Downregulated YTHDF2 expression in systemic lupus erythematosus is associated with inflammatory and neutrophil cytokine production
Objectives An increasing body of evidence suggests that N6-methyladenosine (m6A) plays a crucial role in the etiology of SLE. We focused on YTHDF2 expression in neutrophils and the relationship between YTHDF2 and the pathogenesis of SLE. Methods Sixty-one patients with SLE and 48 healthy controls (H...
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| Veröffentlicht in: | Clinical rheumatology 2025, Vol.44 (1), p.237-246 |
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| creator | Zhao, Hongshuai Lan, Mengfan Huang, Zikun Fu, Peng Fu, Biqi Guo, Yang Li, Junming Luo, Qing |
| description | Objectives
An increasing body of evidence suggests that N6-methyladenosine (m6A) plays a crucial role in the etiology of SLE. We focused on YTHDF2 expression in neutrophils and the relationship between YTHDF2 and the pathogenesis of SLE.
Methods
Sixty-one patients with SLE and 48 healthy controls (HC) were recruited, and their clinical characteristics were recorded. The mRNA levels of m6A “writers” (METTL3, METTL14, WTAP), “erasers” (FTO and ALKBH5), “readers” (YTHDF2), and inflammatory factors (interleukin-1β, interleukin-6, interleukin-8, and TNF-α) in neutrophils were determined by reverse transcription-quantitative PCR. The protein of YTHDF2 was determined by Western blotting. The correlations between the YTHDF2 in neutrophils of SLE patients and clinical features were examined by Spearman’s method. YTHDF2 and TNF-α expression in neutrophils were examined after stimulation by SLE serums.
Results
The mRNA expression of YTHDF2 in neutrophils was significantly decreased, and the protein level of YTHDF2 in neutrophils was decreased. The mRNA expression of YTHDF2 in neutrophils correlated with
L
% (
r
s
= 0.5796,
P
|
| doi_str_mv | 10.1007/s10067-024-07257-z |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_3146665062</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>3154979929</sourcerecordid><originalsourceid>FETCH-LOGICAL-c256t-3deea0c253d2bad475a4e005652c08ebcbf8cb02d49679c09e6fbd2c8f65ac1d3</originalsourceid><addsrcrecordid>eNp9kTFv1TAUhS0Eoo_CH2BAllhYAjd24sQjailFqsRSBqbIsW_6XJI4-Doq6cgvx-0rIDGw-Nq63znH0mHsZQlvS4DmHeVTNQWIqoBG1E1x-4jtykpWhdaVfsx20DRQyFK3R-wZ0TUAiFaXT9mR1Eq1EuSO_TwNN3PEq3U0CR3_enl-eiY4_lgiEvkwcz9z2ijh5C0f12UljnFLe5xMCpRfnrghCtbf62982mfJMJrpDogbN7PjM64phmXvR263FL75GfkSg1ttyhHP2ZPBjIQvHuYx-3L24fLkvLj4_PHTyfuLwopapUI6RAP5Lp3ojaua2lQIUKtaWGixt_3Q2h6Eq7RqtAWNauidsO2gamNLJ4_Zm4Nvjv6-IqVu8mRxHM2MYaVOlpVSqgYlMvr6H_Q6rHHOv8tUXelGa6EzJQ6UjYEo4tAt0U8mbl0J3V1D3aGhLjfU3TfU3WbRqwfrtZ_Q_ZH8riQD8gBQXs1XGP9m_8f2F3lOoJI</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>3154979929</pqid></control><display><type>article</type><title>Downregulated YTHDF2 expression in systemic lupus erythematosus is associated with inflammatory and neutrophil cytokine production</title><source>MEDLINE</source><source>SpringerLink Journals</source><creator>Zhao, Hongshuai ; Lan, Mengfan ; Huang, Zikun ; Fu, Peng ; Fu, Biqi ; Guo, Yang ; Li, Junming ; Luo, Qing</creator><creatorcontrib>Zhao, Hongshuai ; Lan, Mengfan ; Huang, Zikun ; Fu, Peng ; Fu, Biqi ; Guo, Yang ; Li, Junming ; Luo, Qing</creatorcontrib><description>Objectives
An increasing body of evidence suggests that N6-methyladenosine (m6A) plays a crucial role in the etiology of SLE. We focused on YTHDF2 expression in neutrophils and the relationship between YTHDF2 and the pathogenesis of SLE.
Methods
Sixty-one patients with SLE and 48 healthy controls (HC) were recruited, and their clinical characteristics were recorded. The mRNA levels of m6A “writers” (METTL3, METTL14, WTAP), “erasers” (FTO and ALKBH5), “readers” (YTHDF2), and inflammatory factors (interleukin-1β, interleukin-6, interleukin-8, and TNF-α) in neutrophils were determined by reverse transcription-quantitative PCR. The protein of YTHDF2 was determined by Western blotting. The correlations between the YTHDF2 in neutrophils of SLE patients and clinical features were examined by Spearman’s method. YTHDF2 and TNF-α expression in neutrophils were examined after stimulation by SLE serums.
Results
The mRNA expression of YTHDF2 in neutrophils was significantly decreased, and the protein level of YTHDF2 in neutrophils was decreased. The mRNA expression of YTHDF2 in neutrophils correlated with
L
% (
r
s
= 0.5796,
P
< 0.0001), LMR (
r
s
= 0.3524,
P
= 0.0062), WBC (
r
s
= − 0.3186,
P
= 0.0123),
N
(
r
s
= − 0.4141,
P
= 0.0010),
N
% (
r
s
= − 0.4813,
P
< 0.0001), NLR (
r
s
= − 0.5301,
P
< 0.0001), dNLR (
r
s
= − 0.4945,
P
< 0.0001), and SII (
r
s
= − 0.3930,
P
= 0.0019), which were suggested as the inflammatory conditions of SLE. In addition, the mRNA expression of TNF-α in neutrophils was significantly increased in SLE patients. Further analysis revealed that the mRNA expression of YTHDF2 in neutrophils was inversely correlated with TNF-α in SLE. Neutrophils from health control were significantly downregulated in their YTHDF2 expression and upregulated in their TNF-α expression following stimulation by serum from SLE patients.
Conclusion
This study indicates that the levels of YTHDF2 in peripheral blood neutrophils may be involved in the pathogenesis of SLE and could be a novel target for diagnosis and therapy.
Key points
• The mRNA expression of YTHDF2 in neutrophils of SLE and described that decreased mRNA of YTHDF2 in neutrophils correlated with L%, LMR, WBC, N, N%, NLR, dNLR, and SII.
• The mRNA expression of TNF-α in neutrophils was significantly increased and correlated with YTHDF2 in SLE patients.
• Neutrophils from health control were significantly downregulated in their YTHDF2 expression and upregulated in their TNF-α expression following stimulation by serum from SLE patients.</description><identifier>ISSN: 0770-3198</identifier><identifier>ISSN: 1434-9949</identifier><identifier>EISSN: 1434-9949</identifier><identifier>DOI: 10.1007/s10067-024-07257-z</identifier><identifier>PMID: 39668303</identifier><language>eng</language><publisher>Cham: Springer International Publishing</publisher><subject>Adult ; Blood levels ; Case-Control Studies ; Cytokines ; Cytokines - blood ; Cytokines - metabolism ; Down-Regulation ; Female ; Gene expression ; Humans ; Inflammation ; Interleukin 6 ; Interleukin 8 ; Leukocytes (neutrophilic) ; Lupus Erythematosus, Systemic - blood ; Lupus Erythematosus, Systemic - metabolism ; Male ; Medicine ; Medicine & Public Health ; Middle Aged ; N6-methyladenosine ; Neutrophils ; Neutrophils - metabolism ; Original Article ; Pathogenesis ; Peripheral blood ; Reverse transcription ; Rheumatology ; RNA, Messenger - metabolism ; RNA-Binding Proteins - metabolism ; Systemic lupus erythematosus ; Tumor Necrosis Factor-alpha - metabolism ; Tumor necrosis factor-α ; Western blotting ; Young Adult</subject><ispartof>Clinical rheumatology, 2025, Vol.44 (1), p.237-246</ispartof><rights>The Author(s), under exclusive licence to International League of Associations for Rheumatology (ILAR) 2024 Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><rights>2024. The Author(s), under exclusive licence to International League of Associations for Rheumatology (ILAR).</rights><rights>Copyright Springer Nature B.V. Jan 2025</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c256t-3deea0c253d2bad475a4e005652c08ebcbf8cb02d49679c09e6fbd2c8f65ac1d3</cites><orcidid>0009-0001-2023-124X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10067-024-07257-z$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10067-024-07257-z$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39668303$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhao, Hongshuai</creatorcontrib><creatorcontrib>Lan, Mengfan</creatorcontrib><creatorcontrib>Huang, Zikun</creatorcontrib><creatorcontrib>Fu, Peng</creatorcontrib><creatorcontrib>Fu, Biqi</creatorcontrib><creatorcontrib>Guo, Yang</creatorcontrib><creatorcontrib>Li, Junming</creatorcontrib><creatorcontrib>Luo, Qing</creatorcontrib><title>Downregulated YTHDF2 expression in systemic lupus erythematosus is associated with inflammatory and neutrophil cytokine production</title><title>Clinical rheumatology</title><addtitle>Clin Rheumatol</addtitle><addtitle>Clin Rheumatol</addtitle><description>Objectives
An increasing body of evidence suggests that N6-methyladenosine (m6A) plays a crucial role in the etiology of SLE. We focused on YTHDF2 expression in neutrophils and the relationship between YTHDF2 and the pathogenesis of SLE.
Methods
Sixty-one patients with SLE and 48 healthy controls (HC) were recruited, and their clinical characteristics were recorded. The mRNA levels of m6A “writers” (METTL3, METTL14, WTAP), “erasers” (FTO and ALKBH5), “readers” (YTHDF2), and inflammatory factors (interleukin-1β, interleukin-6, interleukin-8, and TNF-α) in neutrophils were determined by reverse transcription-quantitative PCR. The protein of YTHDF2 was determined by Western blotting. The correlations between the YTHDF2 in neutrophils of SLE patients and clinical features were examined by Spearman’s method. YTHDF2 and TNF-α expression in neutrophils were examined after stimulation by SLE serums.
Results
The mRNA expression of YTHDF2 in neutrophils was significantly decreased, and the protein level of YTHDF2 in neutrophils was decreased. The mRNA expression of YTHDF2 in neutrophils correlated with
L
% (
r
s
= 0.5796,
P
< 0.0001), LMR (
r
s
= 0.3524,
P
= 0.0062), WBC (
r
s
= − 0.3186,
P
= 0.0123),
N
(
r
s
= − 0.4141,
P
= 0.0010),
N
% (
r
s
= − 0.4813,
P
< 0.0001), NLR (
r
s
= − 0.5301,
P
< 0.0001), dNLR (
r
s
= − 0.4945,
P
< 0.0001), and SII (
r
s
= − 0.3930,
P
= 0.0019), which were suggested as the inflammatory conditions of SLE. In addition, the mRNA expression of TNF-α in neutrophils was significantly increased in SLE patients. Further analysis revealed that the mRNA expression of YTHDF2 in neutrophils was inversely correlated with TNF-α in SLE. Neutrophils from health control were significantly downregulated in their YTHDF2 expression and upregulated in their TNF-α expression following stimulation by serum from SLE patients.
Conclusion
This study indicates that the levels of YTHDF2 in peripheral blood neutrophils may be involved in the pathogenesis of SLE and could be a novel target for diagnosis and therapy.
Key points
• The mRNA expression of YTHDF2 in neutrophils of SLE and described that decreased mRNA of YTHDF2 in neutrophils correlated with L%, LMR, WBC, N, N%, NLR, dNLR, and SII.
• The mRNA expression of TNF-α in neutrophils was significantly increased and correlated with YTHDF2 in SLE patients.
• Neutrophils from health control were significantly downregulated in their YTHDF2 expression and upregulated in their TNF-α expression following stimulation by serum from SLE patients.</description><subject>Adult</subject><subject>Blood levels</subject><subject>Case-Control Studies</subject><subject>Cytokines</subject><subject>Cytokines - blood</subject><subject>Cytokines - metabolism</subject><subject>Down-Regulation</subject><subject>Female</subject><subject>Gene expression</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Interleukin 6</subject><subject>Interleukin 8</subject><subject>Leukocytes (neutrophilic)</subject><subject>Lupus Erythematosus, Systemic - blood</subject><subject>Lupus Erythematosus, Systemic - metabolism</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Middle Aged</subject><subject>N6-methyladenosine</subject><subject>Neutrophils</subject><subject>Neutrophils - metabolism</subject><subject>Original Article</subject><subject>Pathogenesis</subject><subject>Peripheral blood</subject><subject>Reverse transcription</subject><subject>Rheumatology</subject><subject>RNA, Messenger - metabolism</subject><subject>RNA-Binding Proteins - metabolism</subject><subject>Systemic lupus erythematosus</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Tumor necrosis factor-α</subject><subject>Western blotting</subject><subject>Young Adult</subject><issn>0770-3198</issn><issn>1434-9949</issn><issn>1434-9949</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2025</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kTFv1TAUhS0Eoo_CH2BAllhYAjd24sQjailFqsRSBqbIsW_6XJI4-Doq6cgvx-0rIDGw-Nq63znH0mHsZQlvS4DmHeVTNQWIqoBG1E1x-4jtykpWhdaVfsx20DRQyFK3R-wZ0TUAiFaXT9mR1Eq1EuSO_TwNN3PEq3U0CR3_enl-eiY4_lgiEvkwcz9z2ijh5C0f12UljnFLe5xMCpRfnrghCtbf62982mfJMJrpDogbN7PjM64phmXvR263FL75GfkSg1ttyhHP2ZPBjIQvHuYx-3L24fLkvLj4_PHTyfuLwopapUI6RAP5Lp3ojaua2lQIUKtaWGixt_3Q2h6Eq7RqtAWNauidsO2gamNLJ4_Zm4Nvjv6-IqVu8mRxHM2MYaVOlpVSqgYlMvr6H_Q6rHHOv8tUXelGa6EzJQ6UjYEo4tAt0U8mbl0J3V1D3aGhLjfU3TfU3WbRqwfrtZ_Q_ZH8riQD8gBQXs1XGP9m_8f2F3lOoJI</recordid><startdate>2025</startdate><enddate>2025</enddate><creator>Zhao, Hongshuai</creator><creator>Lan, Mengfan</creator><creator>Huang, Zikun</creator><creator>Fu, Peng</creator><creator>Fu, Biqi</creator><creator>Guo, Yang</creator><creator>Li, Junming</creator><creator>Luo, Qing</creator><general>Springer International Publishing</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope><orcidid>https://orcid.org/0009-0001-2023-124X</orcidid></search><sort><creationdate>2025</creationdate><title>Downregulated YTHDF2 expression in systemic lupus erythematosus is associated with inflammatory and neutrophil cytokine production</title><author>Zhao, Hongshuai ; Lan, Mengfan ; Huang, Zikun ; Fu, Peng ; Fu, Biqi ; Guo, Yang ; Li, Junming ; Luo, Qing</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c256t-3deea0c253d2bad475a4e005652c08ebcbf8cb02d49679c09e6fbd2c8f65ac1d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2025</creationdate><topic>Adult</topic><topic>Blood levels</topic><topic>Case-Control Studies</topic><topic>Cytokines</topic><topic>Cytokines - blood</topic><topic>Cytokines - metabolism</topic><topic>Down-Regulation</topic><topic>Female</topic><topic>Gene expression</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Interleukin 6</topic><topic>Interleukin 8</topic><topic>Leukocytes (neutrophilic)</topic><topic>Lupus Erythematosus, Systemic - blood</topic><topic>Lupus Erythematosus, Systemic - metabolism</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Middle Aged</topic><topic>N6-methyladenosine</topic><topic>Neutrophils</topic><topic>Neutrophils - metabolism</topic><topic>Original Article</topic><topic>Pathogenesis</topic><topic>Peripheral blood</topic><topic>Reverse transcription</topic><topic>Rheumatology</topic><topic>RNA, Messenger - metabolism</topic><topic>RNA-Binding Proteins - metabolism</topic><topic>Systemic lupus erythematosus</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>Tumor necrosis factor-α</topic><topic>Western blotting</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhao, Hongshuai</creatorcontrib><creatorcontrib>Lan, Mengfan</creatorcontrib><creatorcontrib>Huang, Zikun</creatorcontrib><creatorcontrib>Fu, Peng</creatorcontrib><creatorcontrib>Fu, Biqi</creatorcontrib><creatorcontrib>Guo, Yang</creatorcontrib><creatorcontrib>Li, Junming</creatorcontrib><creatorcontrib>Luo, Qing</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Clinical rheumatology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhao, Hongshuai</au><au>Lan, Mengfan</au><au>Huang, Zikun</au><au>Fu, Peng</au><au>Fu, Biqi</au><au>Guo, Yang</au><au>Li, Junming</au><au>Luo, Qing</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Downregulated YTHDF2 expression in systemic lupus erythematosus is associated with inflammatory and neutrophil cytokine production</atitle><jtitle>Clinical rheumatology</jtitle><stitle>Clin Rheumatol</stitle><addtitle>Clin Rheumatol</addtitle><date>2025</date><risdate>2025</risdate><volume>44</volume><issue>1</issue><spage>237</spage><epage>246</epage><pages>237-246</pages><issn>0770-3198</issn><issn>1434-9949</issn><eissn>1434-9949</eissn><abstract>Objectives
An increasing body of evidence suggests that N6-methyladenosine (m6A) plays a crucial role in the etiology of SLE. We focused on YTHDF2 expression in neutrophils and the relationship between YTHDF2 and the pathogenesis of SLE.
Methods
Sixty-one patients with SLE and 48 healthy controls (HC) were recruited, and their clinical characteristics were recorded. The mRNA levels of m6A “writers” (METTL3, METTL14, WTAP), “erasers” (FTO and ALKBH5), “readers” (YTHDF2), and inflammatory factors (interleukin-1β, interleukin-6, interleukin-8, and TNF-α) in neutrophils were determined by reverse transcription-quantitative PCR. The protein of YTHDF2 was determined by Western blotting. The correlations between the YTHDF2 in neutrophils of SLE patients and clinical features were examined by Spearman’s method. YTHDF2 and TNF-α expression in neutrophils were examined after stimulation by SLE serums.
Results
The mRNA expression of YTHDF2 in neutrophils was significantly decreased, and the protein level of YTHDF2 in neutrophils was decreased. The mRNA expression of YTHDF2 in neutrophils correlated with
L
% (
r
s
= 0.5796,
P
< 0.0001), LMR (
r
s
= 0.3524,
P
= 0.0062), WBC (
r
s
= − 0.3186,
P
= 0.0123),
N
(
r
s
= − 0.4141,
P
= 0.0010),
N
% (
r
s
= − 0.4813,
P
< 0.0001), NLR (
r
s
= − 0.5301,
P
< 0.0001), dNLR (
r
s
= − 0.4945,
P
< 0.0001), and SII (
r
s
= − 0.3930,
P
= 0.0019), which were suggested as the inflammatory conditions of SLE. In addition, the mRNA expression of TNF-α in neutrophils was significantly increased in SLE patients. Further analysis revealed that the mRNA expression of YTHDF2 in neutrophils was inversely correlated with TNF-α in SLE. Neutrophils from health control were significantly downregulated in their YTHDF2 expression and upregulated in their TNF-α expression following stimulation by serum from SLE patients.
Conclusion
This study indicates that the levels of YTHDF2 in peripheral blood neutrophils may be involved in the pathogenesis of SLE and could be a novel target for diagnosis and therapy.
Key points
• The mRNA expression of YTHDF2 in neutrophils of SLE and described that decreased mRNA of YTHDF2 in neutrophils correlated with L%, LMR, WBC, N, N%, NLR, dNLR, and SII.
• The mRNA expression of TNF-α in neutrophils was significantly increased and correlated with YTHDF2 in SLE patients.
• Neutrophils from health control were significantly downregulated in their YTHDF2 expression and upregulated in their TNF-α expression following stimulation by serum from SLE patients.</abstract><cop>Cham</cop><pub>Springer International Publishing</pub><pmid>39668303</pmid><doi>10.1007/s10067-024-07257-z</doi><tpages>10</tpages><orcidid>https://orcid.org/0009-0001-2023-124X</orcidid></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0770-3198 |
| ispartof | Clinical rheumatology, 2025, Vol.44 (1), p.237-246 |
| issn | 0770-3198 1434-9949 1434-9949 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_3146665062 |
| source | MEDLINE; SpringerLink Journals |
| subjects | Adult Blood levels Case-Control Studies Cytokines Cytokines - blood Cytokines - metabolism Down-Regulation Female Gene expression Humans Inflammation Interleukin 6 Interleukin 8 Leukocytes (neutrophilic) Lupus Erythematosus, Systemic - blood Lupus Erythematosus, Systemic - metabolism Male Medicine Medicine & Public Health Middle Aged N6-methyladenosine Neutrophils Neutrophils - metabolism Original Article Pathogenesis Peripheral blood Reverse transcription Rheumatology RNA, Messenger - metabolism RNA-Binding Proteins - metabolism Systemic lupus erythematosus Tumor Necrosis Factor-alpha - metabolism Tumor necrosis factor-α Western blotting Young Adult |
| title | Downregulated YTHDF2 expression in systemic lupus erythematosus is associated with inflammatory and neutrophil cytokine production |
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