Authors
Samia Hussein, Ezzat Moustafa Mohamed, Hoda F Ebian, Ahmad Barakat Waley, Mohammed G M Alshamy, Zahraa I Aboafya, Basma S Elsayed, Ashwag Alsharidah, Nora Atef, Maha Mahmoud Hamed Sakr
Published in
Human immunology. Volume 87. Issue 8. Pages 111786. Jul 02, 2026. Epub Jul 02, 2026.
Abstract
Chronic lymphocytic leukemia (CLL) is a hematological malignancy with the accumulation of mature, monoclonal B lymphocytes. CLL cells can escape the host's immune response by inducing T-cell exhaustion. This occurs by upregulation of inhibitory checkpoint receptors, such as T-cell immunoglobulin and mucin domain-containing molecule-3 (TIM-3). Galectin-9 (Gal-9) is a soluble ligand for TIM-3. Its interaction with TIM-3 can induce T-cell exhaustion in various cancers. Therefore, targeting these inhibitory pathways may be a potential therapy for CLL.
This case-control study included 200 participants, divided into two groups. Group 1 included 100 treatment-naïve patients with newly diagnosed CLL. Group 2 (control group) included 100 age- and sex-matched healthy individuals. Gal-9 expression was estimated by real-time polymerase chain reaction, while flow cytometric %TIM-3+ on CD3+, CD3+CD4+, and CD3+CD8+ T cells was measured.
Galectin-9 mRNA expression and flow cytometric %TIM-3+ on CD3+, CD3+CD4+, and CD3+CD8+ T-cells were significantly higher in CLL patients than healthy controls. Both markers were significantly associated with prognostic markers (β2-microglobulin, lactate dehydrogenase (LDH), chromosomal abnormalities, and Rai stage).
Galectin-9/TIM-3 interaction has a possible role in the development and progression of CLL. Gal-9 mRNA expression and %TIM-3+ on CD3+, CD3+CD4+, and CD3+CD8+ T-cells are potential discriminators between CLL patients and healthy controls. This was demonstrated by high sensitivity and specificity. Additionally, they had significant correlations with prognostic markers, including β2-microglobulin, LDH, chromosomal abnormalities, CD38, and Rai stage.
PMID:
42391833
Bibliographic data and abstract were imported from PubMed on 03 Jul 2026.
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