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Introduction: In CLL patients, immune escape mechanisms allow leukemia cells to proliferate and expand. Human
leukocyte antigen G (HLA-G) is a further strategy adopted by CLL cells to evade immune defenses and to create
protected niches where to grow and expand. Toll-like receptors (TLRs) represent major agents of innate immunity
and initiators of adaptive immunity. It has been suggested that the stimulation of TLRs expressed on CLL cells could
increase immunogenicity of tumor cells and thus potentially contribute to the induction of tumor-specific immune
response. We study the total expression of HLA-G and TLR-9 in CLL patients, evaluating their relationships with
other well established clinical and possible laboratory prognostic markers.
Methods: This study enrolled 40 CLL patients selected from the Hematology Department of the medical research
institute and Alexandria Main Hospital. In addition, to 20 healthy subjects matched by age and sex.
Results: In CLL patients, HLA-G showed significant negative correlation to TLR-9 and both of them showed
significant association with disease stage and prognostic index.
Conclusion: This study concluded that expression of HLA-G and TLR-9 could have a prognostic value in CLL
patients; the higher the HLA-G expression, the lower the TLR-9 expression, the worst the outcome. Use of HLA-G
and/or TLR-9 as markers for new targeted therapy in CLL could be valuable.
Hala K. Sultan ; professor of hematology, graduated from Alexandria University in 1984 , She obtained her master degree in Clinical Hematology from Faculty of Medicine at the same University in 1990 and earned her MD degree in benign and malignant Hematology from Hematology department , Medical Research Institute in 1998. She has been working since then as a Hematologist in the same department, currently the Head of the department since June 2018. She has been involved in teaching & clinical research, supervised more than 25 master and MD theses and she has about 20 publications in various international and national journals.