<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>9(3)</volume><submitter>Zhan Y</submitter><pubmed_abstract>&lt;h4>Background&lt;/h4>Primary immune thrombocytopenia (ITP) is an autoimmune-mediated disorder characterized by a decreased platelet count. Systemic lupus erythematosus (SLE) is also an autoimmune disease in which thrombocytopenia is a common hematologic manifestation. Interleukin (IL)-1 family cytokines are major proinflammatory and immunoregulatory mediators. This study aimed to investigate the role of IL-1 cytokines in patients with ITP and SLE and the potential pathophysiologic mechanism to differentiate SLE-associated thrombocytopenia (SLE-TP) from ITP.&lt;h4>Methods&lt;/h4>Multiplex cytokine assay and real-time polymerase chain reaction (RT-PCR) were used to measure IL-1 cytokines in 17 newly diagnosed ITP patients, 17 SLE-TP patients, 19 SLE patients without thrombocytopenia (SLE-NTP), and 10 healthy controls.&lt;h4>Results&lt;/h4>The serum levels of IL-1β, IL-18, IL-36α, IL-36β, IL-36γ, and IL-33 were decreased significantly in ITP patients compared with SLE-TP patients, SLE-NTP patients, and healthy controls (P&lt;0.05). While there was no significant difference in the serum level of IL-37 between ITP and SLE-TP patients, there was a positive correlation between the platelet count and IL-37 level in ITP patients. Our data suggested that serum IL-1β, IL-18, IL-36α, IL-36β, IL-36γ, IL-33, and IL-37 could be considered biomarkers in the diagnosis of ITP.&lt;h4>Conclusions&lt;/h4>Serum IL-1β, IL-18, IL-36α, IL-36β, IL-36γ, and IL-33 could be considered biomarkers to differentiate SLE-TP from ITP patients.</pubmed_abstract><journal>Annals of translational medicine</journal><pagination>222</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7940935</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Interleukin (IL)-1 family cytokines could differentiate primary immune thrombocytopenia from systemic lupus erythematosus-associated thrombocytopenia.</pubmed_title><pmcid>PMC7940935</pmcid><pubmed_authors>Min Z</pubmed_authors><pubmed_authors>Chen P</pubmed_authors><pubmed_authors>Cao J</pubmed_authors><pubmed_authors>Li F</pubmed_authors><pubmed_authors>Ji L</pubmed_authors><pubmed_authors>Yuan L</pubmed_authors><pubmed_authors>Wu B</pubmed_authors><pubmed_authors>Chen H</pubmed_authors><pubmed_authors>Cheng Y</pubmed_authors><pubmed_authors>Zhan Y</pubmed_authors><pubmed_authors>Ke Y</pubmed_authors><pubmed_authors>Sun L</pubmed_authors><pubmed_authors>Hua F</pubmed_authors><pubmed_authors>Cheng L</pubmed_authors></additional><is_claimable>false</is_claimable><name>Interleukin (IL)-1 family cytokines could differentiate primary immune thrombocytopenia from systemic lupus erythematosus-associated thrombocytopenia.</name><description>&lt;h4>Background&lt;/h4>Primary immune thrombocytopenia (ITP) is an autoimmune-mediated disorder characterized by a decreased platelet count. Systemic lupus erythematosus (SLE) is also an autoimmune disease in which thrombocytopenia is a common hematologic manifestation. Interleukin (IL)-1 family cytokines are major proinflammatory and immunoregulatory mediators. This study aimed to investigate the role of IL-1 cytokines in patients with ITP and SLE and the potential pathophysiologic mechanism to differentiate SLE-associated thrombocytopenia (SLE-TP) from ITP.&lt;h4>Methods&lt;/h4>Multiplex cytokine assay and real-time polymerase chain reaction (RT-PCR) were used to measure IL-1 cytokines in 17 newly diagnosed ITP patients, 17 SLE-TP patients, 19 SLE patients without thrombocytopenia (SLE-NTP), and 10 healthy controls.&lt;h4>Results&lt;/h4>The serum levels of IL-1β, IL-18, IL-36α, IL-36β, IL-36γ, and IL-33 were decreased significantly in ITP patients compared with SLE-TP patients, SLE-NTP patients, and healthy controls (P&lt;0.05). While there was no significant difference in the serum level of IL-37 between ITP and SLE-TP patients, there was a positive correlation between the platelet count and IL-37 level in ITP patients. Our data suggested that serum IL-1β, IL-18, IL-36α, IL-36β, IL-36γ, IL-33, and IL-37 could be considered biomarkers in the diagnosis of ITP.&lt;h4>Conclusions&lt;/h4>Serum IL-1β, IL-18, IL-36α, IL-36β, IL-36γ, and IL-33 could be considered biomarkers to differentiate SLE-TP from ITP patients.</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Feb</publication><modification>2025-04-26T16:30:54.993Z</modification><creation>2025-04-06T15:12:29.905Z</creation></dates><accession>S-EPMC7940935</accession><cross_references><pubmed>33708849</pubmed><doi>10.21037/atm-20-4729</doi></cross_references></HashMap>