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Last update 23 Jan 2025

GITRL

Last update 23 Jan 2025

Basic Info

Synonyms

Activation-inducible TNF-related ligand, AITRL, GITRL

+ [6]

Introduction

Cytokine that binds to TNFRSF18/AITR/GITR. Regulates T-cell responses. Can function as costimulator and lower the threshold for T-cell activation and T-cell proliferation. Important for interactions between activated T-lymphocytes and endothelial cells. Mediates activation of NF-kappa-B. Triggers increased phosphorylation of STAT1 and up-regulates expression of VCAM1 and ICAM1 (PubMed:23892569). Promotes leukocyte adhesion to endothelial cells (PubMed:23892569). Regulates migration of monocytes from the splenic reservoir to sites of inflammation (By similarity).

Drugs associated with GITRL

Delta-24-GREAT

Target

GITRL

Mechanism

GITRL modulators

Active Org.

The University of Texas MD Anderson Cancer Center

Originator Org.

The University of Texas MD Anderson Cancer Center

Active Indication

Metastatic breast cancer [+1]

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with GITRL

100 Translational Medicine associated with GITRL

0 Patents (Medical) associated with GITRL

301

Literatures (Medical) associated with GITRL

01 Feb 2025·Translational Oncology

Cellular heterogeneity and cytokine signatures in acute myeloid leukemia: A novel prognostic model

Article

Author: Fang, Dan ; Jiang, Ling ; Li, Tianqi ; Cao, Jinxia ; Wang, Jun ; Hu, Bin

Acute Myeloid Leukemia (AML) is a complex hematological malignancy distinguished by its heterogeneity in genetic aberrations, cellular composition, and clinical outcomes. This diversity complicates the development of effective, universally applicable therapeutic strategies and highlights the necessity for personalized approaches to treatment. In our study, we utilized high-resolution single-cell RNA sequencing from publicly available datasets to dissect the complex cellular landscape of AML. This approach uncovered a diverse array of cellular subpopulations within the bone marrow samples of AML patients. Through meticulous analysis, we identified 156 differentially expressed cytokine-related genes that underscore the nuanced interplay between AML cells and their microenvironment. Leveraging this comprehensive dataset, we constructed a prognostic risk score model based on seven pivotal cytokine-related genes: CCL23, IL2RA, IL3RA, IL6R, INHBA, TNFSF15, and TNFSF18. The mRNA levels of 7 genes in the risk score model have significant different. This model was rigorously validated across several independent AML patient cohorts, showcasing its robust prognostic capability to stratify patients into distinct risk categories. Patients classified under the high-risk category exhibited significantly poorer survival outcomes compared to their low-risk counterparts, underscoring the model's clinical relevance. Additionally, our in-depth investigation into the immune landscape revealed marked differences in immune cell infiltration and cytokine signaling between the identified risk groups, shedding light on potential immune-mediated mechanisms driving disease progression and treatment resistance. This comprehensive analysis not only advances our understanding of the cellular and molecular underpinnings of AML but also introduces a novel, clinically applicable risk score model. This tool holds significant promise for enhancing the precision of prognostic assessments in AML, thereby paving the way for more tailored and effective therapeutic interventions. Our findings represent a pivotal step toward the realization of personalized medicine in the management of AML, offering new avenues for research and treatment optimization in this challenging disease landscape.

15 Dec 2024·The FASEB Journal

Correction to “Genetic and pharmacological inhibition of GITR‐GITRL interaction reduces chronic lung injury induced by bleomycin instillation”

Cuzzocrea, S., Ronchetti, S., Genovese, T., Mazzon, E., Agostini, M., Di Paola, R., Esposito, E., Muià, C., Nocentini, G. and Riccardi, C. (2007), Genetic and pharmacological inhibition of GITR‐GITRL interaction reduces chronic lung injury induced by bleomycin instillation. The FASEB Journal, 21: 117‐129. https://doi.org/10.1096/fj.06‐6611comThe authors report that while preparing Figure 10B, the beta‐tubulin image was placed incorrectly; specifically, it was flipped horizontally. Due to the time that has passed, the original data are no longer available to correct the image. The figure legend has been corrected to clarify that the same beta‐tubulin image was used in Figures 10A and 10B because the blots shown are from the same experiment and beta‐tubulin is the experimental control. The error does not change the results or conclusions of the article.FIGURE 10 Effect of genetic or pharmacological inhibition of GITR‐GITRL interaction on NF‐κB activation in lungs following bleomycin administration. A basal level of IK B‐e was detected in the lung tissues from sham‐treated GITR+/+ and GITR−/−mice (A, Aa), whereas in 7 d bleomycin‐treated GITR+/+ mice IκB‐α levels were substantially reduced (A, Aa). A significant prevention of IκB‐é degradation induced by bleomycin instillation was observed in the lung tissues collected from GITR−/− mice (A, Aa). Western blot with β‐tubulin was performed to verify that equivalent amounts of proteins were loaded in each lane. *p ~ .05 vs. sham; °p ~ .05 vs. bleomycin‐treated GITR+/+ mice. In addition, bleomycin instillation caused a significant increase in the phosphorylation of Ser‐536 in the lung tissues from GITR+/+ mice (B, Ba). A significant reduction of the phosphorylation of p65 on Ser‐536 was observed in the lung tissues from GITR−/− mice (B, Ba). Western blot with β‐tubulin was performed to verify that equivalent amounts of proteins were loaded in each lane. *p < .01 vs. sham; °p < .01 vs. bleomycin‐treated ‐GITR+/+ mice. Moreover, the levels of the NF‐κB p65 subunit protein in the nuclear fractions from lung tissue were also significantly increased after bleomycin instillation com compared to the sham‐treated mice (C, Ca). A significant reduction of the NFκB p65 protein levels was observed in the tissues from GITR−/− mice (C, Ca). *p < .01 vs. sham; °p < .01 vs. bleomycin‐treated GITR+/+ mice. Immunoblotting in (A–C) is representative of one blot out of five analyzed. The results in (Aa, Ba, and Ca) are expressed as mean ± se from five blots. The same blot for β‐tubulin was used in panels (A) and (B) because it is from the same experiment.

01 Sep 2024·Journal of Surgical Oncology

Immune checkpoint expression as prognostic biomarker candidates in non‐small cell lung carcinoma patients

Article

Author: Costa, Guilherme Jorge ; Porto, Débora Maria ; Torres, Leuridan Cavalcante ; Casarini, Dulce Elena

AbstractBackgroundCancer immunotherapy has had an important role in oncologic therapeutics for patients with non‐small cell lung cancer (NSCLC) using checkpoint inhibitors. We will explore the possible prognosis biomarker candidates such as: soluble OX40 (sOX40), OX40L (sOX40L), Glucocorticoid‐induced tumor necrosis factor receptor family‐related receptor (GITR), and their ligand (GITRL), 4‐1BB or tumor necrosis factor receptor superfamily 9 (TNFRS9) and inducible T cell co‐stimulator (ICOS) in peripheral blood of NSCLC patients.MethodsFifty‐eight patients were diagnosed with advanced NSCLC between January 2019 and March 2020.ResultsHigh sOX40 and low s4‐1BB levels in smokers compared non‐smoker NSCLC patients. Lower sOX40L levels were found in the male than female (p < 0.05). High sOX40 and sGITRL in stage III compared to the stage IV (p < 0.05). With follow‐up at 21.4 months, 44.1% and 91.1% were alive in the sGITRhigh and sGITRlow groups, respectively (p = 0.02), and 73.3% and 27.7% were alive in the sGITRLhigh and sGITRLlow groups, respectively (p = 0.02). At 22 months, 38.7% and 92.3% were alive in the sOX40Lhigh and sOX40Llow groups, respectively (p = 0.01).ConclusionsGITR, sGITRL, and sOX40L levels were potential prognostic biomarkers and could have an important role as new targets of immunotherapy in NSCLC patients. sGITR, sGITRL, sOX40L, and sOX40 levels were associated with smoking, sex, stage, and age in NSCLC.

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