The Role of Serum Cytokines IL_17 A and IL_10 in Disease Activity of Acute B Lymphoblastic Leukemia in South Egypt

Acute Lymphoblastic Leukemia, B-Cell

interleukins

Study aimsTo measure the serum levels of IL-17 A and IL-10 in newly diagnosed patients with B-cell acute lymphoblastic leukemia (B-ALL). 2-To study the association between serum cytokine levels (IL-17 A and IL-10) and laboratory parameters, as well as the response to treatment

Acute Lymphoblastic Leukemia (ALL) is a clonal malignant disorder of lymphoid progenitor cells, characterized by uncontrolled proliferation and accumulation of immature lymphoblasts in the bone marrow, peripheral blood, and extramedullary tissues. It is the most common childhood malignancy worldwide. Although survival rates have improved with risk-adapted chemotherapy and immunotherapy, relapse and treatment resistance remain major challenges, particularly among high-risk pediatric patients \[1,2\]. ALL is genetically and cytogenetically heterogeneous, but the bone marrow immune microenvironment also plays a critical role in disease progression. Cytokine-mediated interactions between leukemic blasts and immune cells create a permissive niche that supports proliferation, survival, and immune evasion. The balance between T helper 17 (Th17) cells and regulatory T cells (Tregs) is particularly important, as its disruption may promote chronic inflammation and impair anti-leukemic immune responses \[3,4\]. Interleukin-17A (IL-17A), the signature cytokine of Th17 cells, is a potent pro-inflammatory mediator that induces IL-6 and TNF-α production and activates STAT3 and NF-κB signaling pathways. IL-17A can enhance tumor-associated immune responses, promote angiogenesis, recruit immunosuppressive cells, and support malignant cell survival.\[5\] Conversely, Interleukin-10 (IL-10), produced mainly by Tregs, B cells, and some myeloid cells, is an anti-inflammatory cytokine that maintains immune homeostasis by limiting T cell activation and antigen presentation. Elevated IL-10 levels in ALL are associated with an immunosuppressive bone marrow environment, higher blast burden, and poor treatment response, suggesting its potential as a prognostic biomarker \[6,7\]. Overall, the interplay between pro-inflammatory cytokines such as IL-17A and anti-inflammatory cytokines such as IL-10 shapes the bone marrow microenvironment in ALL. Evaluating serum IL-17A and IL-10 levels may provide valuable prognostic information and enhance understanding of the disease's immunopathogenesis \[1-4\].

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