Cancer is crafty, using a wide range of insidious tricks to ensure it can survive and spread in the body. But now researchers at Rush University and the University of California, San Diego have found a way to intervene in one of these schemes, preventing tumors from recruiting immune cells to help them grow and metastasize.
Myeloid cells are a type of white blood cell that patrols the body looking for pathogens, but there are actually two sub-types of them. The M1 macrophage has been found to suppress tumor growth, while M2s do the opposite – they fight off helpful T cells (the foot soldiers of the immune system) and actively help cancer grow and spread.
The new study uncovered a vital clue to what makes myeloid cells become one macrophage or the other. It turns out that the key is a protein called CD11b that is found on the surface of myeloid cells. When CD11b activity goes up, the number of M1 myeloid cells also increases, while low CD11b causes more M2 cells to develop. To take advantage of this, tumors actively suppress the protein to create more M2 cells and therefore boost their own growth.
With that mechanism uncovered, the researchers then experimented to see if CD11b could be a potential target for cancer treatment. They engineered mice that completely lacked the protein then transplanted tumors into them, and found that those tumors grew much bigger than tumors in control-group mice.
Next, the team tried the inverse. They gave normal mice a molecule called Leukadherin-1 (LA-1), which boosts the function of CD11b, and found that tumors shrank significantly. And finally, to make doubly sure that this protein was the right target, they engineered a mouse that had CD11b active all the time, instead of just sporadically like normal mice. Their tumors also shrank drastically.
The researchers say these results indicate that CD11b is a promising target for new cancer immunotherapy techniques. It will still be a number of years before it may be available as an option for human patients, but the team plans to continue working on it.
The research was published in the journal Nature Communications.
Source: Rush University