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Milka Koupenova: The Role of Platelet RIG-I in Regulating Thrombotic Responses
Nov 12, 2026, 22:52

Milka Koupenova: The Role of Platelet RIG-I in Regulating Thrombotic Responses

Milka Koupenova, Assistant Professor at University of Massachusetts Medical School, shared a post on LinkedIn about a recent article she and her colleagues co-authored, published in Blood, adding:

“Excited to share our latest publication in Blood:

‘The Pathogen Recognition Receptor RIG-I is Functional in Platelets and Limits Thrombotic Responses’ work by my first PhD student Anthony Sciaudone:

Heartfelt thank you to all of our co-authors, the reviewers, and the editor!

Our major findings:

  1. Platelets have functional cytoplasmic RIG-I receptors and downstream signaling.
  2. RIG-I activates a non-classical pathway in platelets: RIG-I signals through MAVS to promote MLKL phosphorylation, oligomerization, and membrane punctures, without uniform α- or δ-granule release or canonical interferon signaling.
  3. RIG-I promotes S100A10 surface translocation and release: RIG-I activation promotes S100A10 surface localization and release, but not S100A8/A9; S100A10 is a S100 that promotes an S100 family protein that facilitates plasmin generation from plasminogen in the presence of uPA or tPA.
  4. RIG-I activation changes the thrombus architecture: Thrombi formed by RIG-I-activated platelets contain otherwise unchanged platelets with membrane punctures.
  5. RIG-I activation reduces platelet aggregation in the presence of plasminogen and facilitates uPA-dependent disaggregation.
  6. In vivo, at the time points when RIG-I expression is highest following infection, disruption of RIG-I/MAVS signaling increases thrombotic burden during mild influenza infection and alters the temporal pattern of leukocyte presence in lung tissue.

Importantly, many viruses encode mechanisms that inhibit RIG-I activation and signaling.

Our conclusion:

Platelets do more than promote thrombosis during infection. Through RIG-I/MAVS signaling, they sense viral RNA and engage non-classical activation mechanisms that limit thrombotic responses and contribute to the regulation of leukocyte transmigration.”

Title: The Pathogen Recognition Receptor RIG-I is Functional in Platelets and Limits Thrombotic Responses

Authors: Anthony R. Sciaudone, Michael L. Jameson, Heather Learnard, Heather Corkrey, Antonina Risitano, Mark Kelly, Timothy P. Fitzgibbons, Sara E. Cahill, Evelyn A. Kurt-Jones, Jane E. Freedman, Fiachra Humphries, Kahraman Tanriverdi, Jennifer P. Wang, Milka Koupenova

Milka Koupenova

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