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<jats:p> DNA–(cytosine-5) methyltransferase (MCMT) methylates newly replicated mammalian DNA, but the factors regulating this activity are unknown. Here, MCMT is shown to bind proliferating cell nuclear antigen (PCNA), an auxiliary factor for DNA replication and repair. Binding of PCNA requires amino acids 163 to 174 of MCMT, occurs in intact cells at foci of newly replicated DNA, and does not alter MCMT activity. A peptide derived from the cell cycle regulator p21 <jats:sup>WAF1</jats:sup> can disrupt the MCMT-PCNA interaction, which suggests that p21 <jats:sup>WAF1</jats:sup> may regulate methylation by blocking access of MCMT to PCNA. MCMT and p21 <jats:sup>WAF1</jats:sup> may be linked in a regulatory pathway, because the extents of their expression are inversely related in both SV40-transformed and nontransformed cells. </jats:p>

<jats:p>The upper cervical corticospinal tract was transected on one side in adult rats. A suspension of ensheathing cells cultured from adult rat olfactory bulb was injected into the lesion site. This induced unbranched, elongative growth of the cut corticospinal axons. The axons grew through the transplant and continued to regenerate into the denervated caudal host tract. Rats with complete transections and no transplanted cells did not use the forepaw on the lesioned side for directed reaching. Rats in which the transplanted cells had formed a continuous bridge across the lesion exhibited directed forepaw reaching on the lesioned side.*</jats:p>

<jats:p> To determine which proteinases are responsible for the lung destruction characteristic of pulmonary emphysema, macrophage elastase–deficient (MME <jats:sup>−/−</jats:sup> ) mice were subjected to cigarette smoke. In contrast to wild-type mice, MME <jats:sup>−</jats:sup> <jats:sup>/</jats:sup> <jats:sup>−</jats:sup> mice did not have increased numbers of macrophages in their lungs and did not develop emphysema in response to long-term exposure to cigarette smoke. Smoke-exposed MME <jats:sup>−</jats:sup> <jats:sup>/</jats:sup> <jats:sup>−</jats:sup> mice that received monthly intratracheal instillations of monocyte chemoattractant protein–1 showed accumulation of alveolar macrophages but did not develop air space enlargement. Thus, macrophage elastase is probably sufficient for the development of emphysema that results from chronic inhalation of cigarette smoke. </jats:p>

<jats:p> There is growing evidence that T helper cell subsets (T <jats:sub>H</jats:sub> 1 and T <jats:sub>H</jats:sub> 2) can be differentially recruited to promote different types of inflammatory reactions. Murine T <jats:sub>H</jats:sub> 1 but not T <jats:sub>H</jats:sub> 2 cells are recruited through P- and E-selectin into inflamed tissues, where they induce delayed-type hypersensitivity reactions. The human eotaxin-receptor CCR3, originally described on eosinophils and basophils, was also found to be expressed by T <jats:sub>H</jats:sub> 2 cells. An antibody to CCR3 was used to isolate T cells from peripheral blood that give rise to T <jats:sub>H</jats:sub> 2-polarized cell lines and to identify T <jats:sub>H</jats:sub> 2 cells derived from naı̈ve T cells in vitro. Eotaxin stimulated increases in intracellular calcium and chemotaxis of CCR3 <jats:sup>+</jats:sup> T cells. The attraction of T <jats:sub>H</jats:sub> 2 cells by eotaxin could represent a key mechanism in allergic reactions, because it promotes the allergen-driven production of interleukin-4 and interleukin-5 necessary to activate basophils and eosinophils. </jats:p>

<jats:p> A selection strategy was devised to identify bacterial genes preferentially expressed when a bacterium associates with its host cell. Fourteen <jats:italic>Salmonella typhimurium</jats:italic> genes, which were under the control of at least four independent regulatory circuits, were identified to be selectively induced in host macrophages. Four genes encode virulence factors, including a component of a type III secretory apparatus. This selection methodology should be generally applicable to the identification of genes from pathogenic organisms that are induced upon association with host cells or tissues. </jats:p>