Recent advances in the understanding of the way that immune system cells operate and how cancer could potentially be prevented are giving doctors and patients fresh hope. The protein CD11b has shown promise in recent trials and could be the key to improving patient outcomes and reducing the impact cancer has on the body. The answer lies in myeloid cells and how they are impacted by cancerous cells – and how that process can be disrupted.
What are Myeloid Cells and Why do They Matter?
Myeloid cells are part of the immune system; according to the National Institutes of Health, myeloid cells are found in the blood and attack dangerous pathogens. These cells are part of the immune system, and when they work properly, they fight illness and infection. These are white blood cells, and when they function normally, they attack cancerous cells and prevent their development. Myeloid cells don’t always do their job properly, though.
When cancerous tumors or cells develop, though, those beneficial myeloid cells can be tricked into seeing the cancer as a beneficial entity – and end up contributing to the growth and wellbeing of the cancer, instead of working to eradicate it. Instead of seeing the cancer as an invading, unwelcome presence that should trigger an immediate response, the myeloid cells are tricked into ignoring the cancer, or worse, helping it grow.
CD11b and Myeloid Cells
Recent research shows that by disrupting the way that cancerous cells interact with myeloid cells could disrupt this process. CD11b has shown promise in disrupting the process and limiting cancer’s ability to trick myeloid cells into boosting its own growth or ignoring it entirely.
The latest research comes from the Department of Internal Medicine at Rush Medical College and focuses on the way that integrins like CD11b can impact the way that a myeloid responds to cancer. Integrins are proteins that regulate a wide range of biological and growth processes; CD11b is an integrin that normally improves myeloid cell migration and the way that these powerful immune system cells fend off illness and infection.
Increasing CD11b Activity Impacts Cancer Growth
Researchers found that this particular protein encourages myeloid cells to develop into a specific type, dubbed the M1 macrophage, which works to suppress cancerous tumor growth. This suppression comes at a cost, though; the tumors work to suppress CD11b involvement, often triggering the development of M2 macrophage. The M2 macrophage ward off the beneficial T cells the body needs to fight off disease and can end up actually feeding developing cancer cells.
The research team focused on modifying CD11b to ensure that beneficial M1 macrophage activity were increased, but that M2 type cells were not activate. Mice were used for testing, and the team found that altering mice to increase CD11b worked to reduce tumor growth, while mice that were not treated to increased CD11b activity had a much larger tumor growth rate.
Based on their testing, researchers found that when left alone, myeloid cells could be recruited and used by cancer to promote growth, but when the right amount of CD11b was applied, those cells would convert to the beneficial M1 versions that actively fight cancer growth. The team conducted further experiments to discover that CD11b could be strategically deployed to target only cancer cells; this would prevent the development of far less beneficial M2 macrophage versions that could cause harm.
The latest research suggests that a more comprehensive understanding of myeloid and how they interact with cancer cells — and how integrin proteins like CD11b can impact the growth rate of cancerous tumors — is needed. This understanding could be an important step in the fight against cancer and could reveal how to prevent the body’s own immune system to contributing to the growth of cancerous cells.
This research could lead to new and novel approaches in the fight against cancer using the immune system and by manipulating the body’s own cells to combat tumors and disease.