Macrophage procoagulants.
From the preceding exposition it is now clear that the regulation of monocyte/macrophage PCA is dependent upon a complex network of interacting pathways, some of which amplify the response of the monocyte/macrophage, while others inhibit. In all probability many more will emerge. The construct illustrated in Figure 3, therefore, is a simplified view of the two major stimulatory pathways: the T cell-dependent pathway, activated by immune recognition and mediated by lymphokine(s); and the T cell-independent pathway, activated by direct perturbation of monocytes by such stimuli as LPS. At least 2 or 3 different PCAs can be expressed by monocyte/macrophages from different species, depending upon the anatomic site of the origin of the cell and the types of stimuli imposed. Inhibition of PCA expression is accomplished by at least one set of regulatory lipoproteins, and other inhibitory loops may be found. The result of these multiple interactions is the deposition of fibrin on the cell surface or in the surrounding milieu. It is our belief that this close relationship between coagulation reactions and inflammatory reactions, resulting in fibrin deposition, represents a fundamental host defense designed to delimit the inflammatory response. Nevertheless, the precise role of monocyte procoagulants in vivo remains unclear. A number of potential mechanisms exist for activation of coagulation in both inflammatory and neoplastic disorders, and the finding of enhanced monocyte procoagulant activity by no means establishes its importance in physiologic or, pathosphysiologic responses in vivo. Further studies, possibly with agents capable of specific inhibition of monocyte procoagulants in vivo, will be necessary to define the precise importance of these procoagulants in clinical disorders.
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D000941:Antigens / Q000502:physiology; D001777:Blood Coagulation / Q000187:drug effects; D001779:Blood Coagulation Factors / Q000096:biosynthesis / Q000494:pharmacology / Q000502:physiology*; D002460:Cell Line; D005165:Factor V / Q000502:physiology; D005167:Factor VII / Q000502:physiology; D005170:Factor X / Q000502:physiology; D015951:Factor Xa; D005337:Fibrin / Q000378:metabolism; D005338:Fibrin Fibrinogen Degradation Products / Q000378:metabolism; D006168:Guinea Pigs; D006801:Humans; D006968:Hypersensitivity, Delayed / Q000503:physiopathology; D007153:Immunologic Deficiency Syndromes / Q000097:blood; D007239:Infections / Q000097:blood; D007249:Inflammation / Q000503:physiopathology; D008070:Lipopolysaccharides / Q000494:pharmacology; D008264:Macrophages / Q000502:physiology*; D051379:Mice; D009000:Monocytes / Q000187:drug effects / Q000378:metabolism / Q000502:physiology; D009369:Neoplasms / Q000097:blood; D009504:Neutrophils / Q000378:metabolism / Q000502:physiology; D011817:Rabbits; D051381:Rats; D013601:T-Lymphocytes / Q000502:physiology; D013923:Thromboembolism / Q000097:blood; D013925:Thromboplastin / Q000502:physiology; D014859:Warfarin / Q000494:pharmacology
D000893:Anti-Inflammatory Agents; D000941:Antigens; D001779:Blood Coagulation Factors; D005338:Fibrin Fibrinogen Degradation Products; D008070:Lipopolysaccharides; C045071:leukocyte procoagulant activity; C045072:macrophage procoagulant activity; C022475:prothrombinase complex; D014859:Warfarin; D005165:Factor V; D005167:Factor VII; D005170:Factor X; D005337:Fibrin; D013925:Thromboplastin; D015951:Factor Xa