Toll‐like receptor 7 (TLR7) mediated transcriptomic changes on human mast cells

Kyung Ah Cho; Da Won Choi; Minhwa Park; Yu Hee Kim; So Youn Woo

doi:10.5021/AD.2021.33.5.402

Toll‐like receptor 7 (TLR7) mediated transcriptomic changes on human mast cells

Kyung Ah Cho, Da Won Choi, Minhwa Park, Yu Hee Kim, So Youn Woo

Department of Microbiology

Research output: Contribution to journal › Article › peer-review

4 Scopus citations

Abstract

Background: Mast cells are skin immune sentinels located in the upper dermis, where wheal formation and sensory nerve stimulation take place. Skin inflammation is occasionally accompanied by mast cell-driven responses with wheals, angioedema, or both. Immunoglobulin E (IgE) antibodies are regarded as typical stimuli to drive mast cell activation. However, various causative factors, including microbial infections, can drive IgE-independent mast cell response. When infected, the innate immunity orchestrates an immune response by activating receptor signaling via Toll-like receptors (TLRs). Objective: In this study, we determined the effect of TLR7 stimulation on mast cells to investigate the possible mechanism of IgE-independent inflammatory response. Methods: Human mast cell (HMC) line, HMC-1 cells were treated with TLR7 agonist and the morphologic alteration was observed in transmission electron microscopy. Further, TLR7 agonist treated HMC-1 cells were conducted to RNA sequencing to compare transcriptomic features. Results: HMC-1 cells treated with TLR7 agonist reveals increase of intracellular vesicles, lipid droplets, and ribosomes. Also, genes involved in pro-inflammatory responses such as angiogenesis are highly expressed, and Il12rb2 was the most highly upregulated gene. Conclusion: Our data suggest that TLR7 signaling on mast cells might be a potential therapeutic target for mast cell-driven, IgE-independent skin inflammation.

Original language	English
Pages (from-to)	402-408
Number of pages	7
Journal	Annals of Dermatology
Volume	33
Issue number	5
DOIs	https://doi.org/10.5021/AD.2021.33.5.402
State	Published - Oct 2021

Bibliographical note

Funding Information:
This work was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea Government (MSIT) (No. NRF-2019R1H1A1035603 and NRF-2020 R1C1C1012769) and RP-Grant 2019 of Ewha Womans University. The funders had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication.

Publisher Copyright:
Copyright © The Korean Dermatological Association and The Korean Society for Investigative Dermatology

Keywords

Mast cell
Skin inflammation
Toll‐like receptor 7

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10.5021/AD.2021.33.5.402

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title = "Toll‐like receptor 7 (TLR7) mediated transcriptomic changes on human mast cells",

abstract = "Background: Mast cells are skin immune sentinels located in the upper dermis, where wheal formation and sensory nerve stimulation take place. Skin inflammation is occasionally accompanied by mast cell-driven responses with wheals, angioedema, or both. Immunoglobulin E (IgE) antibodies are regarded as typical stimuli to drive mast cell activation. However, various causative factors, including microbial infections, can drive IgE-independent mast cell response. When infected, the innate immunity orchestrates an immune response by activating receptor signaling via Toll-like receptors (TLRs). Objective: In this study, we determined the effect of TLR7 stimulation on mast cells to investigate the possible mechanism of IgE-independent inflammatory response. Methods: Human mast cell (HMC) line, HMC-1 cells were treated with TLR7 agonist and the morphologic alteration was observed in transmission electron microscopy. Further, TLR7 agonist treated HMC-1 cells were conducted to RNA sequencing to compare transcriptomic features. Results: HMC-1 cells treated with TLR7 agonist reveals increase of intracellular vesicles, lipid droplets, and ribosomes. Also, genes involved in pro-inflammatory responses such as angiogenesis are highly expressed, and Il12rb2 was the most highly upregulated gene. Conclusion: Our data suggest that TLR7 signaling on mast cells might be a potential therapeutic target for mast cell-driven, IgE-independent skin inflammation.",

keywords = "Mast cell, Skin inflammation, Toll‐like receptor 7",

author = "Cho, {Kyung Ah} and Choi, {Da Won} and Minhwa Park and Kim, {Yu Hee} and Woo, {So Youn}",

note = "Funding Information: This work was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea Government (MSIT) (No. NRF-2019R1H1A1035603 and NRF-2020 R1C1C1012769) and RP-Grant 2019 of Ewha Womans University. The funders had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication. Publisher Copyright: Copyright {\textcopyright} The Korean Dermatological Association and The Korean Society for Investigative Dermatology",

year = "2021",

month = oct,

doi = "10.5021/AD.2021.33.5.402",

language = "English",

volume = "33",

pages = "402--408",

journal = "Annals of Dermatology",

issn = "1013-9087",

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T1 - Toll‐like receptor 7 (TLR7) mediated transcriptomic changes on human mast cells

AU - Cho, Kyung Ah

AU - Choi, Da Won

AU - Park, Minhwa

AU - Kim, Yu Hee

AU - Woo, So Youn

N1 - Funding Information: This work was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea Government (MSIT) (No. NRF-2019R1H1A1035603 and NRF-2020 R1C1C1012769) and RP-Grant 2019 of Ewha Womans University. The funders had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication. Publisher Copyright: Copyright © The Korean Dermatological Association and The Korean Society for Investigative Dermatology

PY - 2021/10

Y1 - 2021/10

N2 - Background: Mast cells are skin immune sentinels located in the upper dermis, where wheal formation and sensory nerve stimulation take place. Skin inflammation is occasionally accompanied by mast cell-driven responses with wheals, angioedema, or both. Immunoglobulin E (IgE) antibodies are regarded as typical stimuli to drive mast cell activation. However, various causative factors, including microbial infections, can drive IgE-independent mast cell response. When infected, the innate immunity orchestrates an immune response by activating receptor signaling via Toll-like receptors (TLRs). Objective: In this study, we determined the effect of TLR7 stimulation on mast cells to investigate the possible mechanism of IgE-independent inflammatory response. Methods: Human mast cell (HMC) line, HMC-1 cells were treated with TLR7 agonist and the morphologic alteration was observed in transmission electron microscopy. Further, TLR7 agonist treated HMC-1 cells were conducted to RNA sequencing to compare transcriptomic features. Results: HMC-1 cells treated with TLR7 agonist reveals increase of intracellular vesicles, lipid droplets, and ribosomes. Also, genes involved in pro-inflammatory responses such as angiogenesis are highly expressed, and Il12rb2 was the most highly upregulated gene. Conclusion: Our data suggest that TLR7 signaling on mast cells might be a potential therapeutic target for mast cell-driven, IgE-independent skin inflammation.

AB - Background: Mast cells are skin immune sentinels located in the upper dermis, where wheal formation and sensory nerve stimulation take place. Skin inflammation is occasionally accompanied by mast cell-driven responses with wheals, angioedema, or both. Immunoglobulin E (IgE) antibodies are regarded as typical stimuli to drive mast cell activation. However, various causative factors, including microbial infections, can drive IgE-independent mast cell response. When infected, the innate immunity orchestrates an immune response by activating receptor signaling via Toll-like receptors (TLRs). Objective: In this study, we determined the effect of TLR7 stimulation on mast cells to investigate the possible mechanism of IgE-independent inflammatory response. Methods: Human mast cell (HMC) line, HMC-1 cells were treated with TLR7 agonist and the morphologic alteration was observed in transmission electron microscopy. Further, TLR7 agonist treated HMC-1 cells were conducted to RNA sequencing to compare transcriptomic features. Results: HMC-1 cells treated with TLR7 agonist reveals increase of intracellular vesicles, lipid droplets, and ribosomes. Also, genes involved in pro-inflammatory responses such as angiogenesis are highly expressed, and Il12rb2 was the most highly upregulated gene. Conclusion: Our data suggest that TLR7 signaling on mast cells might be a potential therapeutic target for mast cell-driven, IgE-independent skin inflammation.

KW - Mast cell

KW - Skin inflammation

KW - Toll‐like receptor 7

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U2 - 10.5021/AD.2021.33.5.402

DO - 10.5021/AD.2021.33.5.402

M3 - Article

AN - SCOPUS:85116756651

SN - 1013-9087

VL - 33

SP - 402

EP - 408

JO - Annals of Dermatology

JF - Annals of Dermatology

IS - 5

ER -

Toll‐like receptor 7 (TLR7) mediated transcriptomic changes on human mast cells

Abstract

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Keywords

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