Home » Health » Title: Hormone Disrupts Immune Response, Offers New Cancer Treatment Target

Title: Hormone Disrupts Immune Response, Offers New Cancer Treatment Target

by Dr. Michael Lee – Health Editor

“Cuddle Hormone” Oxytocin Linked to Immune Suppression in Cancer, New study Reveals

BOSTON, MA – A newly published study in Nature Immunology details how cancer cells may exploit the hormone oxytocin – often dubbed the “cuddle hormone” – to suppress the immune system and⁣ evade treatment.⁢ Researchers⁣ have identified a pathway involving the hormone, the SCG2 receptor, and the LILRB4 receptor on myeloid cells that ultimately hinders the body’s ability to fight tumors.

The research team, led by Zhang, found that receptors on⁣ myeloid cells are stimulated by ‍oxytocin, leading to immune suppression. “Our study suggests that⁣ receptors on these myeloid cells get stimulated by this hormone and end up suppressing the ​immune system,” Zhang stated.

This discovery opens potential new avenues for cancer treatment.Blocking LILRB4 coudl improve patient response to existing therapies, and ⁣researchers suggest testing LILRB4 blockers in combination with checkpoint drugs.Early‍ evidence supports this approach; studies in multiple myeloma have shown that blocking LILRB4 slowed disease progression in laboratory ​and animal models.

The pathway also relies on STAT3, a key regulator within these suppressive cells. A 2025 review highlighted STAT3’s role in promoting ​the growth of these cells and inhibiting T-cells, suggesting a combined LILRB4 and STAT3-focused drug approach could be beneficial.

Conversely, researchers are also exploring the ‍potential of carefully administering SCG2 to calm overactive inflammation in certain conditions, as it can ⁣quiet myeloid‍ cells.

Several key questions remain. Researchers are working to develop reliable tests to measure SCG2 levels‍ and LILRB4 activity in blood and tumor tissue to identify ‍patients moast likely to benefit from these therapies. Safety concerns regarding potential infections due to immune suppression with LILRB4 blocking will be closely monitored in early trials. The possibility of tumors adapting and utilizing option signaling‍ pathways is also being investigated, emphasizing the potential need for combination ‍therapies. Determining which patients would be best suited for LILRB4 blockers, based on SCG2-to-LILRB4 pathway activity within their tumors, is a priority.

future research will focus on:

* ‌developing reliable tests for SCG2 levels and LILRB4 activity.
* Conducting clinical trials combining LILRB4 ‌blockers‍ with checkpoint therapy.
* Mapping this pathway across different cancers and tracking its activity over time.
* Investigating the therapeutic potential of carefully ‌administered SCG2 for inflammatory conditions.

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