This brief overview is focused on the inherent duality of immune responses: on the one hand they may induce inflammation and precipitate injury, on the other, a number of examples of participation in organ and tissue repair is growing. These processes will be reviewed from the nephrological standpoint. Specifically, the role of different leukocyte subsets, innate immunity, nitric oxide production, and stem cells, among others, are presented.
Evolutionary view on regenerationTissue and organ regeneration in amphibians has for years attracted envious attention of mammalian biologists. Urodels (salamanders, newts) and larval anurans (frogs and toads) are capable of regenerating limbs, tails and other organs or tissues swiftly and scarlessly (1). Elements of such a regenerative prowess are detectable in cutaneous wound healing in embryos and early fetuses (2), but later on wounds heal with scars. Needless to say that scar formation in any organ including the kidney results in architectural distortion and functional compromise. This explains the search for molecular mechanisms of scarless healing of inflammatory lesions and in depth studies of fetal peculiarities of regeneration. It has been found that stimulated fetal fibroblasts produce less IL-6 and IL-8 than fibroblasts from adults, thus accounting for the reduced tissue infiltration by neutrophils and monocytes/macrophages (3). Interestingly, application of TGF-β to fetal wounds results in formation of scars upon wound healing, whereas inhibiting TGF-β formation or action in adult wounds reduces scarring (4,5). Among differences in the composition of the extracellular matrix in fetal wounds, the most prominent are the enrichment in hyaluronic acid and tenascin-C, capable of indirect reduction of activity of serine proteinases, cathepsin G, and inhibiting activation of T-cells and secretion of IL-2 (rev in 1). Collectively, these and other investigations shifted the focus from the relatively static studies into immunologic properties of inflammatory infiltrates toward a more dynamic description of mechanisms for resolution of inflammation.