A new research paper was published in Volume 16 of Oncotarget, titled “A novel anti-human CD25 mAb with preferential reactivity to activated T regulatory cells depletes them from the tumour microenvironment.”

In this study, researchers from the National Institute of Allergy and Infectious Diseases, led by first author Maja Buszko and corresponding author Ethan M. Shevach, discovered a new monoclonal antibody that selectively targets a subset of immune cells called regulatory T cells (Tregs).

These cells, while normally important for preventing autoimmunity, also can block the body’s ability to fight cancer by suppressing anti-tumour immune responses.

This discovery could lead to novel cancer therapies that strengthen the immune system’s capacity to attack tumours.

The researchers identified an anti-CD25 monoclonal antibody with several atypical properties and named it 2B010.

To evaluate its effects, they used humanised mice, laboratory mice that are engineered to carry human immune cells, to closely mimic how human immune systems respond to cancer.

The treatment of these mouse models with 2B010 significantly decreased the number of Tregs in tumours and boosted the activity of CD8+ T cells, which are essential for killing cancer cells.

Importantly, 2B010 worked without disrupting other key immune functions.

Unlike traditional Anti-CD25 antibodies, it did not interfere with interleukin-2 (IL-2) signalling, which is essential for the growth and activity of effector T cells that fight cancer.

“2B010 also had no effect on IL-2 induced STAT5 phosphorylation or CD4⁺ T cell proliferation in vitro while both were blocked by Clone D1 further supporting the view that 2B010 does not recognise the IL-2 binding site.”

This finding is especially significant because high levels of Tregs in tumours are associated with poor outcomes in many cancers.

By specifically removing these cells, 2B010 may help overcome one of the main barriers to current immunotherapy approaches.

Its ability to preserve IL-2 signalling could also make it safer and more effective when used alone or in combination with existing therapies such as immune checkpoint inhibitors.

While the 2B010 antibody showed strong effects in reducing Tregs and boosting immune cell activity, the study did not observe changes in tumour size in these models.

Researchers suggest this may be due to limitations in the preclinical systems used, such as the lack of tumour-specific T cells in humanised mice.

Nevertheless, these findings demonstrate that 2B010 has a unique mechanism of action that could complement other cancer immunotherapies in future clinical trials.

In conclusion, the development of 2B010 is a promising step toward selectively disrupting the immune suppressive environment in tumours.

As researchers continue to refine and test this antibody, it could become a powerful tool for enhancing the effectiveness of cancer treatments and improving outcomes for patients.

Source: Impact Journals LLC