Disease activity is associated with changes in the innate immune function in patients with systemic lupus erythematosus
Objective To address the relationship between systemic lupus erythematosus (SLE) disease activity and the functional parameters of the innate immunity. Methods We evaluated a cohort of 26 adult SLE patients and 10 sex and age-paired healthy donors. When the patients had a disease flare (baseline) an...
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creator | Torres-Ruiz, Jiram Rull-Gabayet, Marina Mejía-Domínguez, Nancy R. Carrillo-Vázquez, Daniel Alberto Reyes-Islas, Juan Alberto Cassiano-Quezada, Fabiola Cuellar-Rodríguez, Jennifer Sierra-Madero, Juan Sánchez, Jessica Márquez Serrano-García, Jesús Salvador González, Alexia Esquinca Juárez-Vega, Guillermo Tapia-Rodríguez, Miguel Gómez-Martín, Diana |
description | Objective
To address the relationship between systemic lupus erythematosus (SLE) disease activity and the functional parameters of the innate immunity.
Methods
We evaluated a cohort of 26 adult SLE patients and 10 sex and age-paired healthy donors. When the patients had a disease flare (baseline) and when they achieve clinical response (follow-up), we assessed the systemic lupus erythematosus disease activity index 2 K (SLEDAI 2 K) and the following parameters with flow cytometry and confocal microscopy: monocyte subsets, their expression of TLR2, phagocytic monocytes and neutrophils using the pHrodo Red
E. coli
BioParticles, the respiratory burst with 123-dihydrorhodamine in neutrophils, and the spontaneous and lipopolysaccharide (LPS)-induced production of neutrophil extracellular traps (NETs). We used the Wilcoxon test to compare the paired medians with interquartile range (IQR) and the Mann–Whitney
U
test for independent medians. To assess the effect of prednisone and SLEDAI 2 K on the mentioned parameters, we applied a generalized mixed linear model.
Results
Twenty-three patients (88.4%) were women. The SLEDAI 2 K was higher at baseline 8 (6–14) in comparison to that at follow-up (6 (4–8),
P
= 0.028). At baseline, SLE patients had a decreased percentage of intermediate monocytes, a higher expression of TLR2 in total monocytes, increased phagocytosis in monocytes and neutrophils, a decreased respiratory burst intensity, and an increased production of NETs. In the mix model, the SLEDAI 2 K was the main factor influencing these functional innate immune parameters.
Conclusion
Disease activity regulates the innate immune function in SLE which may contribute to the clinical features and infection predisposition.
Key points
•
This is the first cohort study addressing the effect of disease activity and prednisone use on the innate immune function of lupus patients.
•
Our results show that the disease activity is a key regulator of the respiratory burst, phagocytosis, and the production of neutrophil extracellular traps.
•
Also, we observed a differential proportion of monocyte subsets according to SLE disease activity.
•
We consider that our manuscript contributes to the evidence addressing the intrinsic immune abnormalities of patients with SLE regardless of the use of immunosuppressants and set the bases for new research work considering the disease activity as an element to decide the prescription and duration of antibiotic prophylaxis in SLE patients, wh |
doi_str_mv | 10.1007/s10067-023-06810-6 |
format | Article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2890361560</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2911642284</sourcerecordid><originalsourceid>FETCH-LOGICAL-c375t-251b987d7ac387b1eaff7fd1513bee4a1a83c8dcaabf88f271432cad8aa0b9f43</originalsourceid><addsrcrecordid>eNp9kTtvFDEUhS1ERJbAH6BAlmhohvgx60eJEl5SJJpQW3c8Nutox7PMtYn238fLBJAoaHyL851j-x5CXnH2jjOmL7GdSndMyI4pw1mnnpAN72XfWdvbp2TDtGad5Nack-eId4wxYSx_Rs6ltqpnWm3I_XXCABgo-JJ-pnKkCSkgzj5BCSO9T2VH_Q7y94A0ZVp2oY3cNJqmqeZAY83NOueTeoCSQi642vCIJUzJ0309VKRhOTb3BGXGii_IWYQ9hpeP84J8-_jh9upzd_P105er9zedl3pbOrHlgzV61OCl0QMPEKOOI99yOYTQAwcjvRk9wBCNiUK37wsPowFgg429vCBv19zDMv-oAYubEvqw30MOc0XXFsKk4lvFGvrmH_Rurktur3PCcq56IcwpUKyUX2bEJUR3WNIEy9Fx5k61uLUW12pxv2pxqpleP0bXYQrjH8vvHhogVwCb1Ha9_L37P7EPQgibMw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2911642284</pqid></control><display><type>article</type><title>Disease activity is associated with changes in the innate immune function in patients with systemic lupus erythematosus</title><source>Springer LINK 全文期刊数据库</source><creator>Torres-Ruiz, Jiram ; Rull-Gabayet, Marina ; Mejía-Domínguez, Nancy R. ; Carrillo-Vázquez, Daniel Alberto ; Reyes-Islas, Juan Alberto ; Cassiano-Quezada, Fabiola ; Cuellar-Rodríguez, Jennifer ; Sierra-Madero, Juan ; Sánchez, Jessica Márquez ; Serrano-García, Jesús Salvador ; González, Alexia Esquinca ; Juárez-Vega, Guillermo ; Tapia-Rodríguez, Miguel ; Gómez-Martín, Diana</creator><creatorcontrib>Torres-Ruiz, Jiram ; Rull-Gabayet, Marina ; Mejía-Domínguez, Nancy R. ; Carrillo-Vázquez, Daniel Alberto ; Reyes-Islas, Juan Alberto ; Cassiano-Quezada, Fabiola ; Cuellar-Rodríguez, Jennifer ; Sierra-Madero, Juan ; Sánchez, Jessica Márquez ; Serrano-García, Jesús Salvador ; González, Alexia Esquinca ; Juárez-Vega, Guillermo ; Tapia-Rodríguez, Miguel ; Gómez-Martín, Diana</creatorcontrib><description>Objective
To address the relationship between systemic lupus erythematosus (SLE) disease activity and the functional parameters of the innate immunity.
Methods
We evaluated a cohort of 26 adult SLE patients and 10 sex and age-paired healthy donors. When the patients had a disease flare (baseline) and when they achieve clinical response (follow-up), we assessed the systemic lupus erythematosus disease activity index 2 K (SLEDAI 2 K) and the following parameters with flow cytometry and confocal microscopy: monocyte subsets, their expression of TLR2, phagocytic monocytes and neutrophils using the pHrodo Red
E. coli
BioParticles, the respiratory burst with 123-dihydrorhodamine in neutrophils, and the spontaneous and lipopolysaccharide (LPS)-induced production of neutrophil extracellular traps (NETs). We used the Wilcoxon test to compare the paired medians with interquartile range (IQR) and the Mann–Whitney
U
test for independent medians. To assess the effect of prednisone and SLEDAI 2 K on the mentioned parameters, we applied a generalized mixed linear model.
Results
Twenty-three patients (88.4%) were women. The SLEDAI 2 K was higher at baseline 8 (6–14) in comparison to that at follow-up (6 (4–8),
P
= 0.028). At baseline, SLE patients had a decreased percentage of intermediate monocytes, a higher expression of TLR2 in total monocytes, increased phagocytosis in monocytes and neutrophils, a decreased respiratory burst intensity, and an increased production of NETs. In the mix model, the SLEDAI 2 K was the main factor influencing these functional innate immune parameters.
Conclusion
Disease activity regulates the innate immune function in SLE which may contribute to the clinical features and infection predisposition.
Key points
•
This is the first cohort study addressing the effect of disease activity and prednisone use on the innate immune function of lupus patients.
•
Our results show that the disease activity is a key regulator of the respiratory burst, phagocytosis, and the production of neutrophil extracellular traps.
•
Also, we observed a differential proportion of monocyte subsets according to SLE disease activity.
•
We consider that our manuscript contributes to the evidence addressing the intrinsic immune abnormalities of patients with SLE regardless of the use of immunosuppressants and set the bases for new research work considering the disease activity as an element to decide the prescription and duration of antibiotic prophylaxis in SLE patients, which is of interest to all rheumatologists.</description><identifier>ISSN: 0770-3198</identifier><identifier>EISSN: 1434-9949</identifier><identifier>DOI: 10.1007/s10067-023-06810-6</identifier><identifier>PMID: 37964076</identifier><language>eng</language><publisher>Cham: Springer International Publishing</publisher><subject>Confocal microscopy ; Flow cytometry ; Immune response ; Immunosuppressive agents ; Innate immunity ; Leukocytes (neutrophilic) ; Lipopolysaccharides ; Lupus ; Medicine ; Medicine & Public Health ; Monocytes ; Neutrophils ; Original Article ; Phagocytes ; Phagocytosis ; Prednisone ; Prophylaxis ; Respiratory burst ; Rheumatology ; Systemic lupus erythematosus ; TLR2 protein ; Toll-like receptors</subject><ispartof>Clinical rheumatology, 2024, Vol.43 (1), p.501-509</ispartof><rights>The Author(s), under exclusive licence to International League of Associations for Rheumatology (ILAR) 2023. 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>2023. The Author(s), under exclusive licence to International League of Associations for Rheumatology (ILAR).</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-251b987d7ac387b1eaff7fd1513bee4a1a83c8dcaabf88f271432cad8aa0b9f43</citedby><cites>FETCH-LOGICAL-c375t-251b987d7ac387b1eaff7fd1513bee4a1a83c8dcaabf88f271432cad8aa0b9f43</cites><orcidid>0000-0002-1807-0045</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/s10067-023-06810-6$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10067-023-06810-6$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27923,27924,41487,42556,51318</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37964076$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Torres-Ruiz, Jiram</creatorcontrib><creatorcontrib>Rull-Gabayet, Marina</creatorcontrib><creatorcontrib>Mejía-Domínguez, Nancy R.</creatorcontrib><creatorcontrib>Carrillo-Vázquez, Daniel Alberto</creatorcontrib><creatorcontrib>Reyes-Islas, Juan Alberto</creatorcontrib><creatorcontrib>Cassiano-Quezada, Fabiola</creatorcontrib><creatorcontrib>Cuellar-Rodríguez, Jennifer</creatorcontrib><creatorcontrib>Sierra-Madero, Juan</creatorcontrib><creatorcontrib>Sánchez, Jessica Márquez</creatorcontrib><creatorcontrib>Serrano-García, Jesús Salvador</creatorcontrib><creatorcontrib>González, Alexia Esquinca</creatorcontrib><creatorcontrib>Juárez-Vega, Guillermo</creatorcontrib><creatorcontrib>Tapia-Rodríguez, Miguel</creatorcontrib><creatorcontrib>Gómez-Martín, Diana</creatorcontrib><title>Disease activity is associated with changes in the innate immune function in patients with systemic lupus erythematosus</title><title>Clinical rheumatology</title><addtitle>Clin Rheumatol</addtitle><addtitle>Clin Rheumatol</addtitle><description>Objective
To address the relationship between systemic lupus erythematosus (SLE) disease activity and the functional parameters of the innate immunity.
Methods
We evaluated a cohort of 26 adult SLE patients and 10 sex and age-paired healthy donors. When the patients had a disease flare (baseline) and when they achieve clinical response (follow-up), we assessed the systemic lupus erythematosus disease activity index 2 K (SLEDAI 2 K) and the following parameters with flow cytometry and confocal microscopy: monocyte subsets, their expression of TLR2, phagocytic monocytes and neutrophils using the pHrodo Red
E. coli
BioParticles, the respiratory burst with 123-dihydrorhodamine in neutrophils, and the spontaneous and lipopolysaccharide (LPS)-induced production of neutrophil extracellular traps (NETs). We used the Wilcoxon test to compare the paired medians with interquartile range (IQR) and the Mann–Whitney
U
test for independent medians. To assess the effect of prednisone and SLEDAI 2 K on the mentioned parameters, we applied a generalized mixed linear model.
Results
Twenty-three patients (88.4%) were women. The SLEDAI 2 K was higher at baseline 8 (6–14) in comparison to that at follow-up (6 (4–8),
P
= 0.028). At baseline, SLE patients had a decreased percentage of intermediate monocytes, a higher expression of TLR2 in total monocytes, increased phagocytosis in monocytes and neutrophils, a decreased respiratory burst intensity, and an increased production of NETs. In the mix model, the SLEDAI 2 K was the main factor influencing these functional innate immune parameters.
Conclusion
Disease activity regulates the innate immune function in SLE which may contribute to the clinical features and infection predisposition.
Key points
•
This is the first cohort study addressing the effect of disease activity and prednisone use on the innate immune function of lupus patients.
•
Our results show that the disease activity is a key regulator of the respiratory burst, phagocytosis, and the production of neutrophil extracellular traps.
•
Also, we observed a differential proportion of monocyte subsets according to SLE disease activity.
•
We consider that our manuscript contributes to the evidence addressing the intrinsic immune abnormalities of patients with SLE regardless of the use of immunosuppressants and set the bases for new research work considering the disease activity as an element to decide the prescription and duration of antibiotic prophylaxis in SLE patients, which is of interest to all rheumatologists.</description><subject>Confocal microscopy</subject><subject>Flow cytometry</subject><subject>Immune response</subject><subject>Immunosuppressive agents</subject><subject>Innate immunity</subject><subject>Leukocytes (neutrophilic)</subject><subject>Lipopolysaccharides</subject><subject>Lupus</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Monocytes</subject><subject>Neutrophils</subject><subject>Original Article</subject><subject>Phagocytes</subject><subject>Phagocytosis</subject><subject>Prednisone</subject><subject>Prophylaxis</subject><subject>Respiratory burst</subject><subject>Rheumatology</subject><subject>Systemic lupus erythematosus</subject><subject>TLR2 protein</subject><subject>Toll-like receptors</subject><issn>0770-3198</issn><issn>1434-9949</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp9kTtvFDEUhS1ERJbAH6BAlmhohvgx60eJEl5SJJpQW3c8Nutox7PMtYn238fLBJAoaHyL851j-x5CXnH2jjOmL7GdSndMyI4pw1mnnpAN72XfWdvbp2TDtGad5Nack-eId4wxYSx_Rs6ltqpnWm3I_XXCABgo-JJ-pnKkCSkgzj5BCSO9T2VH_Q7y94A0ZVp2oY3cNJqmqeZAY83NOueTeoCSQi642vCIJUzJ0309VKRhOTb3BGXGii_IWYQ9hpeP84J8-_jh9upzd_P105er9zedl3pbOrHlgzV61OCl0QMPEKOOI99yOYTQAwcjvRk9wBCNiUK37wsPowFgg429vCBv19zDMv-oAYubEvqw30MOc0XXFsKk4lvFGvrmH_Rurktur3PCcq56IcwpUKyUX2bEJUR3WNIEy9Fx5k61uLUW12pxv2pxqpleP0bXYQrjH8vvHhogVwCb1Ha9_L37P7EPQgibMw</recordid><startdate>2024</startdate><enddate>2024</enddate><creator>Torres-Ruiz, Jiram</creator><creator>Rull-Gabayet, Marina</creator><creator>Mejía-Domínguez, Nancy R.</creator><creator>Carrillo-Vázquez, Daniel Alberto</creator><creator>Reyes-Islas, Juan Alberto</creator><creator>Cassiano-Quezada, Fabiola</creator><creator>Cuellar-Rodríguez, Jennifer</creator><creator>Sierra-Madero, Juan</creator><creator>Sánchez, Jessica Márquez</creator><creator>Serrano-García, Jesús Salvador</creator><creator>González, Alexia Esquinca</creator><creator>Juárez-Vega, Guillermo</creator><creator>Tapia-Rodríguez, Miguel</creator><creator>Gómez-Martín, Diana</creator><general>Springer International Publishing</general><general>Springer Nature B.V</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-1807-0045</orcidid></search><sort><creationdate>2024</creationdate><title>Disease activity is associated with changes in the innate immune function in patients with systemic lupus erythematosus</title><author>Torres-Ruiz, Jiram ; Rull-Gabayet, Marina ; Mejía-Domínguez, Nancy R. ; Carrillo-Vázquez, Daniel Alberto ; Reyes-Islas, Juan Alberto ; Cassiano-Quezada, Fabiola ; Cuellar-Rodríguez, Jennifer ; Sierra-Madero, Juan ; Sánchez, Jessica Márquez ; Serrano-García, Jesús Salvador ; González, Alexia Esquinca ; Juárez-Vega, Guillermo ; Tapia-Rodríguez, Miguel ; Gómez-Martín, Diana</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-251b987d7ac387b1eaff7fd1513bee4a1a83c8dcaabf88f271432cad8aa0b9f43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Confocal microscopy</topic><topic>Flow cytometry</topic><topic>Immune response</topic><topic>Immunosuppressive agents</topic><topic>Innate immunity</topic><topic>Leukocytes (neutrophilic)</topic><topic>Lipopolysaccharides</topic><topic>Lupus</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Monocytes</topic><topic>Neutrophils</topic><topic>Original Article</topic><topic>Phagocytes</topic><topic>Phagocytosis</topic><topic>Prednisone</topic><topic>Prophylaxis</topic><topic>Respiratory burst</topic><topic>Rheumatology</topic><topic>Systemic lupus erythematosus</topic><topic>TLR2 protein</topic><topic>Toll-like receptors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Torres-Ruiz, Jiram</creatorcontrib><creatorcontrib>Rull-Gabayet, Marina</creatorcontrib><creatorcontrib>Mejía-Domínguez, Nancy R.</creatorcontrib><creatorcontrib>Carrillo-Vázquez, Daniel Alberto</creatorcontrib><creatorcontrib>Reyes-Islas, Juan Alberto</creatorcontrib><creatorcontrib>Cassiano-Quezada, Fabiola</creatorcontrib><creatorcontrib>Cuellar-Rodríguez, Jennifer</creatorcontrib><creatorcontrib>Sierra-Madero, Juan</creatorcontrib><creatorcontrib>Sánchez, Jessica Márquez</creatorcontrib><creatorcontrib>Serrano-García, Jesús Salvador</creatorcontrib><creatorcontrib>González, Alexia Esquinca</creatorcontrib><creatorcontrib>Juárez-Vega, Guillermo</creatorcontrib><creatorcontrib>Tapia-Rodríguez, Miguel</creatorcontrib><creatorcontrib>Gómez-Martín, Diana</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Health & Medical Collection (Proquest)</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>MEDLINE - Academic</collection><jtitle>Clinical rheumatology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Torres-Ruiz, Jiram</au><au>Rull-Gabayet, Marina</au><au>Mejía-Domínguez, Nancy R.</au><au>Carrillo-Vázquez, Daniel Alberto</au><au>Reyes-Islas, Juan Alberto</au><au>Cassiano-Quezada, Fabiola</au><au>Cuellar-Rodríguez, Jennifer</au><au>Sierra-Madero, Juan</au><au>Sánchez, Jessica Márquez</au><au>Serrano-García, Jesús Salvador</au><au>González, Alexia Esquinca</au><au>Juárez-Vega, Guillermo</au><au>Tapia-Rodríguez, Miguel</au><au>Gómez-Martín, Diana</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Disease activity is associated with changes in the innate immune function in patients with systemic lupus erythematosus</atitle><jtitle>Clinical rheumatology</jtitle><stitle>Clin Rheumatol</stitle><addtitle>Clin Rheumatol</addtitle><date>2024</date><risdate>2024</risdate><volume>43</volume><issue>1</issue><spage>501</spage><epage>509</epage><pages>501-509</pages><issn>0770-3198</issn><eissn>1434-9949</eissn><abstract>Objective
To address the relationship between systemic lupus erythematosus (SLE) disease activity and the functional parameters of the innate immunity.
Methods
We evaluated a cohort of 26 adult SLE patients and 10 sex and age-paired healthy donors. When the patients had a disease flare (baseline) and when they achieve clinical response (follow-up), we assessed the systemic lupus erythematosus disease activity index 2 K (SLEDAI 2 K) and the following parameters with flow cytometry and confocal microscopy: monocyte subsets, their expression of TLR2, phagocytic monocytes and neutrophils using the pHrodo Red
E. coli
BioParticles, the respiratory burst with 123-dihydrorhodamine in neutrophils, and the spontaneous and lipopolysaccharide (LPS)-induced production of neutrophil extracellular traps (NETs). We used the Wilcoxon test to compare the paired medians with interquartile range (IQR) and the Mann–Whitney
U
test for independent medians. To assess the effect of prednisone and SLEDAI 2 K on the mentioned parameters, we applied a generalized mixed linear model.
Results
Twenty-three patients (88.4%) were women. The SLEDAI 2 K was higher at baseline 8 (6–14) in comparison to that at follow-up (6 (4–8),
P
= 0.028). At baseline, SLE patients had a decreased percentage of intermediate monocytes, a higher expression of TLR2 in total monocytes, increased phagocytosis in monocytes and neutrophils, a decreased respiratory burst intensity, and an increased production of NETs. In the mix model, the SLEDAI 2 K was the main factor influencing these functional innate immune parameters.
Conclusion
Disease activity regulates the innate immune function in SLE which may contribute to the clinical features and infection predisposition.
Key points
•
This is the first cohort study addressing the effect of disease activity and prednisone use on the innate immune function of lupus patients.
•
Our results show that the disease activity is a key regulator of the respiratory burst, phagocytosis, and the production of neutrophil extracellular traps.
•
Also, we observed a differential proportion of monocyte subsets according to SLE disease activity.
•
We consider that our manuscript contributes to the evidence addressing the intrinsic immune abnormalities of patients with SLE regardless of the use of immunosuppressants and set the bases for new research work considering the disease activity as an element to decide the prescription and duration of antibiotic prophylaxis in SLE patients, which is of interest to all rheumatologists.</abstract><cop>Cham</cop><pub>Springer International Publishing</pub><pmid>37964076</pmid><doi>10.1007/s10067-023-06810-6</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0002-1807-0045</orcidid></addata></record> |
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subjects | Confocal microscopy Flow cytometry Immune response Immunosuppressive agents Innate immunity Leukocytes (neutrophilic) Lipopolysaccharides Lupus Medicine Medicine & Public Health Monocytes Neutrophils Original Article Phagocytes Phagocytosis Prednisone Prophylaxis Respiratory burst Rheumatology Systemic lupus erythematosus TLR2 protein Toll-like receptors |
title | Disease activity is associated with changes in the innate immune function in patients with systemic lupus erythematosus |
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