Portal de Periódicos da CAPES

Artigo Acesso aberto Produção Nacional Revisado por pares

BIBTEX RIS

Imbalance of Chemokines and Cytokines in the Bone Marrow Microenvironment of Children with B-Cell Acute Lymphoblastic Leukemia

2021; Hindawi Publishing Corporation; Volume: 2021; Linguagem: Inglês

10.1155/2021/5530650

1687-8469

Fábio Magalhães-Gama, Marlon Wendell Athaydes Kerr, Nilberto Dias de Araújo, Hiochelson Najibe Santos Ibiapina, Juliana Costa Ferreira Neves, Fabíola Silva Alves-Hanna, Lilyane de Amorim Xabregas, Maria Perpétuo Socorro Sampaio Carvalho, Eliana Brasil Alves, Andréa Monteiro Tarragô, Olindo Assis Martins‐Filho, Andréa Teixeira−Carvalho, Adriana Malheiro, Allyson Guimarães Costa,

Hematopoietic Stem Cell Transplantation

In the hematopoietic microenvironment, leukemic cells secrete factors that imbalanced chemokine and cytokine production. However, the network of soluble immunological molecules in the bone marrow microenvironment of acute lymphoblastic leukemia (ALL) remains underexplored. Herein, we evaluated the levels of the immunological molecules (CXCL8, CCL2, CXCL9, CCL5, CXCL10, IL-6, TNF, IFN-γ, IL-17A, IL-4, IL-10, and IL-2) in the bone marrow plasma of 47 recently diagnosed B-cell acute lymphoblastic leukemia (B-ALL) patients during induction therapy using cytometric beads arrays. The results demonstrated that B-ALL patients showed high levels of CXCL9, CXCL10, IL-6, and IL-10 at the time of diagnosis, while at the end of induction therapy, a decrease in the levels of these immunological molecules and an increase in CCL5, IFN-γ, and IL-17A levels were observed. These findings indicate that B-ALL patients have an imbalance in chemokines and cytokines in the bone marrow microenvironment that contributes to suppressing the immune response. This immune imbalance may be associated with the presence of leukemic cells since, at the end of the induction therapy, with the elimination and reduction to residual cells, the proinflammatory profile is reestablished, characterized by an increase in the cytokines of the Th1 and Th17 profiles.