Group 2 Innate Lymphoid Cells Participate in Renal Fibrosis in Diabetic Kidney Disease Partly via TGF-β1 Signal Pathway

Aim. To explore the role of group 2 innate lymphoid cells (ILC2s) in the pathogenesis of renal fibrosis in diabetic kidney disease (DKD). Methods. The proportion of ILC2s and the levels of Th2 cytokines (IL-4, IL-5, and IL-13) in the peripheral blood of normal control subjects (NC) or patients with...

Full description

Saved in:
Bibliographic Details
Published inJournal of diabetes research Vol. 2019; no. 2019; pp. 1 - 12
Main Authors Long, Yang, Xu, Yong, Jiang, Zongzhe, Guo, Man, Zhang, Ting, Gao, Chenlin, Zhou, Luping, Ding, Jingya, Qin, Ludan, Liu, Cuiping, Huang, Wei
Format Journal Article
LanguageEnglish
Published Cairo, Egypt Hindawi Publishing Corporation 2019
Hindawi
John Wiley & Sons, Inc
Wiley
Subjects
Online AccessGet full text
ISSN2314-6745
2314-6753
2314-6753
DOI10.1155/2019/8512028

Cover

Abstract Aim. To explore the role of group 2 innate lymphoid cells (ILC2s) in the pathogenesis of renal fibrosis in diabetic kidney disease (DKD). Methods. The proportion of ILC2s and the levels of Th2 cytokines (IL-4, IL-5, and IL-13) in the peripheral blood of normal control subjects (NC) or patients with type 2 diabetes mellitus (DM), early diabetic kidney disease (DKD1), or late diabetic kidney disease (DKD2) were analyzed by flow cytometry and ELISA. The expression of transforming growth factor-β1 (TGF-β1), fibronectin (FN), collagen1, IL-4Rα, and IL-13Rα1 in renal tubular epithelial cells (HK-2) induced by IL-4, IL-13, or high glucose was analyzed by ELISA or qPCR. Results. The proportion of ILC2s and the levels of IL-4, IL-5, and IL-13 were significantly increased in DKD patients and were positively correlated with the severity of DKD (P<0.05). The expression of TGF-β1, FN, and collagen1 was significantly upregulated in HK-2 cells induced by IL-4 or IL-13 (P<0.05). Moreover, the IL-4Rα and IL-13Rα1 mRNA in HK2 cells were increased followed by high glucose alone or combined with IL-4 or IL-13, but the differences were not statistically significant (P>0.05). However, compared with high-glucose stimulation alone, the expression of TGF-β1, FN, and collagen1 was significantly increased in HK-2 cells induced by high glucose combined with IL-4 or IL-13 (P<0.05). Conclusions. ILC2s may participate in renal fibrosis in DKD partly via TGF-β1 signal pathway.
AbstractList To explore the role of group 2 innate lymphoid cells (ILC2s) in the pathogenesis of renal fibrosis in diabetic kidney disease (DKD).AIMTo explore the role of group 2 innate lymphoid cells (ILC2s) in the pathogenesis of renal fibrosis in diabetic kidney disease (DKD).The proportion of ILC2s and the levels of Th2 cytokines (IL-4, IL-5, and IL-13) in the peripheral blood of normal control subjects (NC) or patients with type 2 diabetes mellitus (DM), early diabetic kidney disease (DKD1), or late diabetic kidney disease (DKD2) were analyzed by flow cytometry and ELISA. The expression of transforming growth factor-β1 (TGF-β1), fibronectin (FN), collagen1, IL-4Rα, and IL-13Rα1 in renal tubular epithelial cells (HK-2) induced by IL-4, IL-13, or high glucose was analyzed by ELISA or qPCR.METHODSThe proportion of ILC2s and the levels of Th2 cytokines (IL-4, IL-5, and IL-13) in the peripheral blood of normal control subjects (NC) or patients with type 2 diabetes mellitus (DM), early diabetic kidney disease (DKD1), or late diabetic kidney disease (DKD2) were analyzed by flow cytometry and ELISA. The expression of transforming growth factor-β1 (TGF-β1), fibronectin (FN), collagen1, IL-4Rα, and IL-13Rα1 in renal tubular epithelial cells (HK-2) induced by IL-4, IL-13, or high glucose was analyzed by ELISA or qPCR.The proportion of ILC2s and the levels of IL-4, IL-5, and IL-13 were significantly increased in DKD patients and were positively correlated with the severity of DKD (P < 0.05). The expression of TGF-β1, FN, and collagen1 was significantly upregulated in HK-2 cells induced by IL-4 or IL-13 (P < 0.05). Moreover, the IL-4Rα and IL-13Rα1 mRNA in HK2 cells were increased followed by high glucose alone or combined with IL-4 or IL-13, but the differences were not statistically significant (P > 0.05). However, compared with high-glucose stimulation alone, the expression of TGF-β1, FN, and collagen1 was significantly increased in HK-2 cells induced by high glucose combined with IL-4 or IL-13 (P < 0.05).RESULTSThe proportion of ILC2s and the levels of IL-4, IL-5, and IL-13 were significantly increased in DKD patients and were positively correlated with the severity of DKD (P < 0.05). The expression of TGF-β1, FN, and collagen1 was significantly upregulated in HK-2 cells induced by IL-4 or IL-13 (P < 0.05). Moreover, the IL-4Rα and IL-13Rα1 mRNA in HK2 cells were increased followed by high glucose alone or combined with IL-4 or IL-13, but the differences were not statistically significant (P > 0.05). However, compared with high-glucose stimulation alone, the expression of TGF-β1, FN, and collagen1 was significantly increased in HK-2 cells induced by high glucose combined with IL-4 or IL-13 (P < 0.05).ILC2s may participate in renal fibrosis in DKD partly via TGF-β1 signal pathway.CONCLUSIONSILC2s may participate in renal fibrosis in DKD partly via TGF-β1 signal pathway.
Aim. To explore the role of group 2 innate lymphoid cells (ILC2s) in the pathogenesis of renal fibrosis in diabetic kidney disease (DKD). Methods. The proportion of ILC2s and the levels of Th2 cytokines (IL-4, IL-5, and IL-13) in the peripheral blood of normal control subjects (NC) or patients with type 2 diabetes mellitus (DM), early diabetic kidney disease (DKD1), or late diabetic kidney disease (DKD2) were analyzed by flow cytometry and ELISA. The expression of transforming growth factor-β1 (TGF-β1), fibronectin (FN), collagen1, IL-4Rα, and IL-13Rα1 in renal tubular epithelial cells (HK-2) induced by IL-4, IL-13, or high glucose was analyzed by ELISA or qPCR. Results. The proportion of ILC2s and the levels of IL-4, IL-5, and IL-13 were significantly increased in DKD patients and were positively correlated with the severity of DKD (P<0.05). The expression of TGF-β1, FN, and collagen1 was significantly upregulated in HK-2 cells induced by IL-4 or IL-13 (P<0.05). Moreover, the IL-4Rα and IL-13Rα1 mRNA in HK2 cells were increased followed by high glucose alone or combined with IL-4 or IL-13, but the differences were not statistically significant (P>0.05). However, compared with high-glucose stimulation alone, the expression of TGF-β1, FN, and collagen1 was significantly increased in HK-2 cells induced by high glucose combined with IL-4 or IL-13 (P<0.05). Conclusions. ILC2s may participate in renal fibrosis in DKD partly via TGF-β1 signal pathway.
Author Xu, Yong
Zhang, Ting
Gao, Chenlin
Ding, Jingya
Liu, Cuiping
Jiang, Zongzhe
Guo, Man
Huang, Wei
Qin, Ludan
Long, Yang
Zhou, Luping
AuthorAffiliation 1 Luzhou Key Laboratory of Cardiovascular and Metabolic Diseases, Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, China
3 State Key Laboratory of Quality Research in Chinese Medicine, Faculty of Chinese Medicine, Macau University of Science and Technology, Avenida Wai Long, Taipa, Macau
2 Department of Endocrinology, Zigong Fourth People's Hospital, Zigong, Sichuan, China
AuthorAffiliation_xml – name: 2 Department of Endocrinology, Zigong Fourth People's Hospital, Zigong, Sichuan, China
– name: 3 State Key Laboratory of Quality Research in Chinese Medicine, Faculty of Chinese Medicine, Macau University of Science and Technology, Avenida Wai Long, Taipa, Macau
– name: 1 Luzhou Key Laboratory of Cardiovascular and Metabolic Diseases, Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, China
Author_xml – sequence: 1
  fullname: Long, Yang
– sequence: 2
  fullname: Xu, Yong
– sequence: 3
  fullname: Jiang, Zongzhe
– sequence: 4
  fullname: Guo, Man
– sequence: 5
  fullname: Zhang, Ting
– sequence: 6
  fullname: Gao, Chenlin
– sequence: 7
  fullname: Zhou, Luping
– sequence: 8
  fullname: Ding, Jingya
– sequence: 9
  fullname: Qin, Ludan
– sequence: 10
  fullname: Liu, Cuiping
– sequence: 11
  fullname: Huang, Wei
BookMark eNpdkt9u0zAUxiM0xMbYHdfIEjdIKCyOfRL7BgkVWioqMcG4tvwvravULnGykdfiQXgmnLYaGr6xfc7vfLI_fc-zMx-8zbKXuHiHMcB1WWB-zQCXRcmeZBclwTSvaiBnD2cK59lVjNsiLU44A_YsOyeYAJScXmS_Fl0Y9qhES-9lb9Fq3O03wRk0s20b0Y3seqfdfmo5j75ZL1s0d6oL0cWp8tFJZROCvjjj7Zju0cpoD4PtiO6cRLeLef7nN0bf3XqavpH95l6OL7KnjWyjvTrtl9mP-afb2ed89XWxnH1Y5YZQznKMNShGK46VgVIqRRkzyhCmNYAqC15RqimAblSdWI1rq7GuSWW4pY3E5DJbHnVNkFux79xOdqMI0olDIXRrcfhjawVOBlFudFXomrJCMtDSJMdUAxaSXtJ6f9TaD2pnjba-72T7SPRxx7uNWIc7UVWkAk6TwJuTQBd-Djb2YueiTk5Lb8MQRVkmkjIMVUJf_4duw9AlAxNFi7oCoDVP1NsjtXHeyHv38BZciCkgYgqIOAUk0a-OtE2MbeQ_GteEFDX5CwOmtss
ContentType Journal Article
Copyright Copyright © 2019 Cuiping Liu et al.
Copyright © 2019 Cuiping Liu et al. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
Copyright © 2019 Cuiping Liu et al. 2019
Copyright_xml – notice: Copyright © 2019 Cuiping Liu et al.
– notice: Copyright © 2019 Cuiping Liu et al. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
– notice: Copyright © 2019 Cuiping Liu et al. 2019
DBID ADJCN
AHFXO
RHU
RHW
RHX
3V.
7RV
7X7
7XB
8C1
8FI
8FJ
8FK
ABUWG
AFKRA
AZQEC
BENPR
CCPQU
DWQXO
FYUFA
GHDGH
K9.
KB0
M0S
M0T
NAPCQ
PHGZM
PHGZT
PIMPY
PJZUB
PKEHL
PPXIY
PQEST
PQQKQ
PQUKI
7X8
5PM
DOA
DOI 10.1155/2019/8512028
DatabaseName الدوريات العلمية والإحصائية - e-Marefa Academic and Statistical Periodicals
معرفة - المحتوى العربي الأكاديمي المتكامل - e-Marefa Academic Complete
Hindawi Publishing Complete
Hindawi Publishing Subscription Journals
Hindawi Publishing Open Access
ProQuest Central (Corporate)
Nursing & Allied Health Database
Health & Medical Collection
ProQuest Central (purchase pre-March 2016)
Public Health Database
ProQuest Hospital Collection
Hospital Premium Collection (Alumni Edition)
ProQuest Central (Alumni) (purchase pre-March 2016)
ProQuest Central (Alumni)
ProQuest Central UK/Ireland
ProQuest Central Essentials
ProQuest Central
ProQuest One Community College
ProQuest Central Korea
Proquest Health Research Premium Collection
Health Research Premium Collection (Alumni)
ProQuest Health & Medical Complete (Alumni)
Nursing & Allied Health Database (Alumni Edition)
ProQuest Health & Medical Collection
Healthcare Administration Database (Proquest)
Nursing & Allied Health Premium
ProQuest Central Premium
ProQuest One Academic
Publicly Available Content Database
ProQuest Health & Medical Research Collection
ProQuest One Academic Middle East (New)
ProQuest One Health & Nursing
ProQuest One Academic Eastern Edition (DO NOT USE)
ProQuest One Academic
ProQuest One Academic UKI Edition
MEDLINE - Academic
PubMed Central (Full Participant titles)
DOAJ Directory of Open Access Journals
DatabaseTitle Publicly Available Content Database
ProQuest One Academic Middle East (New)
ProQuest Central Essentials
ProQuest Health & Medical Complete (Alumni)
ProQuest Central (Alumni Edition)
ProQuest One Community College
ProQuest One Health & Nursing
ProQuest Central
ProQuest Health & Medical Research Collection
Health Research Premium Collection
Health and Medicine Complete (Alumni Edition)
ProQuest Central Korea
Health & Medical Research Collection
ProQuest Central (New)
ProQuest Public Health
ProQuest One Academic Eastern Edition
ProQuest Health Management
ProQuest Nursing & Allied Health Source
ProQuest Hospital Collection
Health Research Premium Collection (Alumni)
ProQuest Hospital Collection (Alumni)
Nursing & Allied Health Premium
ProQuest Health & Medical Complete
ProQuest One Academic UKI Edition
ProQuest Nursing & Allied Health Source (Alumni)
ProQuest One Academic
ProQuest One Academic (New)
ProQuest Central (Alumni)
MEDLINE - Academic
DatabaseTitleList MEDLINE - Academic

Publicly Available Content Database


Database_xml – sequence: 1
  dbid: RHX
  name: Hindawi Publishing Open Access
  url: http://www.hindawi.com/journals/
  sourceTypes: Publisher
– sequence: 2
  dbid: DOA
  name: DOAJ Directory of Open Access Journals
  url: https://www.doaj.org/
  sourceTypes: Open Website
– sequence: 3
  dbid: BENPR
  name: ProQuest Central
  url: http://www.proquest.com/pqcentral?accountid=15518
  sourceTypes: Aggregation Database
DeliveryMethod fulltext_linktorsrc
Discipline Medicine
EISSN 2314-6753
Editor Okamoto, Hiroshi
Editor_xml – sequence: 1
  givenname: Hiroshi
  surname: Okamoto
  fullname: Okamoto, Hiroshi
EndPage 12
ExternalDocumentID oai_doaj_org_article_109349dc60c7480a85cad985bf5e5d9e
PMC6636594
10_1155_2019_8512028
1173307
GeographicLocations Beijing China
China
GeographicLocations_xml – name: China
– name: Beijing China
GrantInformation_xml – fundername: Education Department of Sichuan Province
  grantid: 17CZ0041
– fundername: National Natural Science Foundation of China
  grantid: 81800741
GroupedDBID 0R~
24P
4.4
53G
5VS
7RV
7X7
8C1
8FI
8FJ
AAFWJ
AAKDD
AAMMB
ABDBF
ABUWG
ACCMX
ACUHS
ADBBV
ADJCN
ADRAZ
AEFGJ
AENEX
AFKRA
AFPKN
AGXDD
AHFXO
AIDQK
AIDYY
ALMA_UNASSIGNED_HOLDINGS
AOIJS
BAWUL
BCNDV
BENPR
CCPQU
DIK
EBD
EBS
EJD
EMOBN
ESX
FYUFA
GROUPED_DOAJ
H13
HMCUK
HYE
IAO
IEA
IHR
IHW
INH
INR
ITC
KQ8
M0T
M48
NAPCQ
OK1
PGMZT
PHGZM
PHGZT
PIMPY
PJZUB
PPXIY
PUEGO
RPM
SV3
TUS
UKHRP
~8M
AAJEY
ADMBK
RHU
RHW
RHX
3V.
7XB
8FK
ALIPV
AZQEC
DWQXO
K9.
PKEHL
PQEST
PQQKQ
PQUKI
7X8
5PM
ID FETCH-LOGICAL-d3498-11c5b84691bd52abb488dbd38cc55b209644c455cfb711cc17ec1c736d9e4fa13
IEDL.DBID M48
ISSN 2314-6745
2314-6753
IngestDate Wed Aug 27 01:31:36 EDT 2025
Thu Aug 21 18:30:43 EDT 2025
Thu Sep 04 21:18:36 EDT 2025
Fri Jul 25 20:48:24 EDT 2025
Sun Jun 02 18:51:59 EDT 2024
Thu Sep 25 15:03:13 EDT 2025
IsDoiOpenAccess true
IsOpenAccess true
IsPeerReviewed true
IsScholarly true
Issue 2019
Language English
License This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
LinkModel DirectLink
MergedId FETCHMERGED-LOGICAL-d3498-11c5b84691bd52abb488dbd38cc55b209644c455cfb711cc17ec1c736d9e4fa13
Notes ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 14
content type line 23
Academic Editor: Hiroshi Okamoto
ORCID 0000-0002-1955-181X
0000-0003-4668-0681
0000-0003-3473-956X
0000-0002-9744-8762
0000-0002-9671-2939
0000-0001-7646-669X
0000-0003-4305-743X
0000-0003-2464-9325
0000-0002-9534-6252
0000-0003-1065-6604
OpenAccessLink http://journals.scholarsportal.info/openUrl.xqy?doi=10.1155/2019/8512028
PMID 31355294
PQID 2407655479
PQPubID 4727240
PageCount 12
ParticipantIDs doaj_primary_oai_doaj_org_article_109349dc60c7480a85cad985bf5e5d9e
pubmedcentral_primary_oai_pubmedcentral_nih_gov_6636594
proquest_miscellaneous_2266348156
proquest_journals_2407655479
hindawi_primary_10_1155_2019_8512028
emarefa_primary_1173307
PublicationCentury 2000
PublicationDate 2019-00-00
PublicationDateYYYYMMDD 2019-01-01
PublicationDate_xml – year: 2019
  text: 2019-00-00
PublicationDecade 2010
PublicationPlace Cairo, Egypt
PublicationPlace_xml – name: Cairo, Egypt
– name: Cairo
PublicationTitle Journal of diabetes research
PublicationYear 2019
Publisher Hindawi Publishing Corporation
Hindawi
John Wiley & Sons, Inc
Wiley
Publisher_xml – name: Hindawi Publishing Corporation
– name: Hindawi
– name: John Wiley & Sons, Inc
– name: Wiley
SSID ssj0000939858
ssib050733531
Score 2.2064881
Snippet Aim. To explore the role of group 2 innate lymphoid cells (ILC2s) in the pathogenesis of renal fibrosis in diabetic kidney disease (DKD). Methods. The...
To explore the role of group 2 innate lymphoid cells (ILC2s) in the pathogenesis of renal fibrosis in diabetic kidney disease (DKD).AIMTo explore the role of...
SourceID doaj
pubmedcentral
proquest
hindawi
emarefa
SourceType Open Website
Open Access Repository
Aggregation Database
Publisher
StartPage 1
SubjectTerms Antibodies
Cytokines
Diabetes
Diabetic nephropathy
Diabetic retinopathy
Flow cytometry
Genes
Glucose
Homeostasis
Inflammation
Kidney diseases
Pathogenesis
Studies
Variance analysis
SummonAdditionalLinks – databaseName: DOAJ Directory of Open Access Journals
  dbid: DOA
  link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV1Lb9QwELZQpSIuiPIMFGSkXqONNx47PtKKpTyKKmil3iK_QiOtvIhtKfu3-kP6mzp2vGVz4sIxfkmez2N_Y09mCNkTVhtUG9S0ivOSG65KNJtZ6WspmbO66VIugqOv4vCUfzqDs41UX9EnbAgPPAhuEsMdceWsqKzkTaUbsNqpBkwHHpzycfetVLVhTOFKgpiKEPL7VtqTVY19Unq6mvFSSA5rL3iACR6CaoLUY1rFpOwpdn_6QVfjIYUH1vZ5NI-v-hEJHbtQbpxJs0fkYSaT9N0wiR1yz4fH5P5Rfi5_Qv6kmyU6pR9DQE5Jv6wQu0Xv6IGfz5f0WK99qj3tA_3m42AztJ8Xy34ZSwZ3md7Sz70LfoXf6TUndZyv6O9e05MPs_LmmtHv_Y_Y-xgJ5ZVePSWns_cnB4dlTrVQOpQu2pHMgkEqophxMNXGoF474-rGWgCDAkbaZDmA7YzEtpZJb5mVtUAEeKdZ_YxshUXwLwhFvgFe4SDeW2611L7DFVCJxkgjnKkKsh8F3P4comm0Mb51KkDU24x6-y_UC_I8w3M3DmOIeSULspfh-lsT7RyANsLcZpgLsrvGss1au2yjdSuQX0lVkLd31ahv8RFFB7-4xDbIaOoUY6cgcrQGRjMa14T-PEXuxq4CFH_5P0TwijyIExqug3bJ1sWvS_8aCdKFeZN04RbAlwrT
  priority: 102
  providerName: Directory of Open Access Journals
– databaseName: Hindawi Publishing Open Access
  dbid: RHX
  link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwjV3LbtQwFL2ilUBsEG8CBRmp24h44ke8LFWH4VFUlVaaXeRXaKSRB5GWMr_VD-Gbeu3xFAIblvErTo5vfI6vcw2wK6w2aDZoaRVjJTNMlSibaelrKamzuunSWQSHn8XslH2Y83kOkjT868LH2Q7lOVVvkBigTG-2YKsRcfAez-abYcPjuYM8O7PSB1jVqkkncyJ5YaWQjG-2vP_VXA7Un_7G1Tgj4ex0-yxq4ct-xDjH-yX_mICm9-FeZo5kbw31A7jlw0O4c5h944_gZ1pGIhPyPgQkkOTTCoFa9o7s-8ViIEd6s4Hakz6QYx8bm6JYXg79EFPWe2N6Sz72LvgVXifXTaq4WJEfvSYn76blrytKvvRfY-0jZI-XevUYTqcHJ_uzMp-rULqaKRSN1HKDvENR4_hEG4NG7IyrG2s5NxMUNYxZxrntjMSylkpvqZW1cMqzTtP6CWyHZfDPgCC54F5hI95bZrXUvkO4K9EYaYQzVQFv4wtuv61DZ7QxmHVKQIDbbBvRCY79clZUVrKm0g232iGCpuOe4z0LeJrhuWmHUsS8kgXsZrh-50RRw3kbYW4zzAXsbLBss4kObZSyAsmUVAW8vslG44oeEx388gLLIH2pU0CdAuRoDIyeaJwT-rMUphurCq7Y8__r4wu4Gy_Xqzs7sH3-_cK_RL5zbl6l0X4N3YH30g
  priority: 102
  providerName: Hindawi Publishing
– databaseName: ProQuest Central
  dbid: BENPR
  link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwfV1Lb9QwEB6VrUBcEM8SKMhIvUYbb-w4PiBEqy7l0dWqtFJvkV9pI62S0m0p-7f4Ifwmxl6nJReOsWPnMTOebzzjGYCdwiiNYoOSljGWMs1kimYzTV0uBLVGlXWoRXA4Kw5O2JdTfroBs_4sjA-r7NfEsFDbzvg98rG3PArUfUJ-uPiR-qpR3rval9BQsbSCfR9SjN2DTVySeTaCzd392fyo5zDuSxTy6PcKa7XMZRmKeCLOYWkhGO-j4zkfo3KUY4Qkk8wXaw85_cPBXYXKCxXZ_XNvNt80A3A6DK38R1dNH8OjCDLJxzVXPIEN1z6FB4fRjf4MfoUdJzIhn9sWsSb5tkKado0le26xWJK56mOtHWlacuT8ZFO0q7tls_Qt6zCaxpCvjW3dCq-DlycMXKzIz0aR40_T9M9vSr43Z370HIHmjVo9h5Pp_vHeQRpLMKQ2ZxLtS2q4RogiqbZ8orRGebfa5qUxnOsJ2j-MGca5qbXAew0VzlAj8sJKx2pF8xcwarvWvQSCOIQ7iZM4Z5hRQrkaOSMrSi10YXWWwK7_wdXFOstG5fNeh4bu8qyKYuT95fhe1hSZEazMVMmNskhBXXPH8ZkJbEXy3M5DKdI8EwnsRHLd9Xj7h_PKk7mKZE5gu6dlFaV5Wd3xXgLvbrtRDr1zRbWuu8Z7EOnkIfdOAmLAA4MvGva0zXnI6I1DCy7Zq_8__DU89K-63gDahtHV5bV7g5DoSr-NfP4XdfkItg
  priority: 102
  providerName: ProQuest
Title Group 2 Innate Lymphoid Cells Participate in Renal Fibrosis in Diabetic Kidney Disease Partly via TGF-β1 Signal Pathway
URI https://search.emarefa.net/detail/BIM-1173307
https://dx.doi.org/10.1155/2019/8512028
https://www.proquest.com/docview/2407655479
https://www.proquest.com/docview/2266348156
https://pubmed.ncbi.nlm.nih.gov/PMC6636594
https://doaj.org/article/109349dc60c7480a85cad985bf5e5d9e
Volume 2019
hasFullText 1
inHoldings 1
isFullTextHit
isPrint
link http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1bb9MwFD7aRUx7QVxHxqiMtNdA3Nhx_IAQq1bKZVNVVqlvkW_dIlUpaze2_C1-CL-JYzfdCOKJl0iJYyf28Ym_z-fkHIDDzCiNaoOaljAWM81kjLSZxi4Vglqj8mnIRXBymg3G7POETzZgnW20GcDlP6mdzyc1Xsze3F7W71Hh3wWF5xz5O5VvETkgj883YTtYirwT3z3Q5z41IW_sXeEbLVOZh-SdiG9YnAnG117xfzW4CzspxUW5K1kT1j_8u6tw_cK17MGFZ843ZQuftr0r_1iu-o_gYYMzyYfVxHgMG656AjsnjSX9KdyGTSfSJZ-qCuEm-VqjWOelJT03my3JUK3drR0pKzJyvrE-Uuv5slz6KytPmtKQL6WtXI3nwdATKs5q8qNU5OxjP_71k5Jv5bmvPUSseaPqZzDuH5_1BnGThSG2KZNIManhGlGKpNryrtIaVd5qm-bGcK67SIEYM4xzM9UC7zVUOEONSDMrHZsqmj6HrWpeuRdAEIpwJ7ER5wwzSig3xcmRZLkWOrM6ieDID3DxfRVoo_Chr8OF-eK8aDTJm8zxvazJEiNYnqicG2VRmHrKHcdnRrDXiOeuHUpR_ImI4LAR132Jp0CcF17iRSPxCA7WsizW87HwxDdD6CVkBK_vilEVvX1FVW5-jfcg2ElD-J0IRGsOtHrULqnKixDUG6tmXLL9_675EnZ9L1bbQwewdbW4dq8QMF3pDmyKicBj3qMd2D46Ph2OOmHzoRO0BI-jweQ3kTIWhA
linkProvider Scholars Portal
linkToHtml http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwtV1Lb9QwEB6VrXhcEG8CBYxUjtHmYcebQ4Vo6bLLPrQqW6m31K9tI62S0m0p-7f4AfwEfhNjr9OyF249Jo4dJzPj-cYzngHYzpSQKDYoaRGlIZU0D9FsjkOTch5rJTozV4tgNM56h_TrETvagN_NWRgbVtmsiW6h1rWye-Rta3lkqPt4_vHse2irRlnvalNCQ_jSCnrHpRjzBzsGZnmFJtxip_8Z6f0hSbr7071e6KsMhDqlOZpQsWIStXAeS80SISWytJY67SjFmEwQ4lOqKGNqJjk-q2JuVKx4munc0JmIUxz3DmxSu4HSgs3d_fHkoOFoZksiMu9nc7ohT_OOKxqKuIqGGaesicZnrI3KOG8jBEoiWxze1RBwB4UFKktUnHdPrZl-Va6B4fVQzn90Y_cRPPSglnxaceFj2DDVE7g38m77p_DT7XCRhPSrCrEtGS6Rh-pSkz0zny_IRDSx3YaUFTkwdrAu2vH1olzYO6uwnVKRQakrs8Rr51VyHedL8qMUZPqlG_75FZNv5YntPUFgeyWWz-DwVojxHFpVXZmXQBD3MJPjIMYoqgQXZoacGGUdyWWmZRTArv3Bxdkqq0dh82y7G_X5SeHF1vrncV5aZZHitBOJDlNCIwXljBmG7wzghSfP9ThxjDSPeADbnlw3LdbeYqywZC48mQPYamhZ-NVjUdzwegDvr5tR7q0zR1SmvsRnEFmlLtdPAHyNB9a-aL2lKk9dBnHsmrGcvvr_y9_B_d50NCyG_fHgNTyw015tPm1B6-L80rxBOHYh33qeJ3B822L2F7TARaM
linkToPdf http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwtV1Lb9QwEB6VVlRcEG8CBYxUjtHmYcfJoUL0sXTZdrUqrdRb8CttpFVSui3L_i1-Bgd-E2Ov07IXbj0mjh0nM-P5xjOeAdjMlJAoNihpEaUhlbQI0WyOQ5NyHmsl8srVIjgcZfsn9MspO12B391ZGBtW2a2JbqHWrbJ75D1reWSo-3jRq3xYxHi3__Hie2grSFlPa1dOQ_gyC3rLpRvzhzyGZj5Dc266NdhF2n9Ikv7e8c5-6CsOhDqlBZpTsWISNXIRS80SISWyt5Y6zZViTCYI9ylVlDFVSY7PqpgbFSueZrowtBJxiuPegzWOWh8NwbXtvdH4qONuZssjMu9zc3qiSIvcFRBFjEXDjFPWReYz1kPFXPQQDiWRLRTv6gm4Q8MCFScq0fvn1mSf1UvAeDms8x892X8EDz3AJZ8WHPkYVkzzBNYPvQv_Kfx0u10kIYOmQZxLDubIT22tyY6ZTKZkLLo4b0PqhhwZO1gfbfp2Wk_tnUUIT63IsNaNmeO18zC5jpM5-VELcvy5H_75FZOv9ZntPUaQOxPzZ3ByJ8R4DqtN25iXQBADMVPgIMYoqgQXpkKujLJccplpGQWwbX9webHI8FHanNvuRnt5VnoRtr56nJdWWaQ4zSORMyU0UlBWzDB8ZwAvPHluxoljpHnEA9j05LptsbYXY6Ulc-nJHMBGR8vSryTT8pbvA3h_04xrgHXsiMa01_gMoqzU5f0JgC_xwNIXLbc09bnLJo5dM1bQV_9_-TtYR3ErDwaj4Wt4YGe92IfagNWry2vzBpHZlXzrWZ7At7uWsr8kCknn
openUrl ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Group+2+Innate+Lymphoid+Cells+Participate+in+Renal+Fibrosis+in+Diabetic+Kidney+Disease+Partly+via+TGF-%CE%B21+Signal+Pathway&rft.jtitle=Journal+of+diabetes+research&rft.au=Liu%2C+Cuiping&rft.au=Qin%2C+Ludan&rft.au=Ding%2C+Jingya&rft.au=Zhou%2C+Luping&rft.date=2019&rft.pub=Hindawi&rft.issn=2314-6745&rft.eissn=2314-6753&rft.volume=2019&rft_id=info:doi/10.1155%2F2019%2F8512028&rft_id=info%3Apmid%2F31355294&rft.externalDocID=PMC6636594
thumbnail_l http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=2314-6745&client=summon
thumbnail_m http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=2314-6745&client=summon
thumbnail_s http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=2314-6745&client=summon