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Several studies of human cancers have established that chronic and insidious inflammation promotes the process of carcinogenesis and exacerbates the growth of existing tumors. Conversely, acute inflammation seems to have the opposite effect. Recent discoveries indicate that this dualism in the role of inflammation in cancer is mirrored by the effects of the complement system on this disease process. Previous studies have suggested that complement proteins can contribute to the immune surveillance of malignant tumors. However, a very recent study has indicated that complement proteins can also promote tumor growth. Here, we describe our current understanding of the role of complement in tumor development and progression. [Copyright &y& Elsevier]

The convergence between complement and the clotting system extends far beyond the chemical nature of the complement and coagulation components, both of which form proteolytic cascades. Complement effectors directly enhance coagulation. These effects are supplemented by the interactions of complement with other inflammatory mediators that can increase the thrombogenicity of blood. In addition, complement inhibits anticoagulant factors. The crosstalk between complement and coagulation is also well illustrated by the ability of certain coagulation enzymes to activate complement components. Understanding the interplay between complement and coagulation has fundamental clinical implications in the context of diseases with an inflammatory pathogenesis, in which complement–coagulation interactions contribute to the development of life-threatening complications. Here, we review the interactions of the complement system with hemostasis and their roles in various diseases. [Copyright &y& Elsevier]

Abstract: The anatomic localization and unique vasculature of the liver, along with its cell properties, make this organ an efficient line of defense against blood-borne infections, either systemic or arising in the abdomen. Liver cells can modify the host immune response by releasing immunomodulatory molecules, interacting with cells of the immune system and acting as scavengers for inflammatory mediators. However, these defensive functions do not protect the liver itself from the severe injury that may be caused by pathogens, toxins or pollutant xenobiotics. Therefore, the mammalian liver has developed a unique adaptation in the form of an astonishing regenerative capability. The complexity of regeneration requires a well-orchestrated system to control this process. Growing evidence suggest the importance of immune mechanisms as a part of this system. It seems likely that the mechanisms that serve to eliminate infections (and may simultaneously cause liver injury) are also active in restoring the structural and functional integrity of the damaged liver. [Copyright &y& Elsevier]