Abstract
The prognostic significance of sCD86 in patients with hematologic malignancies is unclear. We evaluated sCD86 levels in 63 newly diagnosed AML and 16 controls by enzyme-linked immunosorbent assay and then analyzed how its levels and various clinical parameters related to overall survival. Levels of sCD86 in patients were high (1.22 ± 1.34) compared with the controls (0.51 ± 0.23) but were not significant (p = 0.096). The patients’ outcome and whether they achieved complete remission and if they were sCD86 positive or negative didn’t have any significance (p = 0.1). High levels of sCD86 were detected in patients with hypercellular marrow (with a high percentage of bone marrow blasts), FLT-3 mutated type, and in FAB M4-M5. The overall survival among sCD86-positive and sCD86-negative patients was not significant (p = 0.16). The overall survival of patients regarding clinical parameters showed no significance except for FLT-3 type (p = 0.001).
Highlights
CD4+ T helper cells (TH) cell activation is initiated by the interaction of the T-cell receptor (TCR) CD3 complex with antigen presenting cell (APC) through the antigenic peptide bound to the MHC class II molecule on its surface [1].Naïve T lymphocytes require two diverse signals from APCs to be a functional cell
In our study we assessed levels of soluble CD86 (sCD86) in 63 de novo acute myeloid leukemia patients compared with 16 volunteers in the control group to determine if there is any correlation with prognosis, outcome, and overall survival
For a better understanding of the molecular, cytogenetic and immunological mechanisms of acute myeloid leukemia (AML) and its poor chemotherapy outcome, the detection of novel diagnostic and prognostic markers is vital because we can use them as a guide to develop new targeted chemotherapies or immunotherapeutic agents
Summary
CD4+ T helper cells (TH) cell activation is initiated by the interaction of the T-cell receptor (TCR) CD3 complex with antigen presenting cell (APC) through the antigenic peptide bound to the MHC class II molecule on its surface [1]. Naïve T lymphocytes require two diverse signals from APCs to be a functional cell. A second signal can be provided by APC-borne ligands for the CD28 and cytotoxic lymphocyte-associated antigen-4 (CTLA-4) receptors on T cells [2]. The B7 molecules CD80 and CD86 are expressed predominantly by activated APCs, and they generate, following binding to their T-cell ligands (CD28, CTLA-4), bi-directional signals that are critical in the regulation of antitumor responses. The B7:CD28 interaction enhances and the B7:CTLA-4 inhibits both APC and effector cell function [3]. Despite having the same ligands, CD80 and CD86 appear to be involved in different mechanisms: CD80 can be more potent than CD86 in inducing an antitumoral response, while CD86 preferentially induces the production of a helper (Th) 2 response
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