A s bstract. Within any chronically inflamed tissue, there is an increased number of macrophages, pluripotential phagocytic cells that, while critical to host defenses, are also able to profoundly damage parenchymal structure and function. Because of their central role in the inflammatory response, considerable attention has been focused on the mechanisms resulting in an expansion of the macrophage population within an inflamed tissue. Although recruitment of precursor monocytes from the circulation into inflamed tissues clearly plays an important role in macrophage accumulation, it is also possible that replication of tissue macrophages contributes to the expansion of macrophage numbers in inflammation. Because of the accessibility of tissue macrophages with the technique of bronchoalveolar lavage, the lung provides an ideal opportunity to test this hypothesis in humans. To accomplish this, bronchoalveolar lavage was performed to obtain alveolar macrophages from normals (n = 5) and individuals with chronic lung inflammation (normal smokers [n = 5], idiopathic pulmonary fibrosis [n = 13], sarcoidosis [n = 18], and other chronic interstitial lung disorders [n = 1 1]). Alveolar macrophage replication was quantified by three independent methods: (a) DNA synthesis, assessed by autoradiographic analysis of macrophages cultured for 16 h in the presence of [3H]thymidine; (b) DNA content, assessed by flow cytometric analysis of macrophages fixed immediately after recovery from the lower respiratory tract; and (c) cell division, assessed by cluster formation in semisolid medium. While the proportion of replicating macrophages

Substantial evidence is now available that Peyer's patches (pp)l are a major source of precursors of IgA-secreting plasma cells (1-3). These cells are generated in PP by exposure to antigen-specific or nonspecific stimuli. They then exit the PP, migrate through mesenteric lymph nodes, the thoracic duct, and systemic circulation, and finally localize in secretory tissues, where they differentiate into IgA-producing plasma cells (3). There is also considerable evidence that the IgA-predominant antibody production by PP B cells in gut-associated lymphoid tissues (GALT) is controlled by immunoregulatory T cells, such as class-specific helper and suppressor T cells (4-7). More recently, the existence of another type of regulatory T cell in PP, a contrasuppressor-inducer T cell, has been demonstrated, which suggests that IgA production is also influenced by a contrasuppressor regulatory circuit (8). Thus, immunoregulation of the mucosal immune response appears to be quite complicated.As a new approach to the elucidation of the mechanisms governing IgA production in GALT we have studied the effect of cloned T cell lines on in vitro IgA synthesis. Accordingly, we have established concanavalin A (Con A)-induced cloned T cells from both murine PP and spleen and have determined the ability of these cells to regulate IgA immunoglobulin (Ig) synthesis and secretion by lipopolysaccharide (LPS)-driven PP B cells. In addition, we have analyzed the effect of co-cultured Con A-induced cloned T cells on the surface Ig (sIg) profile of PP and spleen B cells.The data obtained strongly suggest that in murine PP there is a special type of T cell that causes switching of sIgM-bearing B cells directly to sIgA-bearing B cells.

It is now well established that Peyer's patches (pp)l are lymphoid follicles that give rise to cells that are committed to IgA development and that ultimately localize in mucosal areas (1-5). However, the mechanisms governing such commitment are not completely understood. On the one hand, PP B cells and their clonal progeny could represent a class of B cells that secrete IgA, because they are exposed to a particular kind and pattern of specific (antigenic) and/or nonspecific (T cell and/or B cell) stimuli (6, 7); on the other hand, IgA B cells may develop in PP because PP contain Ig class-specific PP T cells that direct PP B cells along certain lines of differentiation (8, 9). Recently, we have provided additional evidence favoring the latter possibility, in that we have obtained T cell clones from PP which are capable of influencing PP B cell differentiation so that it follows a pathway that leads directly from IgM expression to IgA expression (10, 11). However, these IgA-specific T cells (switch T cells) cannot in themselves provide help for terminal differentiation of PP B cells since the effect of the switch T cells is to induce cells to become surface IgA-bearing B cells rather than plasma cells secreting IgA.Newer information regarding immunologic mechanisms governing B cell differentiation of all Ig classes are of relevance to IgA B cell differentiation. In this regard, there are extensive data which indicate that T cells or T cell-derived factors, and/or macrophages or macrophage-derived factors induced by specific and nonspecific stimuli can profoundly affect the proliferation and differentiation of T and/or B cells (12-26). These cells and the factors derived from these cells

The U.S. Consumer Product Safety Commission (CPSC) staff completed a series of investigations that estimated the potential exposure and risk of young children to arsenic while playing on playground equipment composed of CCA (chromated copper arsenate)-treated wood. Prior to sampling in-use field structures composed of CCA-treated wood, studies were undertaken to create a standard sampling protocol for quantifying arsenic migration from CCA-treated wood and to establish a correlation between the amount of chemical removed by a human hand and a cloth surrogate. These studies resulted in: 1) the development of an efficient extraction method for chemical residues collected on a human hand, 2) the development of a sampling device for consistent surrogate measurements, 3) establishment of a correlation between surrogate and hand measurements, and 4) the development of a standard human hand and surrogate sampling protocol for quantifying arsenic migration from CCA-treated wood. These studies also examined factors such as approaching a maximum hand load, effects of re-rubbing the same area of a board, and comparison of surrogate materials. The results from sampling CCA-treated wood with methods described in this article were later employed to obtain field data used in exposure and risk assessments.These videos were made several years ago by CPSC for a different issue concerning playground equipment.

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