Both acute and chronic inflammatory diseases, including autoimmune diseases, allergies, and infections, promote dysregulation of haemostasis, leading to immunothrombosis. Inflammatory mediators such as enhanced pathogenic immune cell populations, increased proinflammatory cytokines and chemokines levels, and diminished tolerogenic Treg cell responses coincide with and promote aberrant coagulation. This enhanced procoagulant state feeds back to amplify inflammation, inducing further expansion of proinflammatory immune cells, enhanced TF expression in myeloid cells, NET production and inhibition of tolerogenic Treg responses that impair thrombolysis and clot resolution.