scholarly journals Interleukin-6 and Related Proteins as Biomarkers in Systemic Sclerosis

2017 ◽  
Vol 2 (2_suppl) ◽  
pp. S13-S19 ◽  
Author(s):  
Christopher P. Denton ◽  
Voon H. Ong
Keyword(s):  
Systemic Sclerosis ◽  
Interleukin 6 ◽  
Cell Function ◽  
Immune Cell ◽  
Family Members ◽  
Surrogate Marker ◽  
Response To Therapy ◽  
Janus Kinase ◽  
Response To Treatment ◽  
Early Stage Disease

The search for biomarkers in systemic sclerosis (SSc) is driven by a goal to stratify patients, identify potential subgroups for treatment, and help assess response to therapy. Emerging evidence indicates that interleukin-6 (IL-6) and some family members are key biomarkers involved in SSc pathogenesis and therefore suitable targets for therapy. Recent studies evaluating IL-6 and its canonical Janus kinase/signal transducers and activators of transcription downstream pathways in modulating fibrotic response and immune cell function suggest a pivotal role for IL-6 in SSc pathogenesis. Although the significance and effect of local tissue expression of IL-6 and its family members are less well established, high levels of circulating IL-6 may identify subgroups of patients with early-stage disease, particularly those at risk for progressive lung fibrosis. In addition, higher disease activity may portend poor prognostic outcome in terms of survival and skin disease. Longitudinal assessment of serum levels of IL-6 and its signaling associates may prove valuable in monitoring response to treatment. As an IL-6–dependent surrogate marker, C-reactive protein may assist cohort enrichment if targeted treatment for IL-6 demonstrates efficacy, especially in subgroups with high IL-6 levels. Although IL-6 appears to be a key factor in the hierarchy of the complex network of disease-associated molecules, the systemic or autocrine/paracrine manner in which IL-6 asserts its profibrotic effects—particularly its interaction with other key pathogenic factors in SSc—is unknown. Ongoing clinical trials will help to delineate the mechanisms of IL-6 in SSc pathogenesis and inform on the role of these biomarkers.

scholarly journals Longitudinal high-dimensional analysis identifies biomarkers of response to anti-PD-1 immunotherapy

2021 ◽  
Author(s):  
Run-Ze Li ◽  
Xing-Xing Fan ◽  
Ze-Bo Jiang ◽  
Jumin Huang ◽  
Hu-Dan Pan ◽  
...  
Keyword(s):  
Clinical Response ◽  
Mononuclear Cells ◽  
Cell Function ◽  
Immune Cell ◽  
Response To Therapy ◽  
High Dimensional ◽  
Meso Scale Discovery ◽  
Peripheral Blood Mononuclear ◽  
Poor Outcomes ◽  
Nsclc Patients

Abstract The response to immunotherapy could be better predicted by using a wide set of biomarkers, including serum tumor markers; however, robust immune markers associated with efficacy have yet to be validated. In this study, changes in immune cell subsets from NSCLC patients treated with anti-PD1 therapy were longitudinally monitored by high-dimensional cytometry by time of flight (CyTOF) and Meso Scale Discovery (MSD) multi-cytokines kits. The frequencies of circulating CD8+ and CD8+CD101hiTIM3+ (CCT T) subsets were significantly correlated with clinical response and survival. Enrichment of these populations in peripheral blood mononuclear cells (PBMCs) indicated a poor clinical response to ICB therapy. Cell function assays revealed that these subsets were remarkably impaired, which supported the poor outcomes observed. Additionally, longitudinal analysis showed that KLRG1 expression and cytokines were associated with the response to therapy. Overall, our results provide novel potential biomarkers for guiding the management of NSCLC patients eligible to anti-PD-1 therapy, and contribute insights for new therapeutic strategies.

Skewed X chromosomal inactivation impacts T regulatory cell function in systemic sclerosis

2010 ◽  
Vol 69 (12) ◽  
pp. 2213-2216 ◽  
Author(s):  
Jasper C A Broen ◽  
Ingrid L M Wolvers-Tettero ◽  
Lenny Geurts-van Bon ◽  
Madelon C Vonk ◽  
Marieke J H Coenen ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Systemic Sclerosis ◽  
T Regulatory Cells ◽  
Mononuclear Cells ◽  
Cell Function ◽  
Immune Cell ◽  
Magnetic Bead ◽  
T Regulatory Cell ◽  
Myeloid Dendritic Cells ◽  
Peripheral Blood Mononuclear

ObjectivesTo investigate the role of X chromosomal inactivation (XCI) in systemic sclerosis (SSc) and its effects on forkhead box P3 (Foxp3) expression in T regulatory cells (Tregs).Methods217 women with SSc and 107 healthy women (controls) were included in the study. From these subjects, DNA was isolated from total peripheral blood mononuclear cells, plasmacytoid dendritic cells, T cells, B cells, myeloid dendritic cells and monocytes after magnetic bead separation. All samples were assessed for skewed XCI patterns with the Human Androgen Receptor Assay. The outcome was assessed by linear regression. CD4+CD25+ cells were then isolated and intracellular Foxp3 expression was assessed by flow cytometry.ResultsSkewing was not associated with increased age in patients with SSc, in contrast to the control population (r=0.45, p<0.0001). Taking this into account, a significantly higher frequency of skewed XCI was found in patients with SSc compared with controls (p=0.001). No difference in skewing was observed between the immune cell subsets. In addition, a higher concentration of Foxp3+ cells exhibiting a lower Foxp3 mean fluorescence intensity was found in the patients with SSc, with profound XCI skewing (both p<0.001) associated with less efficient suppressive activity (p=0.012).ConclusionsSkewed XCI plays a role in susceptibility to SSc, is not restricted and influences Foxp3 expression and the suppressive capacity of Tregs.

Biologic treatments for psoriatic arthritis apart from TNF inhibition

2018 ◽  
Author(s):  
Philip Mease
Keyword(s):  
Psoriatic Arthritis ◽  
Mechanism Of Action ◽  
Structural Damage ◽  
Cell Function ◽  
Immune Cell ◽  
Initial Response ◽  
Tnf Inhibitors ◽  
Janus Kinase ◽  
Oral Medications ◽  
Tnf Inhibition

Psoriatic arthritis (PsA) is an immunologically mediated inflammatory disease characterized by arthritis, enthesitis, dactylitis, spondylitis, and psoriasis. Prior to the introduction of targeted biologic medications, such as TNF inhibitors, the ability to control disease activity was limited, with only modest effects noted with traditional oral medications such as methotrexate and sulfasalazine. The introduction of TNF inhibitors substantially changed the outlook of PsA patients, yielding significant response in all relevant clinical domains and demonstrating the ability to inhibit progressive structural damage of joints. However, not all patients responded to these agents and many patients displayed initial response which waned over time, partly due to immunogenicity (development of antibodies which blocked full therapeutic effect of the biologic protein), or because of tolerability and side effect issues. Thus, it has been important to develop new medicines which target other key cytokines and immunologic pathways. Several medicines with a different mechanism of action have been approved or are in development for the treatment of PsA. Ustekinumab inhibits both IL12 and IL23 and thus is felt to work in both the TH1 and TH7 pathways of inflammation. The oral medicine apremilast inhibits phosphodiesterase 4, thus modulating the cyclic AMP pathway in immunologic cells, yielding an anti-inflammatory effect. Both of these medicines have been approved for the treatment of PsA as well as psoriasis. An emerging group of therapies, the IL17 inhibitors, has demonstrated significant effectiveness in psoriasis and PsA and one of these, Secukinumab, has been approved for psoriasis, PsA, and AS. Other medicines in development include the co-stimulatory blockade agent, abatacept, oral Janus Kinase (JAK) inhibitors, and an emerging group of therapies which inhibit IL23. As modulators of immune cell function, these agents have the potential to increase risk for infection, as well as other side effects. These must be discussed with the patient and considered when determining overall risk benefit analysis regarding their use. The emergence of medicines with a different mechanism of action than TNF inhibition has broadened and strengthened our ability to effectively treat PsA.

Characterizing the gut microbiome of patients with triple-negative breast cancer.

2019 ◽  
Vol 37 (15_suppl) ◽  
pp. e14186-e14186 ◽  
Author(s):  
April T. Swoboda ◽  
Anukriti Sharma ◽  
Olufunmilayo I. Olopade ◽  
Rita Nanda ◽  
Jack Gilbert
Keyword(s):  
Breast Cancer ◽  
16S Rrna ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Residual Disease ◽  
Response To Therapy ◽  
Response To Treatment ◽  
Rrna Gene ◽  
Sequencing Analysis ◽  
Early Stage Disease

e14186 Background: The human microbiome has been postulated to play a role in carcinogenesis, and there is evidence that commensal intestinal bacteria are capable of promoting tumor immunosurveillance and controlling the immune system’s response to therapy by modulating the tumor microenvironment. Methods: We characterized the stool microbiome of 30 patients (pts) with triple-negative breast cancer (TNBC) using 16S rRNA gene sequencing. Analysis of composition of microbiomes (ANCOM) was used to identify differential abundant exact-sequence-variants (ESVs) with p-values adjusted using Benjamini-Hochberg False Discovery Rate (pFDR) correction. We correlated the stool microbiome with clinicopathologic features and response to treatment. Results: The cohort included 7 pts with metastatic breast cancer and 23 pts with early-stage disease. 19 pts were treated with neoadjuvant chemotherapy (NACT). Bacteroides ovatus ESV was enriched (pFDR < 0.05) in black pts (n = 14), whereas ESV from Prevotella copri was abundant (pFDR < 0.05) in white pts (n = 13). ESVs from Clostridium and family Ruminococcaceae were enriched (pFDR < 0.05) in pts with distant metastatic recurrence (n = 6) compared to pts without metastatic disease. Notably, we identified specific taxa that differentiated between pts with a pathological complete response to NACT (pCR, n = 6) and those with residual disease (n = 13). ESVs from Bacteroides and Ruminococcaceae were relatively more abundant in pts with a pCR (pFDR < 0.05). Furthermore, among pts with residual disease after NACT, Bacteroides caccae was significantly enriched in pts with a partial response (n = 4) compared to pts with no response (n = 9). Conclusions: To our knowledge, this is the first time that 16S rRNA amplicon sequencing has been used to identify microbial signatures correlating with clinical phenotypes and response to treatment in pts with TNBC. This small study provides insight into the potential role of microbes in novel therapeutic interventions to correct dysbiosis and shift towards a gut microbial ecosystem that enhances the body’s immune response to TNBC.

scholarly journals POS0359 MOLECULAR PROFILING OF RADIOGRAPHIC AXIAL SPONDYLOARTHRITIS PATIENTS REVEALS AN ASSOCIATION BETWEEN INNATE AND ADAPTIVE CELL POPULATIONS AND THERAPEUTIC RESPONSE TO ADALIMUMAB

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 410.1-410
Author(s):  
D. Sobral ◽  
A. F. Fernandes ◽  
A. Mashayekhi Sardoo ◽  
M. Bernardes ◽  
P. Pinto ◽  
...  
Keyword(s):  
Disease Activity ◽  
Immune Cell ◽  
Axial Spondyloarthritis ◽  
Therapeutic Option ◽  
Differential Expression Analysis ◽  
Differentially Expressed Gene ◽  
Molecular Profiling ◽  
Response To Therapy ◽  
Differentially Expressed ◽  
Response To Treatment

Background:The response to treatment in spondylarthropaties is heterogeneous, due to factors yet to be better described. For that reason, it is important to find tools that might help clinicians to decide what is the best available therapeutic option for each patient.Objectives:The goal of this study is to use comprehensive molecular profiling to characterize clinical response to therapy in a real-world setting. Specifically, to identify molecular biomarkers differentiating good responders and non-responders to TNF inhibitors (TNFi) treatment, using adalimumab, in radiographic axial spondyloarthritis | ankylosing spondylitis (r-axSpA|AS) patients context.Methods:Whole-blood mRNA and plasma proteins were measured in a cohort of biologic naïve r-axSpA|AS patients (n = 35) from the Bioefficacy study (Biomarkers identification of anti-TNF alpha agent efficacy in AS patients using RNA sequencing and mass spectrometry), pre and post (14 weeks) TNFi treatment using adalimumab. Response to treatment was categorized according to ASAS20. Results of differential expression analysis were used to identify the most enriched pathways and in predictive models to distinguish responses to TNFi.Results:A treatment-related signature, independent of the type of response, suggests a reduction in inflammatory disease activity. We found genes and proteins robustly differentially expressed between baseline and week 14 in responders, including the GWAS AS-associated genes TNFRSF1A, FCGR2A, TYK2, TBKBP1, IL1R1, IL6R, ICOSLG, IL7R, HHAT and LTBR. Moreover, CRP and HP proteins showed strong and early decrease in the plasma of AS patients, while a cluster of apolipoproteins (APO1, APO2, APO3) showed an increased expression at week 14. Good responders to TNFi treatment tend to have higher expression of innate immunity genes at baseline, and lower expression of markers associated with adaptive immunity, particularly B-cells. A logistic regression model incorporating ASDAS-CRP, gender and Gene x, the top differentially expressed gene at baseline between responders and non-responders, enabled an accurate prediction of response to adalimumab in our cohort (AUC=0.97).Conclusion:Differences in disease activity and/or innate/adaptive immune cell type composition at baseline may be a major contributor to response to adalimumab in r-axSpA|AS. Alternatively, a model including clinical and gene expression variables could be considered, particularly in patients with mild disease activity.Disclosure of Interests:None declared

Baricitinib: The Second FDA-Approved JAK Inhibitor for the Treatment of Rheumatoid Arthritis

2019 ◽  
Vol 53 (9) ◽  
pp. 947-953 ◽  
Author(s):  
Amanda Mogul ◽  
Katherine Corsi ◽  
Laura McAuliffe
Keyword(s):  
Rheumatoid Arthritis ◽  
Randomized Clinical Trials ◽  
Cell Function ◽  
Immune Cell ◽  
Data Extraction ◽  
Oral Treatment ◽  
Growth Factor Receptor ◽  
Janus Kinase ◽  
Inadequate Response ◽  
Jak Inhibitor

Objective: To review the pharmacology, pharmacokinetics, safety, and efficacy of baricitinib, a recently approved selective Janus Kinase (JAK) inhibitor for the treatment of rheumatoid arthritis (RA), and explore its potential role in therapy. Data Sources: Articles were identified using a PubMed search from inception through January 2019 using the terms rheumatoid arthritis, Olumiant, baricitinib, and LY3009104, its molecular name. Study Selection and Data Extraction: Articles relating to randomized clinical trials, pharmacology, pharmacokinetics, efficacy, and safety of baricitinib were evaluated. Data Synthesis: Baricitinib exerts its effects by inhibiting JAK1 and JAK2 enzymes, targeting cytokine and growth factor receptor stimulation, thus reducing downstream immune cell function. Four trials have demonstrated the efficacy of baricitinib with or without methotrexate in patients naïve to disease-modifying antirheumatic drugs (DMARDs) and those who had an inadequate response to or intolerance to both conventional and biological DMARDs. Furthermore, baricitinib was associated with delayed radiographic progression. Despite baricitinib 4 mg often demonstrating greater efficacy compared with the 2 mg dose, only the 2 mg dose is Food and Drug Administration approved because of safety concerns with the 4 mg dose, primarily thromboembolism. Relevance to Patient Care and Clinical Practice: Baricitinib provides an oral treatment option for patients failing tumor necrosis factor inhibitors (TNFis). Safety, cost, and comparative effectiveness to tofacitinib should be considered prior to prescribing baricitinib. Conclusion: Baricitinib is the second medication in its class and has been proven efficacious for the treatment of RA. Given concerns for adverse effects associated with baricitinib, it should be reserved for patients who have failed one or more TNFis.

scholarly journals Acquired Resistance to Immune Checkpoint Blockade Therapies

Cancers ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1161
Author(s):  
Xianda Zhao ◽  
Dechen Wangmo ◽  
Matthew Robertson ◽  
Subbaya Subramanian
Keyword(s):  
Immune Checkpoint ◽  
Cell Function ◽  
Immune Cell ◽  
Current Knowledge ◽  
Clinical Investigation ◽  
Acquired Resistance ◽  
Genomic Analysis ◽  
Immune Checkpoint Blockade ◽  
Checkpoint Blockade ◽  
Response To Treatment

Immune checkpoint blockade therapy (ICBT) has revolutionized the treatment and management of numerous cancers, yet a substantial proportion of patients who initially respond to ICBT subsequently develop resistance. Comprehensive genomic analysis of samples from recent clinical trials and pre-clinical investigation in mouse models of cancer provide insight into how tumors evade ICBT after an initial response to treatment. Here, we summarize our current knowledge on the development of acquired ICBT resistance, by examining the mechanisms related to tumor-intrinsic properties, T-cell function, and tumor-immune cell interactions. We discuss current and future management of ICBT resistance, and consider crucial questions remaining in this field of acquired resistance to immune checkpoint blockade therapies.

ZAP-70 Expression in Chronic Lymphocytic Leukemia (CLL) Is Independent of Rai Stage: A Retrospective Review of 38 Patients (pts).

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 4811-4811
Author(s):  
Blanche H. Mavromatis ◽  
Bruce D. Cheson ◽  
Nicole D. Zantek ◽  
Dan-Paul Hartmann ◽  
Craig Kessler ◽  
...  
Keyword(s):  
Early Stage ◽  
Therapy Response ◽  
Clinical Information ◽  
Previous Treatment ◽  
Response To Therapy ◽  
Lymphocytic Leukemia ◽  
Stage Iii ◽  
Response To Treatment ◽  
Early Stage Disease ◽  
Negative Patient

Abstract ZAP-70 is a tyrosine kinase protein involved in T cell signaling, overexpression of which is associated with a poor prognosis in CLL. Clinical information on 32 pts with CLL, and 6 pts with prolymphocytic transformation (PLT) followed at our institution was retrospectively reviewed for Rai stage, ZAP-70, CD38, FISH and response to treatment to determine the prognostic association among these factors. Ages ranged from 37 to 78 (median 59). 5/32 pts with CLL had received prior initial therapy, while 17/19 pts had not. They eventually were all treated with fludarabine based regimens either as salvage or upfront. The remaining 8/32 had not required therapy. Response to therapy was correlated with ZAP-70 expression as measured by immunohistochemistry using a monoclonal antibody to ZAP-70 (clone 2F3.2).17/32 patients (53%) were ZAP-70 positive, as were 3/6 (50%) of the patients with PLT. Of the patients with CLL who were ZAP-70 positive, 5 (30%) were stage 0-II, and 12 (70%) were stage III/IV, while18% did not require therapy. Of the 13 who were treated there were 4 (31%) CR, and 5 (38%) PR. Of the patients who were ZAP-70 negative, 50% (7/14) had stages 0-II and 50% had stage III/IV disease. 5/14(36%) were not treated. Of the 9 who were treated there were 2 CR 22%, and 7 PR 78% (p=0.01). 3 PLT patients were previously treated for CLL with fludarabine-based combinations. When they required therapy for PLT, two achieved a CR (one to rituximab/fludarabine/cytoxan_ZAP-70 positive patient, and one to R-CHOP combination_ZAP-70 negative), and another a PR (to R-EPOCH combination_ZAP-70 negative patient). Of the previously untreated PLT patients, two ZAP-70 positive patients achieved a CR (one to rituximab/fludarabine/cyclophosphamide, and one to R-CHOP). One ZAP-70 negative patient was refractory to fludarabine/rituximab combination. Conclusion: ZAP-70 positive CLL is more likely to be refractory to treatment, while ZAP-70 negative pts achieved a higher ORR (p=0.01). Although pts who were ZAP-70 positive were more likely to have advanced stage, 30% of these pts had early stage disease. As such, ZAP-70 did not closely correlate with stage, and may be an independent prognostic factor in these pts. Response to treatment could also not be predicted by ZAP-70 expression. ZAP-70 Number of Pts Previous Treatment Number of Pts Response Positive 16 No 10 3CR, 4PR Yes 3 1CR, 1PR Negative 14 No 7 2CR, 5PR Yes 2 2PR

Predicting Response to Therapy for Graft-vs-Host Disease (GvHD) with a Rapid Immune Function Assay.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 5012-5012
Author(s):  
Elias J. Anaissie ◽  
Jose A. Diaz ◽  
Monica L. Grazziutti ◽  
Marisa H. Miceli ◽  
Michele Fox-Cottler ◽  
...  
Keyword(s):  
Immune Function ◽  
Immunosuppressive Therapy ◽  
Cell Function ◽  
Immune Cell ◽  
Chronic Gvhd ◽  
Organ Transplant ◽  
Response To Therapy ◽  
Solid Organ ◽  
Hematopoietic Stem ◽  
Atp Production

Abstract Background: GvHD following allogeneic hematopoietic stem cell transplantation (allo-HSCT) increases morbidity and mortality and is difficult to predict for. We explored the use of a novel immune function assay to determine whether an immunologic response to changes in immunosuppressive therapy for GvHD could predict clinical response. Methods: The FDA-approved Cylex ® Immune Cell Function assay (ICF) measures the response of whole blood CD4+ lymphocytes to stimulation with phytohemagglutinin (PHA) with as read-out ATP production. The assay is quick and results are available on the same day. Use of this test in solid-organ transplant recipients demonstrated its utility in monitoring changes in immunosuppressive therapy. A retrospective analysis of the ICF assay results from allo-HSCT patients treated at our center for acute or chronic GvHD was conducted. Results: 13 GvHD events (11 chronic, 2 acute) occurring in 8 patients between 35 and 2118 days post-transplant (682 +/− 556 d) were analyzed. At diagnosis of GvHD, the average ICF value was 425 +/− 111 ng/mL ATP. Same day white blood cell (WBC) and absolute neutrophil count (ANC) values were 10.6 +/− 3.2 x 103 cells/μL and 9.2 +/− 3.3 x 103 cells/μL, respectively. Treatment for GvHD consisted of increasing calcineurin inhibitor dose and addition of prednisone and/or other immunosuppressants. Ten GvHD events responded to therapy within 10 +/−7 days with a corresponding significant decrease of ICF values from 430 +/− 109 ng/mL to 239 +/− 130 ng/mL (p=0.002) and a decrease of WBC from 11.2 to 8.0 x103 cells/μL (p=0.027). ANC and C - reactive protein values were not statistically different (p=0.09 and p>0.5 respectively). In contrast, no significant decrease in the ICF values before and after therapy (406 to 465 ng/mL ATP) was observed for the 3 GvHD events that failed to respond to therapy. Conclusion: These preliminary data suggest that the ICF assay is a good predictor of response of GvHD to immunosuppressive therapy and could be used to intensify immunosuppression early in non-responders.

scholarly journals Expression and Pathogenic Analysis of Integrin Family Genes in Systemic Sclerosis

2021 ◽  
Vol 8 ◽  
Author(s):  
Dan Xu ◽  
Ting Li ◽  
Ruikang Wang ◽  
Rong Mu
Keyword(s):  
Systemic Sclerosis ◽  
Pathway Analysis ◽  
Cell Function ◽  
Immune Cell ◽  
Functional Enrichment ◽  
Skin Tissue ◽  
Receptor Interaction ◽  
Skin Thickness ◽  
Endothelial Cell Function ◽  
Integrin Family

Objectives: Emerging evidence shows that integrin members are involved in inflammation and fibrosis in systemic sclerosis (SSc). This study aimed at evaluating the expression of integrin family genes in the skin tissue from SSc patients and exploring the potential pathogenic mechanism.Methods: We utilized the public datasets of SSc skin tissue from the Gene Expression Omnibus (GEO) database to analyze the expression and clinical significance of integrin family genes in SSc. The expression of integrin members in skin tissue was also assessed by immunohistochemistry. In addition, functional enrichment and pathway analysis were conducted.Results: Compared with healthy controls, the mRNA and protein levels of ITGA5, ITGB2, and ITGB5 were upregulated in the skin of SSc patients. Further analysis indicated that the mRNA expression levels of ITGA5, ITGB2, and ITGB5 were positively correlated with modified Rodnan skin thickness score (mRSS). Functional enrichment and pathway analysis showed that integrin members may play multiple roles in the pathogenesis of SSc. Among them, ITGA5, ITGB2, and ITGB5 might synergistically promote SSc through affecting extracellular matrix (ECM) turnover, ECM–receptor interaction, focal adhesion, and leukocyte trans-endothelial migration, while ITGA5 and ITGB5 also might affect angiogenesis and endothelial cell function. In addition, ITGA5, ITGB2, and ITGA5 were associated with different pathways, respectively. ITGA5 was uniquely enriched for actin organization, while ITGB5 was for TGF-β signaling and ITGB2 for immune cell activation.Conclusion: Our results implied that the abnormal expression of integrin family genes including ITGA5, ITGB2, and ITGB5 may participate in multiple pathological processes in SSc. Further investigations are required for confirming this speculation.

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