Cytokine: X最新文献

{"title":"Progress of exosome research in systemic lupus erythematosus","authors":"Jie Shen ,&nbsp;Mengyu Zhang ,&nbsp;Meiyu Peng","doi":"10.1016/j.cytox.2022.100066","DOIUrl":"10.1016/j.cytox.2022.100066","url":null,"abstract":"<div><p>Systemic lupus erythematosus (SLE) is a global chronic autoimmune disease that invades most organs of the body, with kidney injury being the most prominent feature. Exosomes are extracellular vesicles that carry a variety of proteins, lipids and genetic material, participate in the exchange of local and intersystem information, and play an important immunoregulatory role in a variety of autoimmune diseases. At the same time, the use of exosomes as disease biomarkers and drug delivery carriers also shows great application prospects. This article reviews current progress in the application of exosomes in the pathogenesis, diagnosis and treatment of SLE.</p></div>","PeriodicalId":37028,"journal":{"name":"Cytokine: X","volume":"4 2","pages":"Article 100066"},"PeriodicalIF":0.0,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2590153222000052/pdfft?md5=8e1262d0b533437ba12c3dbd70d1c219&pid=1-s2.0-S2590153222000052-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45649243","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An exploratory study of circulating cytokines and chemokines in patients with muscle disorders proposes CD40L and CCL5 represent general disease markers while CXCL10 differentiates between patients with an autoimmune myositis","authors":"Boel De Paepe ,&nbsp;Ken R. Bracke ,&nbsp;Jan L. De Bleecker","doi":"10.1016/j.cytox.2022.100063","DOIUrl":"10.1016/j.cytox.2022.100063","url":null,"abstract":"<div><p>Discriminating an autoimmune myositis from other disorders and subtyping of patient groups within this heterogeneous group of conditions remain diagnostic challenges. In our study we explored the potential of cytokine and chemokine typing in patient sera as an addition to the expanding set of blood-accessible diagnostic biomarkers available today. We selected sets of ten patients within well-characterized disease groups representing healthy controls, and patients with hereditary muscular dystrophies, immune-mediated necrotizing myopathy (IMNM) and sporadic inclusion body myositis (IBM). Prescreening using proteome arrays singled out three biomarker candidates, being the cytokine CD40L, and chemokines CXCL10 and CCL5. Enzyme-linked immunosorbent assays showed all three markers to be elevated in muscle disease irrespective of patient subgroup. CXCL10 levels on the other hand were higher in autoimmune myositis only, and levels were significantly higher in IBM compared to IMNM. The strong CXCL10 expression observed in the auto-aggressive inflammatory cells within IBM muscle tissues possibly represents a major source of circulating CXCL10. We conclude that CXCL10 levels could represent a convenient marker for autoimmune myositis indicative of patient subgroups.</p></div>","PeriodicalId":37028,"journal":{"name":"Cytokine: X","volume":"4 1","pages":"Article 100063"},"PeriodicalIF":0.0,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/15/b0/main.PMC8803590.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39772132","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Plasminogen activator inhibitor-1 mediate downregulation of adiponectin in type 2 diabetes patients with metabolic syndrome","authors":"Shaik Sarfaraz Nawaz,&nbsp;Khalid Siddiqui","doi":"10.1016/j.cytox.2022.100064","DOIUrl":"10.1016/j.cytox.2022.100064","url":null,"abstract":"<div><h3>Introduction</h3><p>Metabolic syndrome (MetS) is a multifactorial disease characterized by metabolic abnormalities. Plasminogen activator inhibitor-1(PAI-1) is a key factor of the fibrinolysis its expression is elevated in insulin resistance, obesity, and MetS. In addition, an adiponectin produced by adipocytes is also key factor in MetS. This study aimed to investigate the relationship between PAI-1, adiponectin levels in MetS.</p></div><div><h3>Patients and Methods</h3><p>A total of 379 subjects were analyse in this cross-sectional study. MetS was defined by NCEP ATP-III criteria. Anthropometric, fasting blood glucose, HbA1c, total cholesterol, high-density lipoprotein, low-density lipoprotein, triglycerides, PAI-1, and adiponectin were measured.</p></div><div><h3>Results</h3><p>PAI-1 levels were higher in MetS compared with non-MetS. In addition, adiponectin levels were significantly lower in MetS compared to non-MetS. Furthermore, increased level of PAI-1 corresponds with increase in prevalence of MetS. PAI-1 levels were significantly associated with MetS (OR = 2.51, CI = 1.23 – 5.14; p = 0.039).</p></div><div><h3>Conclusion</h3><p>PAI-1 increases the risk of MetS. PAI-1 and adiponectin regulation is useful in assesing the presence and severity of MetS. Further pharmacological targeting of PAI-1 studies are necessary for MetS management.</p></div>","PeriodicalId":37028,"journal":{"name":"Cytokine: X","volume":"4 1","pages":"Article 100064"},"PeriodicalIF":0.0,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/f7/6a/main.PMC8803603.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39772133","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TNFAIP8 modulates the survival and immune activity of Th17 cells via p53/ p21/ MDM2 pathway after acute insult","authors":"Xiaobin Cheng ,&nbsp;Xiaocheng Shen ,&nbsp;Min Wang ,&nbsp;Jing Li ,&nbsp;Gang Li","doi":"10.1016/j.cytox.2022.100062","DOIUrl":"10.1016/j.cytox.2022.100062","url":null,"abstract":"<div><p>Th17 cells induced immunosuppression plays a vital role in sepsis. As a member of the tumor necrosis factor α induced protein 8 (TNFAIP8) family, TNFAIP8 is associated with different physiopathological conditions with immunological responses. However, its potential roles in regulating Th17 cells after the acute insult have not been fully elucidated. In this study, sepsis was induced by cecal ligation and puncture (CLP) in the male adult C57BL/6 mice. The stable TNFAIP8 knockdown (KD) Th17 cells were established by infecting with lentivirus carrying TNFAIP8-specific shRNA. CCK-8 assay was conducted to evaluate Th17 cell proliferation, and Annexin V/7-AAD assay was applied for apoptosis measurement by flow cytometry. The alterations of p53/ p21/ MDM2 pathway were assessed by Western blot. We observed that a high TNFAIP8 expression level was related to acute injury in septic mice. TNFAIP8 silencing suppressed Th17 cell proliferation and cytokine production in vivo and in vitro. In addition, TNFAIP8 KD increased Th17 cell apoptosis in septic mice. Furthermore, TNFAIP8 seems to affect the immune function of Th17 cells by regulating p53/ p21/ MDM2 signaling processes. We found that TNFAIP8 KD caused the up-regulation of P21 and MDM2, and also elevated p53 protein level during sepsis. Pharmacological inhibition of p53 partially rescued cell proliferation and apoptotic effects of TNFAIP8 KD. In summary, our work suggests that TNFAIP8 modulates the survival and immune function of Th17 cells after acute insult, which was possibly mediated through the p53/ p21/ MDM2 pathway.</p></div>","PeriodicalId":37028,"journal":{"name":"Cytokine: X","volume":"4 1","pages":"Article 100062"},"PeriodicalIF":0.0,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/02/b6/main.PMC8803581.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39772130","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Interferon stimulated binding of ISRE is cell type specific and is predicted by homeostatic chromatin state","authors":"Sivan Leviyang","doi":"10.1016/j.cytox.2021.100056","DOIUrl":"10.1016/j.cytox.2021.100056","url":null,"abstract":"<div><p>The type I interferon (IFN) signaling pathway involves binding of the transcription factor ISGF3 to IFN-stimulated response elements, ISREs. Gene expression under IFN stimulation is known to vary across cell types, but variation in ISGF3 binding to ISRE across cell types has not been characterized. We examined ISRE binding patterns under IFN stimulation across six cell types using existing ChIPseq datasets. We find that ISRE binding is largely cell specific for ISREs distal to transcription start sites (TSS) and largely conserved across cell types for ISREs proximal to TSS. We show that bound ISRE distal to TSS associate with differential expression of ISGs, although at weaker levels than bound ISRE proximal to TSS. Using existing ATACseq and ChIPseq datasets, we show that the chromatin state of ISRE at homeostasis is cell type specific and is predictive of cell specific, ISRE binding under IFN stimulation. Our results support a model in which the chromatin state of ISRE in enhancer elements is modulated in a cell type specific manner at homeostasis, leading to cell type specific differences in ISRE binding patterns under IFN stimulation.</p></div>","PeriodicalId":37028,"journal":{"name":"Cytokine: X","volume":"3 4","pages":"Article 100056"},"PeriodicalIF":0.0,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.cytox.2021.100056","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39324451","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exclusive inhibition of IL-6 trans-signaling by soluble gp130FlyRFc","authors":"Anna F. Berg,&nbsp;Julia Ettich,&nbsp;Hendrik T. Weitz,&nbsp;Matthias Krusche,&nbsp;Doreen M. Floss,&nbsp;Jürgen Scheller,&nbsp;Jens M. Moll","doi":"10.1016/j.cytox.2021.100058","DOIUrl":"10.1016/j.cytox.2021.100058","url":null,"abstract":"<div><p>gp130 is the signal-transducing receptor for the Interleukin (IL)-6 type cytokines IL-6 and IL-11. To induce signaling, IL-6 forms a complex with IL-6 receptor (IL-6R) and IL-11 with IL-11 receptor (IL-11R). Membrane-bound IL-6R and IL-11R in complex with gp130 and the cytokine mediate classic-signaling, whereas trans-signaling needs soluble IL-6R and IL-11R variants. Interleukin (IL)-6 trans-signaling is of particular importance because it drives the development of autoimmune diseases, including rheumatoid arthritis and chronic inflammatory bowel diseases, whereas a role for IL-11 trans-signaling remains elusive. Soluble gp130 selectively inhibits trans-signaling of IL-6 whereas both, classic- and trans-signaling are abrogated by IL-6- and IL-6R-antibodies. Recently, we described an optimized sgp130 variant, which carries three amino acid substitutions T102Y/Q113F/N114L (sgp130^FlyFc) resulting in reduced inhibition of IL-11 trans-signaling by increasing the affinity of sgp130 for the site I of IL-6. Moreover, we described that the patient mutation R281Q in gp130 results in reduced IL-11 signaling. Here, we show that the combination of T102<u>Y</u>/Q113<u>F</u>/N114<u>L</u> and R281Q in the new variant sgp130^FlyRFc results in complete preservation of IL-11 mediated trans-signaling, whereas inhibition of IL-6 trans-signaling is maintained. Since sgp130Fc (olamkicept) has successfully completed a phase IIa trial in Crohn’s disease (CD) and ulcerative colitis, sgp130^FlyRFc might serve as second-generation therapeutic to diminish IL-11 <em>trans</em>-signaling cross-reactivity.</p></div>","PeriodicalId":37028,"journal":{"name":"Cytokine: X","volume":"3 4","pages":"Article 100058"},"PeriodicalIF":0.0,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8649222/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39828940","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Interferon-gamma impairs phagocytosis of Escherichia coli by primary murine peritoneal macrophages stimulated with LPS and differentially modulates proinflammatory cytokine release","authors":"Sandra Schütze ,&nbsp;Annika Kaufmann ,&nbsp;Stephanie Bunkowski ,&nbsp;Sandra Ribes ,&nbsp;Roland Nau","doi":"10.1016/j.cytox.2021.100057","DOIUrl":"10.1016/j.cytox.2021.100057","url":null,"abstract":"<div><h3>Introduction</h3><p>Interferon-γ levels are increased upon viral infections and during inflamm-aging. Resistance to infections due to <em>Escherichia coli</em> (<em>E. coli</em>), a major cause of bacteriaemia and sepsis, is impaired in aged individuals, partly due to altered phagocytic capacity and cytokine release of immune cells. Here, we analyzed the effect of IFN-γ on phagocytosis of <em>E. coli</em> K1 and release of proinflammatory cytokines by macrophages in resting condition and upon stimulation with different bacterial Toll-like receptor (TLR) agonists.</p></div><div><h3>Methods</h3><p>Primary peritoneal macrophages from C57BL/6 mice were exposed to medium or stimulated with agonists of TLR4 (LPS), 1/2 (Pam₃CSK₄), and 9 (CpG-DNA) in the presence and absence of IFN-γ (100 U/ml) for 24 h. TNF-α, IL-6, and KC were measured in the cell culture supernatant by ELISA. Macrophages were exposed to viable <em>E. coli</em> K1. After 90 min, intracellular phagozytosed bacteria were quantified by quantitative plating.</p></div><div><h3>Results</h3><p>Macrophages treated with LPS 1 µg/ml in the presence of IFN-γ ingested more than 10-fold lower numbers of <em>E. coli</em> than macrophages treated with LPS alone. Phagocytosis of <em>E. coli</em> by macrophages in resting condition or upon stimulation with Pam₃CSK₄ or CpG was not significantly affected by IFN-γ. Cytokine release was differentially modulated by IFN-γ, with reduced KC release by TLR-stimulated macrophages in the presence of IFN-γ being the most striking effect.</p></div><div><h3>Conclusions</h3><p><em>In vitro</em>, IFN-γ reduces the phagocytosis of <em>E. coli</em> by LPS-stimulated macrophages and differentially modulates cytokine release of macrophages activated by different bacterial TLR agonists. Elevated levels of IFN-γ might lead to reduced bacterial clearance and worse outcome of bacterial infections, e.g., in aged individuals and after viral infections and other inflammatory events.</p></div>","PeriodicalId":37028,"journal":{"name":"Cytokine: X","volume":"3 3","pages":"Article 100057"},"PeriodicalIF":0.0,"publicationDate":"2021-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/95/86/main.PMC8498232.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39516087","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Disruption of type I interferon signaling causes sexually dimorphic dysregulation of anti-viral cytokines","authors":"Maedeh Darzianiazizi ,&nbsp;Katrina E. Allison ,&nbsp;Raveendra R. Kulkarni ,&nbsp;Shayan Sharif ,&nbsp;Khalil Karimi ,&nbsp;Byram W. Bridle","doi":"10.1016/j.cytox.2021.100053","DOIUrl":"10.1016/j.cytox.2021.100053","url":null,"abstract":"<div><p>Type I interferons (IFNs) play a crucial role in the establishment of an antiviral state via signaling through their cognate type I IFN receptor (IFNAR). In this study, a replication-competent but highly attenuated strain of VSV (rVSVΔm51) carrying a deletion at position 51 of the matrix protein to remove suppression of anti-viral type I IFN responses was used to explore the effect of disrupted IFNAR signaling on inflammatory cytokine responses in mice. The kinetic responses of interleukin-6, tumor necrosis factor-α and interleukin-12 were evaluated in virus-infected male and female mice with or without concomitant antibody-mediated IFNAR-blockade. Unlike controls, both male and female IFNAR-blocked mice showed signs of sickness by 24-hours post-infection. Female IFNAR-blocked mice experienced greater morbidity as demonstrated by a significant decrease in body temperature. This was not the case for males. In addition, females with IFNAR-blockade mounted prolonged and exaggerated systemic inflammatory cytokine responses to rVSVΔm51. This was in stark contrast to controls with intact IFNAR signaling and males with IFNAR-blockade; they were able to down-regulate virus-induced inflammatory cytokine responses by 24-hours post-infection. Exaggerated cytokine responses in females with impaired IFNAR signaling was associated with more effective control of viremia than their male counterparts. However, the trade-off was greater immune-mediated morbidity. The results of this study demonstrated a role for IFNAR signaling in the down-regulation of antiviral cytokine responses, which was strongly influenced by sex. Our findings suggested that the potential to mount toxic cytokine responses to a virus with concomitant disruption of IFNAR signaling was heavily biased towards females.</p></div>","PeriodicalId":37028,"journal":{"name":"Cytokine: X","volume":"3 2","pages":"Article 100053"},"PeriodicalIF":0.0,"publicationDate":"2021-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.cytox.2021.100053","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39041201","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Resistin in pregnancy: Analysis of determinants in pairs of umbilical cord blood and maternal serum","authors":"Anne Floeck ,&nbsp;Nina Ferrari ,&nbsp;Christine Joisten ,&nbsp;Maria T. Puth ,&nbsp;Brigitte Strizek ,&nbsp;Ramona Dolscheid-Pommerich ,&nbsp;Ulrich Gembruch ,&nbsp;Waltraut M. Merz","doi":"10.1016/j.cytox.2021.100052","DOIUrl":"10.1016/j.cytox.2021.100052","url":null,"abstract":"<div><h3>Objective</h3><p>Despite intensive research on the cytokine resistin only few studies investigated mother-newborn-pairs during healthy pregnancy and reported about interactions with clinical obstetric variables or other cytokines. Comparison of existing studies is difficult due to differences between assays, sample collection, gestational age, definition of healthy controls and patient characteristics. Furthermore, differences between rodent models and humans do not allow for a direct comparison.</p></div><div><h3>Methods</h3><p>In this cross-sectional, prospective study 109 healthy mother-newborn pairs were analyzed. Maternal venous blood samples were taken on admission to the labor ward; newborn venous blood samples were drawn from the placental part of the umbilical cord (UC), immediately after clamping. Resistin, leptin, adiponectin, TNF-α, IL-6 and brain derived neurotrophic factor (BDNF) serum concentrations were measured with commercially available immunoassays. Determinants of maternal and newborn resistin levels were analyzed using simple and multiple linear regression.</p></div><div><h3>Results</h3><p>UC resistin levels were higher than maternal concentrations (median 17.69 ng/mL, IQR 7.36 vs. median 8.04 ng/mL, IQR 4.30). Correlation between UC and maternal resistin levels was moderate (R = 0.503, p &lt; 0.01). In multiple regression analysis levels of maternal resistin and newborn TNF-α remained significant determining factors for UC resistin levels. Gestational age and maternal BDNF-levels remained significant factors for maternal resistin levels.</p></div><div><h3>Conclusion</h3><p>In healthy, term newborns and their respective mothers a positive correlation between maternal and newborn levels and an association with gestational age around term can be found and point to a placental source of resistin. Further investigations are needed to clarify the possible contribution of transplacental transport of resistin into the fetal circulation. Except for gestational age most of the clinical obstetric variables tested do not seem to be determining factors for fetal or maternal resistin. Interactions of resistin with other cytokines like TNF-α and BDNF could be the missing link for the conflicting results in literature.</p></div>","PeriodicalId":37028,"journal":{"name":"Cytokine: X","volume":"3 2","pages":"Article 100052"},"PeriodicalIF":0.0,"publicationDate":"2021-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.cytox.2021.100052","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39251202","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Relationships between plasma levels and six proinflammatory interleukins and body composition using a new magnetic resonance imaging voxel-based technique","authors":"Robin Strand ,&nbsp;Joel Kullberg ,&nbsp;Håkan Ahlström ,&nbsp;Lars Lind","doi":"10.1016/j.cytox.2020.100050","DOIUrl":"10.1016/j.cytox.2020.100050","url":null,"abstract":"<div><h3>Background</h3><p>Obesity has previously been linked to inflammation. Here we investigated how plasma levels of six interleukins were related to body fat distribution.</p></div><div><h3>Methods</h3><p>In 321 subjects, all aged 50 years, in the population-based POEM study (mean BMI 26–27 kg/m²), six interleukins were measured together with a DXA scan for determination of fat and lean mass. Also a whole-body magnetic resonance imaging (MRI) scan, in which fat content measurements were acquired in &gt; 1 million voxels was performed. Interleukin levels were related to each of these voxels by the voxel-based technique “Imiomics” to create a 3D-view of how these measurements were related to size of each part of the body.</p></div><div><h3>Results</h3><p>Levels of IL-1RA and IL-6 were related to traditional DXA and MRI measurements of adipose tissue at all locations. Neither IL-6R, nor IL-8 or IL-18, showed any consistent significant relationships vs the traditional measurements of body composition, while IL-16 showed relationships being of borderline significance. The Imiomics evaluation further strengthen the view that IL-1RA and IL-6 were related to subcutaneous adipose tissue (SAT), as well to ectopic fat distribution. In women, IL-16 levels were weakly related to expansion of SAT in the upper part of the body, while on the contrary, IL-8 levels were related to a reduction of SAT volume.</p></div><div><h3>Conclusion</h3><p>Of the six evaluated interleukins, plasma IL-1RA and IL-6 levels were related to the amount of adipose tissue in all parts of the body, while a diverse picture was seen for other interleukins, suggesting that different interleukins are related to fat distribution in different ways.</p></div>","PeriodicalId":37028,"journal":{"name":"Cytokine: X","volume":"3 1","pages":"Article 100050"},"PeriodicalIF":0.0,"publicationDate":"2021-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.cytox.2020.100050","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25388144","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}