Accumulating evidence suggests that innate immunity interacts with the adaptive immune system to identify potentially harmful antigens and eliminate them from the host. A central facet of innate immunity is complement, which for some time has been recognized as a contributor to inflammation in transplant rejection but without detailed analysis of its role in what is principally a T cell mediated process. Moreover, epithelial and vascular tissues at local sites of inflammation secrete complement components; however, the role of such local synthesis remains unclear. Here we show that the absence of locally synthesized complement component C3 is capable of modulating the rejection of renal allografts in vivo and regulating T-cell responses in vivo and in vitro. The results indicate that improved success in kidney transplantation could come from therapeutic manipulation of innate immunity in concert with T cell directed immunosuppression.

Resistin is a small adipocyte-specific secretory hormone molecule. It has been associated with a number of cellular and metabolic processes. It has also been essentially implicated to have a vital role in the interplay between insulin resistance, obesity, and type II diabetes. Numerous clinical studies have demonstrated an association between many pathological illnesses with elevated serum resistin levels. It has also been shown to affect and modulate various molecular processes such as atherosclerosis, cancer cell metabolism, and inflammation. Periodontitis is a widespread inflammatory disease affecting human beings. Periapical periodontitis is an inflammatory disease that manifests as a sequela of untreated dental caries. Therefore, in this article, we summarize the divergent physiological roles played by resistin and its association with the mechanism of various pathologies. Moreover, current scientific studies discussing its association and role in common dental pathologies, periodontitis, and apical periodontitis are reviewed.