SUMMARY FtsZ, a bacterial homolog of tubulin, is well established as forming the cytoskeletal framework for the cytokinetic ring. Recent work has shown that purified FtsZ, in the absence of any other division proteins, can assemble Z rings when incorporated inside tubular liposomes. Moreover, these artificial Z rings can generate a constriction force, demonstrating that FtsZ is its own force generator. Here we review light microscope observations of how Z rings assemble in bacteria. Assembly begins with long-pitch helices that condense into the Z ring. Once formed, the Z ring can transition to short-pitch helices that are suggestive of its structure. FtsZ assembles in vitro into short protofilaments that are ∼30 subunits long. We present models for how these protofilaments might be further assembled into the Z ring. We discuss recent experiments on assembly dynamics of FtsZ in vitro, with particular attention to how two regulatory proteins, SulA and MinC, inhibit assembly. Recent efforts to develop antibacterial drugs that target FtsZ are reviewed. Finally, we discuss evidence of how FtsZ generates a constriction force: by protofilament bending into a curved conformation.

The recent discovery of CD4 + T cells characterized by secretion of interleukin (IL)-17 (T H 17 cells) and the naturally occurring regulatory FOXP3 + CD4 T cell (nT reg ) has had a major impact on our understanding of immune processes not readily explained by the T H 1/T H 2 paradigm. T H 17 and nT reg cells have been implicated in the pathogenesis of human autoimmune diseases, including multiple sclerosis, rheumatoid arthritis, inflammatory bowel disease and psoriasis 1,2 . Our recent data and the work of others demonstrated that transforming growth factor-β (TGF-β) and IL-6 are responsible for the differentiation of naive mouse T cells into T H 17 cells, and it has been proposed that IL-23 may have a critical role in stabilization of the T H 17 phenotype [3][4][5] . A second pathway has been discovered in which a combination of TGF-β and IL-21 is capable of inducing differentiation of mouse T H 17 cells in the absence of ). However, TGF-β and IL-6 are not capable of differentiating human T H 17 cells 2,9 and it has been suggested that TGF-β may in fact suppress the generation of human T H 17 cells 10 . Instead, it has been recently shown that the cytokines IL-1β, IL-6 and IL-23 are capable of driving IL-17 secretion in short-term CD4 + T cell lines isolated from human peripheral blood 11 , although the factors required for differentiation of naive human CD4 to T H 17 cells are still unknown. Here we confirm that whereas IL-1β and IL-6 induce IL-17A secretion from human central memory CD4 + T cells, TGF-β and IL-21 uniquely promote the differentiation of human naive CD4 + T cells into T H 17 cells accompanied by expression of the transcription factor RORC2. These data will allow the investigation of this new population of T H 17 cells in human inflammatory disease.To better understand regulation of IL-17A secretion from human CD4 + T cells, we used a strategy that would allow us to evaluate the effects of various combinations of cytokine on expansion of T H 17 cells from memory T cells versus differentiation of naive CD4 + lymphocytes into T H 17 cells. Specifically, we used high-speed flow cytometry for sorting these two distinct populations of CD4 + T cells from the peripheral blood of healthy subjects: CD4 + CD25 − CD62L + CD45RA hi cells highly enriched for naive T cells and CD4 + CD25 − CD62L + CD45RA − cells enriched for central memory T cells (T CM ; Fig. 1a). All cells enriched for a naive or a central memory phenotype expressed the chemokine receptor CCR7 (data not shown). These two T cell populations were then stimulated with plate-bound