Monocytes, a special type of white blood cell, play an important role in the innate immune system and contribute to host defense in the blood by secreting large quantities of pro-inflammatory cytokines. Now, researchers at the University Hospital Bonn (UKB) and the University of Bonn have discovered that platelets, also known as thrombocytes, communicate with monocytes and increase their inflammatory capacity. These new findings may help to improve the treatment of immune disorders and associated diseases.

The new study is published in EMBO Molecular Medicine in an article titled, “Platelet transcription factors license the pro-inflammatory cytokine response of human monocytes.”

“In humans, blood Classical CD14+ monocytes contribute to host defense by secreting large amounts of pro-inflammatory cytokines. Their aberrant activity causes hyper-inflammation and life-threatening cytokine storms, while dysfunctional monocytes are associated with ‘immunoparalysis,’ a state of immune hypo responsiveness and reduced pro-inflammatory gene expression, predisposing individuals to opportunistic infections. Understanding how monocyte functions are regulated is critical to prevent these harmful outcomes. We reveal platelets’ vital role in the pro-inflammatory cytokine responses of human monocytes.”

Senior and corresponding author Bernardo Franklin, PhD, a professor from the Institute of Innate Immunity at the UKB and the Cluster of Excellence ImmunoSensation at the University of Bonn, and his research team had already identified platelets as an important regulator of inflammation. In their current study, the team discovered that a low platelet count in the rare blood disorder immune thrombocytopenia (ITP) or the artificial removal of platelets from healthy monocytes results in “immunoparalysis.”

The Bonn researchers discovered that the pro-inflammatory signals, including NF-κB and p38 MAPK, propagate from platelets to monocytes and maintain their inflammatory capacity. “Platelet vesicles as an extended arm of platelets control this intercellular communication,” said co-first author Lukas Rossnagel, a PhD student at the University of Bonn at the Institute of Innate Immunity of the UKB.

The results of the study point to a new intercellular communication mechanism in which platelets regulate monocyte function. “Clinically, this suggests potential therapeutic strategies to counteract monocyte immune paralysis in conditions such as ITP and other inflammatory diseases with the addition of platelets,” explained Franklin, who hopes that an understanding of platelet-monocyte interactions will lead to improved treatment of immune disorders and related diseases.