T-lymphocytes Expression of Toll-like Receptors 2 and 4 in Acute Myeloid Leukemia Patients with Invasive Fungal

Muhamad R Abdel Hammed1, Sherein G Elgendy2, Mohamed A El-Mokhtar2

  • 1Internal Medicine Department and Hematology Unit, Assiut University Hospitals and South Egypt Cancer Institute Bone Marrow Transplantation Unit, Assiut University, Assiut, Egypt.

Abstract

Insights

Toll-like receptor 4 (TLR4) expression is elevated in acute myeloid leukemia (AML) patients experiencing invasive fungal infections (IFIs). This finding suggests TLRs may serve as biomarkers for IFIs in AML patients undergoing chemotherapy.

Area of Science:

  • Immunology
  • Hematology
  • Infectious Diseases

Background:

  • Invasive fungal infections (IFIs) are a significant cause of mortality in acute myeloid leukemia (AML) patients undergoing intensive induction chemotherapy.
  • Toll-like receptors (TLRs), particularly TLR2 and TLR4, are crucial in host defense against pathogens.
  • While TLR signaling in innate immunity is well-studied, their expression on adaptive immune cells and association with IFIs in AML remain unclear.

Purpose of the Study:

  • To investigate the association between T-lymphocyte expression of Toll-like receptors 2 and 4 (TLR2 and TLR4) and the occurrence of IFIs in AML patients.
  • To explore the potential of TLR expression as a biomarker for IFIs in AML.

Main Methods:

  • Evaluated 122 newly diagnosed AML patients and 20 healthy controls.
  • Diagnosed IFIs using culture, microscopy, histopathology, galactomannan assay, and PCR.
  • Analyzed TLR2 and TLR4 expression on T-lymphocytes via flow cytometry.

Main Results:

  • TLR4 expression was significantly higher in AML patients with IFIs compared to healthy controls (p = 0.001).
  • Both TLR2 and TLR4 expressions were significantly increased in AML patients with mixed fungal and bacterial infections versus healthy controls (p=0.002 and p=0.001, respectively).

Conclusions:

  • TLR expressions may serve as important biological markers for predicting IFIs in non-M3 AML patients post-intensive induction chemotherapy.

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