According to the team, platelets could be one of the key players in the immune confusion that leads to bone marrow failure.

In everyday life, platelets help seal cuts and prevent bleeding. The team’s viewpoint at Xuanwu Hospital highlights that these tiny cells also release powerful chemical signals that communicate with the immune system in aplastic anaemia. One of these mediator proteins is PF4/CXCL4, which can influence how T-cells behave and their functions.

This matters because T-cells need a lot of energy to launch strong immune responses. When PF4 and other platelet signals push T-cells into overdrive, the result can be an excess of inflammatory molecules called cytokines. Mitochondrial energy metabolism also plays a crucial role in this process. Two of the most harmful cytokines are interferon-gamma and TNF-alpha, both of which can damage bone marrow.

What makes this theory especially exciting is that it reframes an assumption. In the past, low platelet counts in aplastic anaemia were seen simply as a consequence of bone marrow failure. This research team suggests the opposite may also be true: platelets could be involved much earlier, helping to set the destructive immune reaction in motion. If this is correct, future treatments might target platelet signals directly, not just the T-cells that cause the damage.

The team’s innovative paper has already attracted international attention, with more than 800 downloads shortly after publication and invitations for the researchers to present their findings at international academic conferences.

Part of what makes their work stand out is its potential to reshape how doctors think about treatment. Current therapies suppress the immune system or try to boost blood production, but they do not address platelet-driven signalling. By revealing platelets as active communicators in the immune network, Tan, Feng, Sun, and their colleagues provide a clearer picture of what might be going wrong in aplastic anaemia.

In their latest work, the team used single-cell sequencing in animal models of bone-marrow failure to map out which cells are involved and how they behave. This kind of detailed “cell landscape” could guide the development of more targeted, effective treatments in the future, especially those focused on how platelets and immune cells interact.