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EHA 2026 | Immune dysregulation in ITP and warm AIHA
Alessandro Lucchesi, MD, Istituto Scientifico Romagnolo per lo Studio e la Cura dei Tumori (IRST) IRCCS, Meldola, Italy, discusses the role of chronic inflammation and immune dysregulation in immune thrombocytopenia (ITP) and warm autoimmune hemolytic anemia (wAIHA). He highlights emerging therapeutic strategies targeting the inflammasome, BTK, and SYK pathways, and explains how these agents may improve outcomes beyond conventional antibody-directed therapies. This interview took place at the 31st Congress of the European Hematology Association (EHA) in Stockholm, Sweden.
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Transcript
Well, this is an important question and it’s very complex because we discovered that in the pathophysiology of both ITP and ITP and AIHA, not only are the disorders characterized by the presence of antibodies, circulating antibodies, but they are characterized by chronic inflammation. And chronic inflammation is probably what drives some of the clinical features of the two disorders. For example, fatigue, for example, thrombosis...
Well, this is an important question and it’s very complex because we discovered that in the pathophysiology of both ITP and ITP and AIHA, not only are the disorders characterized by the presence of antibodies, circulating antibodies, but they are characterized by chronic inflammation. And chronic inflammation is probably what drives some of the clinical features of the two disorders. For example, fatigue, for example, thrombosis. These elements cannot be explained by auto-antibodies, but they should depend on chronic inflammation. Chronic inflammation is driven by the innate immunity and from the inflammasome. The inflammasome at the end can eventually cause immune dysregulation by increasing TH17 and decreasing Tregs. So the disease becomes chronic and the inflammation drives autoimmunity and makes the patient not responding to many of the commonly used agents in ITP and AIHA. So there are new agents that are able to modulate the activity of the inflammasome, acting on BTK inhibition and SYK inhibition. SYK is a little bit upstream. BTK is at the crossroad between many downstream pathways so the use of these agents in monotherapy but also in the future probably in combination could be beneficial for our patients.
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