Increased TIM-3 and GAL-9 serum levels in patients with advanced systemic mastocytosis.
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BORIS DOI
Date of Publication
October 2023
Publication Type
Article
Division/Institute
Contributor
Konantz, Martina | |
Williams, Margaret | |
Merkel, Tamara | |
Reiss, Antonia | |
Dirnhofer, Stefan | |
Valent, Peter | |
George, Tracy I | |
Tzankov, Alexandar | |
Hartmann, Karin |
Subject(s)
Series
Journal of allergy and clinical immunology
ISSN or ISBN (if monograph)
1097-6825
Publisher
Elsevier
Language
English
Publisher DOI
PubMed ID
37423405
Uncontrolled Keywords
Description
BACKGROUND
Systemic mastocytosis is characterized by expansion of clonal mast cells in various tissues. Several biomarkers with diagnostic and therapeutic potential have recently been characterized in mastocytosis, such as the serum marker tryptase and the immune checkpoint molecule PD-L1.
OBJECTIVE
We aimed to investigate whether serum levels of other checkpoint molecules are altered in systemic mastocytosis and whether these proteins are expressed in mastocytosis infiltrates in the bone marrow.
METHODS
Levels of different checkpoint molecules were analyzed in serum of patients with different categories of systemic mastocytosis and healthy controls and correlated to disease severity. Bone marrow biopsies from systemic mastocytosis patients were furthermore stained to confirm expression.
RESULTS
Serum levels of TIM-3 and GAL-9 were increased in systemic mastocytosis, particularly in advanced subtypes, compared to healthy controls. TIM-3 and GAL-9 levels were also found to correlate with other biomarkers of systemic mastocytosis such as serum tryptase and KIT D816V variant allele frequency in the peripheral blood. Moreover, we observed expression of TIM-3 and GAL-9 in mastocytosis infiltrates in bone marrow.
CONCLUSIONS
Together, our results demonstrate for the first time that serum levels of TIM-3 and GAL-9 are increased in advanced systemic mastocytosis. Moreover, TIM-3 and GAL-9 are expressed in bone marrow infiltrates in mastocytosis. These findings provide a rationale for exploring TIM-3 and GAL-9 as diagnostic markers and eventually also therapeutic targets in systemic mastocytosis, particularly in advanced forms.
Systemic mastocytosis is characterized by expansion of clonal mast cells in various tissues. Several biomarkers with diagnostic and therapeutic potential have recently been characterized in mastocytosis, such as the serum marker tryptase and the immune checkpoint molecule PD-L1.
OBJECTIVE
We aimed to investigate whether serum levels of other checkpoint molecules are altered in systemic mastocytosis and whether these proteins are expressed in mastocytosis infiltrates in the bone marrow.
METHODS
Levels of different checkpoint molecules were analyzed in serum of patients with different categories of systemic mastocytosis and healthy controls and correlated to disease severity. Bone marrow biopsies from systemic mastocytosis patients were furthermore stained to confirm expression.
RESULTS
Serum levels of TIM-3 and GAL-9 were increased in systemic mastocytosis, particularly in advanced subtypes, compared to healthy controls. TIM-3 and GAL-9 levels were also found to correlate with other biomarkers of systemic mastocytosis such as serum tryptase and KIT D816V variant allele frequency in the peripheral blood. Moreover, we observed expression of TIM-3 and GAL-9 in mastocytosis infiltrates in bone marrow.
CONCLUSIONS
Together, our results demonstrate for the first time that serum levels of TIM-3 and GAL-9 are increased in advanced systemic mastocytosis. Moreover, TIM-3 and GAL-9 are expressed in bone marrow infiltrates in mastocytosis. These findings provide a rationale for exploring TIM-3 and GAL-9 as diagnostic markers and eventually also therapeutic targets in systemic mastocytosis, particularly in advanced forms.
File(s)
| File | File Type | Format | Size | License | Publisher/Copright statement | Content | |
|---|---|---|---|---|---|---|---|
| 1-s2.0-S0091674923008606-main.pdf | text | Adobe PDF | 3.03 MB | Attribution-NonCommercial-NoDerivatives (CC BY-NC-ND 4.0) | accepted |