electronic)
IS  - 0033-7587 (Linking)
VI  - 187
IP  - 4
DP  - 2017 Apr
TI  - Radiation-Induced Dermatitis is Mediated by IL17-Expressing gammadelta T Cells.
PG  - 454-464
LID - 10.1667/RR007CC.1 [doi]
AB  - Radiation dermatitis is a serious cutaneous injury caused by radiation therapy or
      upon accidental nuclear exposure. However, the pathogenic immune mechanisms
      underlying this injury are still poorly understood. We seek to discover how the
      dysregulated immune response after irradiation orchestrates skin inflammation.
      The skin on the left flank of C57BL/6J wild-type and C57BL/6J Tcrd-/- mice, which
      are deficit in gammadelta T cells, was exposed to a single X-ray dose of 25 Gy,
      and the right-flank skin was used as a sham-irradiated control. At 4 weeks
      postirradiation, the wild-type skin exhibited signs of depilation, erythema and
      desquamation. Histological analysis showed hyperproliferation of keratinocytes
      and acanthosis. Dramatic elevation of IL17-expressing T cells was identified from
      the irradiated skin, which was mainly contributed by gammadelta T cells and
      innate lymphoid cells, rather than Th17 cells. Furthermore, protein levels of
      critical cytokines for IL17-expressing gammadelta T cell activation, IL1beta and 
      IL23 were found markedly upregulated. Lastly, radiation-induced dermatitis was
      significantly attenuated in gammadelta T cell knockout mice. In vitro, normal
      human epidermal keratinocytes (NHEKs) could be initiator cells of inflammation by
      providing a great number of pro-inflammatory mediators upon radiation, and as
      well as effector cells of epidermal hyperplasia in response to exogenous IL17
      and/or IL22 treatment. Our findings implicate a novel role of IL17-expressing
      gammadelta T cells in mediating radiation-induced skin inflammation. This study
      reveals the innate immune response pathway as a potential therapeutic target for 
      radiation skin injury.
FAU - Liao, Wupeng
AU  - Liao W
AD  - a Department of Radiation Oncology.
FAU - Hei, Tom K
AU  - Hei TK
AD  - b Center for Radiological Research, College of Physicians and Surgeons, Columbia 
      University, New York, New York 10032; and.
AD  - c Department of Environmental Health Sciences, Mailman School of Public Health,
      Columbia University, New York, New York 10032.
FAU - Cheng, Simon K
AU  - Cheng SK
AD  - a Department of Radiation Oncology.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Radiat Res
JT  - Radiation research
JID - 0401245
RN  - 0 (Interleukin-17)
RN  - 0 (Receptors, Antigen, T-Cell, gamma-delta)
SB  - IM
SB  - S
MH  - Animals
MH  - Humans
MH  - Inflammation/etiology/immunology
MH  - Interleukin-17/*biosynthesis/immunology
MH  - Keratinocytes/immunology/radiation effects
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Radiation Injuries, Experimental/*immunology
MH  - Radiodermatitis/*immunology
MH  - Receptors, Antigen, T-Cell, gamma-delta/*immunology
MH  - T-Lymphocytes/immunology/*radiation effects
EDAT- 2017/04/14 06:00
MHDA- 2017/04/15 06:00
CRDT- 2017/04/14 06:00
AID - 10.1667/RR007CC.1 [doi]
PST - ppublish
SO  - Radiat Res. 2017 Apr;187(4):454-464. doi: 10.1667/RR007CC.1.

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