Inflammatory Monocyte Subsets Correlation with Iron Levels in Low Vitamin D Pediatric Transfusion-Dependent Thalassemia.

Abstract

Background: Patients with transfusion-dependent thalassemia experience iron dysregulation, which affects the immune response. Surface proteins such as FcγRIII (CD16), lipopolysaccharide receptor (CD14), and human leukocyte antigen (HLA-DR) on monocytes are crucial for innate and adaptive responses. Blood monocytes, identified by their CD14 and CD16 expression, show functional diversity during injury or inflammation. Considering the mechanisms of vitamin D activation and its potential interaction with monocytes, further investigation of its immunomodulatory role in transfusion-dependent thalassemia is essential.

Purpose: This study evaluated monocyte subsets, population, and surface receptor expression (CD14, CD16, and HLA-DR), and their association with iron status and vitamin D levels in patients with transfusion-dependent thalassemia.

Patients and methods: Fifty lysed erythrocyte-heparinized whole blood samples from transfusion-dependent thalassemia patients were analyzed by flow cytometry and classified into three monocyte subsets: CD14++CD16- (classical), CD14++CD16+ (intermediate), and CD14+CD16++ (non-classical). Cell percentage referred to the monocyte subset population. Median fluorescence intensity (MFI) indicated surface protein expression. The 25(OH)vitamin D level was used to measure vitamin D levels. Iron status was assessed using ferritin and serum iron levels. A correlational study was performed.

Results: We did not find a correlation between low vitamin D levels (22.9 ng/mL ± 3.9) and monocyte characteristics, iron status, or hematology profile. However, we observed a negative correlation between the percentage of intermediate and non-classical monocytes and hemoglobin and ferritin levels (P = 0.02, r = -0.3; P = 0.04, r = -0.3). Additionally, we found a positive correlation between the median fluorescence intensity (MFI) of CD14 in non-classical monocytes and serum iron (P = 0.04, r = 0.3).

Conclusion: Our findings suggest that iron overload and anemia may influence the function of inflammatory monocyte subsets. Considering the immunomodulatory role of vitamin D through monocyte modulation during pathogen insult, further research utilizing a whole-blood stimulation assay is imperative.