Aged or senescent RBC form in our bloodstream approximately 120 days after they are produced in the bone marrow. Removal of these cells is critical for maintaining a constant number of RBC in the blood and avoiding potential problems they can cause like thrombosis. We have discovered a previously unrecognised physiological function for platelets in the removal of old or senescent RBC, whereby platelets recognise and bind senescent RBC in the circulation and produce platelet-red blood cell complexes (Ningtyas et al 2024 in press). These complexes target the destruction of old cells in the spleen via phagocytosis. We think platelets are therefore important for binding and clearing senescent RBC, and disruptions in platelet count or complex formation and clearance negatively affect RBC homeostasis. When this mechanism is disturbed by diseases such as thrombocytopenia and asplenia, older red cells and complexes remain in the circulation. This may explain why people with these conditions experience and elevated risk of thrombosis.

There are several new lines of enquiry and projects stemming from these findings:

What are the molecules on platelets and senescent red blood cells that drive complex formation?

How do platelets stimulate phagocytosis of red blood cells?

How do anti-thrombotic drugs affect P-RBC complex formation and clearance?

Like the fate of platelet-bound senescent red blood cells, does platelet binding to Plasmodium-infected cells drive their clearance from the bloodstream?

Image

Image

A platelet-erythrocyte complex viewed by scanning electron microscopy.

Related reading

Ningtyas, D.C., et al., Platelets mediate the clearance of senescent red blood cells by forming pro-phagocytic platelet-cell complexes. Blood, 2024 143(6):535-547.

Vautrinot, J. and A.W. Poole. Platelets tell old red cells to clear off. Blood 2024 143(6) 480-481.