Illustration of T-cells attacking AML blasts and MDSCs, demonstrating the BiTE antibody's action.

Targeting Cancer's Weak Spot: How a New Antibody Construct Could Revolutionize AML Treatment

Soraya Malik in Health & Wellness December 2025 • 4 min read.

"Unlocking the Power of the Immune System: A Deep Dive into CD33/CD3-bispecific T-cell engaging (BiTE®) antibody's potential in treating Acute Myeloid Leukemia (AML)."

Acute Myeloid Leukemia (AML), a particularly aggressive form of blood cancer, presents a formidable challenge in the world of oncology. Despite advances in treatment, the 5-year survival rate remains discouragingly low, hovering around 30%. This sobering statistic underscores the critical need for innovative therapeutic approaches that can effectively combat this devastating disease.

Recent research has illuminated a significant hurdle in AML treatment: the ability of the disease to evade and suppress the body's natural defenses. Myeloid-derived suppressor cells (MDSCs), a type of immune cell, have emerged as key players in this immune evasion strategy. These cells, which share characteristics with both monocytes and granulocytes, create an environment that hinders the effectiveness of anti-cancer immune responses and therapies.

In this context, a groundbreaking study has unveiled the potential of a novel antibody construct to revolutionize AML treatment. This construct, known as a CD33/CD3-bispecific T-cell engaging (BiTE®) antibody, is designed to target and eliminate both AML blasts (cancer cells) and MDSCs. This dual-action approach aims to not only kill cancer cells directly but also to dismantle the immune-suppressing environment that allows the disease to thrive.

Understanding the Enemy Within: The Role of MDSCs in AML

Illustration of T-cells attacking AML blasts and MDSCs, demonstrating the BiTE antibody's action.

MDSCs are a diverse group of cells that share the common ability to suppress the immune system, creating a safe haven for cancer cells. In AML, these cells can resemble either monocytes or granulocytes, sharing common characteristics such as an immature phenotype, and the ability to hinder the function of immune cells, like T-cells. This immunosuppressive activity is a major factor in why AML can be so difficult to treat.

The study highlights how AML blasts can induce the production of MDSCs, effectively turning the body's own defenses against itself. These MDSCs then work to suppress the immune system, allowing the cancer cells to evade detection and destruction. This complex interplay between cancer cells and the immune system underscores the need for therapies that can overcome this suppression.

MDSCs are a heterogeneous population of cells with myeloid origin.
They possess an immature phenotype.
They actively suppress T-cell function.
AML blasts can induce MDSC production.
MDSCs contribute to immune evasion, hindering treatment effectiveness.

The CD33/CD3-bispecific T-cell engaging (BiTE®) antibody is designed to counteract these immune evasion tactics. By targeting both AML blasts and MDSCs, this construct aims to unleash the power of the immune system to effectively combat the disease. The potential to eliminate MDSCs could be a crucial factor in improving treatment outcomes and long-term survival rates for AML patients.

Looking Ahead: The Future of AML Treatment

The findings of this study offer a beacon of hope in the fight against AML. By targeting both cancer cells and the immune-suppressing MDSCs, the CD33/CD3-bispecific T-cell engaging (BiTE®) antibody could pave the way for a new era of more effective and durable treatments. Further research and clinical trials are essential to fully realize the potential of this innovative approach and to ultimately improve the lives of those affected by AML. The path forward may involve combining this new therapy with other treatments to help enhance its effects. There is also the possibility of using MDSC levels as a biomarker to better understand the effectiveness of this type of treatment.

About this Article -

This article was crafted using a human-AI hybrid and collaborative approach. AI assisted our team with initial drafting, research insights, identifying key questions, and image generation. Our human editors guided topic selection, defined the angle, structured the content, ensured factual accuracy and relevance, refined the tone, and conducted thorough editing to deliver helpful, high-quality information.See our About page for more information.

This article is based on research published under:

DOI-LINK: 10.1186/s40425-018-0432-9, Alternate LINK

Title: Cd33/Cd3-Bispecific T-Cell Engaging (Bite®) Antibody Construct Targets Monocytic Aml Myeloid-Derived Suppressor Cells

Subject: Cancer Research

Journal: Journal for ImmunoTherapy of Cancer

Publisher: BMJ

Authors: Regina Jitschin, Domenica Saul, Martina Braun, Sehmus Tohumeken, Simon Völkl, Roman Kischel, Michael Lutteropp, Cedric Dos Santos, Andreas Mackensen, Dimitrios Mougiakakos

Published: 2018-11-05

Everything You Need To Know

Why is there a need for new treatment strategies in Acute Myeloid Leukemia (AML)?

Despite advances in treatment, the 5-year survival rate for Acute Myeloid Leukemia (AML) remains low, hovering around 30%. This highlights the urgent need for innovative therapeutic approaches. One significant challenge is the ability of AML to evade the body's immune defenses, making it difficult to treat effectively. New treatments are being designed to target the mechanisms cancer uses to hide from the immune system.

What are Myeloid-Derived Suppressor Cells (MDSCs), and what role do they play in Acute Myeloid Leukemia (AML)?

Myeloid-Derived Suppressor Cells (MDSCs) are a type of immune cell that shares characteristics with both monocytes and granulocytes. In Acute Myeloid Leukemia (AML), MDSCs play a critical role in suppressing the immune system, creating a safe environment for cancer cells to thrive. They actively hinder the function of other immune cells, such as T-cells, preventing them from effectively targeting and destroying cancer cells. AML blasts induce the production of MDSCs, turning the body's defenses against itself.

How does the CD33/CD3-bispecific T-cell engaging (BiTE®) antibody work to combat Acute Myeloid Leukemia (AML)?

The CD33/CD3-bispecific T-cell engaging (BiTE®) antibody is designed to target and eliminate both Acute Myeloid Leukemia (AML) blasts (cancer cells) and Myeloid-Derived Suppressor Cells (MDSCs). This dual-action approach aims to directly kill cancer cells and dismantle the immune-suppressing environment that allows the disease to thrive. By engaging T-cells, this construct redirects them to attack and destroy the targeted cells.

What are the potential implications of targeting Myeloid-Derived Suppressor Cells (MDSCs) in Acute Myeloid Leukemia (AML) treatment?

Targeting Myeloid-Derived Suppressor Cells (MDSCs) in Acute Myeloid Leukemia (AML) treatment could significantly improve treatment outcomes and long-term survival rates. By eliminating MDSCs, the immune system can regain its ability to effectively fight the cancer. The elimination of MDSCs could be a crucial factor in improving treatment outcomes and long-term survival rates for Acute Myeloid Leukemia (AML) patients. Further research and clinical trials are essential to fully realize the potential of this innovative approach.

Beyond the CD33/CD3-bispecific T-cell engaging (BiTE®) antibody, what other avenues are being explored to improve Acute Myeloid Leukemia (AML) treatment?

Research is underway to explore combining the CD33/CD3-bispecific T-cell engaging (BiTE®) antibody with other treatments to enhance its effects. Additionally, there is potential in using Myeloid-Derived Suppressor Cell (MDSC) levels as a biomarker to better understand the effectiveness of treatments. Further avenues may explore treatments that interrupt the pathways that cause AML blasts to induce MDSC production.