Journal of the Reticuloendothelial Society最新文献

Purified rat plasma fibronectin (Fn) was studied for its ability to influence nonspecific lymphocyte transformation to various mitogens. Fn added to lymph node cells (LNC) stimulated with phytohemagglutinin (PHA), concanavalin A (Con A), or bacterial lipopolysaccharide (LPS) resulted in a noncytotoxic dose-dependent inhibition of the blastogenic response. Effective inhibition (greater than 50%) of LNC responses to PHA and LPS occurred with concentrations of Fn that ranged from 10-50 micrograms/culture. The proliferative response to Con A was less affected by the presence of Fn: 50% inhibition was observed only with the highest concentration of Fn studied. Fn at low concentrations was more effective than Fn-depleted plasma in inhibiting lymphocyte responses to PHA. Optimal expression of the regulatory activity of Fn occurs during and following the peak proliferative period for both PHA and LPS responses. In order to evoke maximum inhibition it is necessary for Fn to be present within 12 hours following stimulation of LNC with mitogen. Inhibition does not appear to be the result of Fn-mitogen complexes which reduce the amount of mitogen available for stimulation, since increasing concentrations of either PHA or LPS did not significantly reduce the inhibitory effect. Furthermore, inhibition was not influenced by the concentration of fetal calf serum present in the culture medium. Thus, Fn may function as an important nonspecific immunoregulatory factor at inflammatory sites and in areas of tissue repair.

FMC-17a monoclonal antibody reactive with peripheral blood monocytes was used to identify cells of monocyte origin in sections of normal and inflamed human tissues. FMC-17 + ve cells were found in all samples tested. The distribution, HLA-DR staining characteristics, and enzyme profiles (ACP and ATPase) of FMC-17 + ve cells indicated that interdigitating (dendritic) cells, Langerhans cells, tissue histiocytes, and the classical inflammatory phagocytic macrophages belonged to the reactive population. The antigen recognized by this antibody was found on monocytic and promonocytic cells in bone marrow, yet appeared to be lost following activation in the later stages of inflammatory conditions. Further studies are necessary to elucidate at what stage in the differentiation/maturation pathway the antigen is acquired and again whether or not FMC-17--ve cells are an activated or degenerating population.

Acid-acting (pH 6-7) (presumably lysosomal) ribonuclease and neutral-acting (pH 7-8) calcium-dependent phospholipase A2 (presumably the enzyme releasing arachidonic acid from membrane phospholipids) were demonstrated by the peroxidase-antiperoxidase (PAP) immunocytochemical technique in rabbit professional phagocytes: pulmonary alveolar macrophages (AM), oil-induced peritoneal exudate macrophages (M phi) and glycogen-induced peritoneal exudate polymorphonuclear granulocytes (PMN). All three cell types stained positively with antisera to purified rabbit lung RNase and purified rabbit granulocyte phospholipase A2. The RNase and phospholipase A2 were also demonstrated by the PAP technique in the activated macrophages and granulocytes present in tissue sections of tuberculous (BCG) lesions. The intensity of staining of these two enzymes in individual macrophages did not change appreciably as the BCG lesions developed and regressed, but there were more macrophages rich in both enzymes when the lesions reached their peak size at 21 days. When the anti-RNase serum was fractionated by immunoabsorbent chromatography, the anti-delta RNase serum fraction stained exudate M phi and PMN better than AM; and the anti-beta RNase fraction stained AM better than M phi and PMN. Similar to isolated phagocytes, tissue granulocytes stained best with the anti-delta fraction; and activated tissue macrophages stained best with the anti-beta fraction. Thus, macrophages and granulocytes contain two types of RNase, beta and delta; and the beta RNase is associated with macrophage activation.

Metallophilic cells, which had dendritic morphology in vivo, were localized almost exclusively in the cortico-medullary zone of the control rat thymus. The patterns of thymic regeneration after a single (300 mg/kg) or consecutive injections (5 X 60 mg/kg) of Cyclophosphamide were well correlated with the changes in the number and topographical distribution of the metallophilic cell population. The specific staining with aldehyde fuchsin of metallophilic cells diffusely distributed throughout the cortex during the regeneration clearly demonstrated that these cells were identical with aldehyde fuchsin-positive metallophilic cells in the cortico-medullary zone of the normal rat thymus. The results presented suggest that metallophilic cells play some role in the process of normal thymocytopoiesis and represent a hitherto undescribed component of the thymic microenvironment.

Effects of a metastatic and nonmetastatic tumor on radiocolloid localization in regional lymph nodes in the rat were studied in order to examine further the hypothesis that suppression of radiocolloid uptake results from inhibition of macrophage phagocytic function by tumor products. On the basis of data obtained in the present model using homogenates of autologous spleen and two weakly immunogenic tumors introduced into the foot pad of rats, it is proposed that decreased radiocolloid uptake induced by a regional neoplasm may result from proliferation of nonphagocytic cellular elements within the regional lymph nodes and alterations in the cell population at the site of radiocolloid injection, which impede the transport of interstitially administered radiocolloid and its access to phagocytic macrophages, within primary and secondary regional lymph nodes. In its inception, therefore, suppression of radiocolloid uptake is not unique to neoplasia and may not directly reflect altered phagocytosis.

We examined the involvement of the T cell recognition system in hepatic granuloma formation in nude mice infected with Mycobacterium bovis BCG and subsequently injected with spleen cells. After syngeneic spleen cell transfer, granuloma was seen in nude mouse strains of several different genetic backgrounds. When allogeneic spleen cells were transferred, only those from mice that were H-2 I-region compatible with the recipients induced granuloma formation. Adoptive transfer of BCG-immunized spleen cells to splenectomized BCG-infected nude mice also showed H-2 K-end restriction. The effect of graft-versus-host (GVH) reaction on the generation of immune T cells was examined by time course observations after transfer of H-2-compatible and -incompatible allogeneic spleen cells and by cotransferring allogeneic and syngeneic spleen cells. Under these conditions, H-2-compatible sensitized T cells were generated. The fate of completely allogeneic T cells in nude mice was examined by double transfer experiments. Allogeneic spleen cells were recovered 3, but not 8 or more, days after the transfer.

This study describes the morphological and immunocytochemical aspects of the spleen in rabbits with experimentally induced chronic serum sickness. Thirty-seven rabbits were immunized with daily injections of bovine serum albumin (BSA) and six served as non-immunized controls. The most significant lesions were found in rabbits with chronic serum sickness induced by high doses of BSA. The spleens were increased in size and in weight. Granular deposits of BSA, rabbit IgG and C3, presumably immune complexes (IC), were found in the basement membranes of the venous sinuses and of the capillaries in the marginal zone, in the walls of splenic arterioles and, occasionally, between the macrophages in the splenic cords and lymphoid cells in lymphatic follicles. An increased number of degranulated polymorphonuclear leukocytes, macrophages and giant cells, degenerative changes of dendritic cells and, in some instances, splenic fibrosis were also seen. These splenic lesions developed when the concentration of BSA-antibodies in the sera decreased. The spleens of rabbits receiving high doses of BSA in a stage between acute and chronic serum sickness were also increased in size and in weight. The red pulp was enlarged, and immune deposits were observed within macrophages but not in splenic structures. The spleens of non-responder rabbits had a slight decrease in number of lymphatic follicles and germinal centers only. The spleens of non-immunized rabbits were consistently normal. The results indicate that in rabbits receiving multiple injections of high doses of BSA, chronic serum sickness is associated with splenomegaly and IC-splenitis and that these lesions occur when the level of circulating BSA antibody declines. IC-splenitis could impair the clearance of IC and influence the immune function of the spleen. These findings could have implications in the pathogenesis of splenomegaly and of defective splenic function in human IC-mediated diseases.

The acridine orange technique was used to explore phagosome-lysosome fusion (P-L fusion) in thioglycollate-elicited rat peritoneal macrophages. Sheep red blood cells were coated with IgG or IgM plus complement, or treated with neuraminidase, tannic acid or glutaraldehyde; then both their capacity to be ingested by macrophages and their ability to induce P-L fusion after ingestion were assayed. Their capacity to be engulfed by macrophages was similar, but glutaraldehyde-treated erythrocytes were far more efficient than the other particles in triggering P-L fusion. Hence, both processes must be driven by different mechanisms. No correlation was found between the surface charge of test particles (as assayed by cell electrophoresis) and their ability to trigger phagocytosis or P-L fusion. However, glutaraldehyde-treated erythrocytes were found to be more hydrophobic than the other particles, as previously reported. Hence, particle hydrophobicity might favor P-L fusion. The implication of these findings are discussed.

The cAMP receptor protein and cAMP-dependent protein kinase activity in rabbit peritoneal neutrophils have been identified. The cAMP receptor protein in either the plasma membrane or cytosol fractions, identified by photoaffinity labeling with 8-N3-[32P]cAMP, has an apparent molecular weight of 54,000. The cytosol and membrane receptor proteins have apparent dissociation constants for 8-N3-[32P]cAMP of 0.20 microM and 0.06 microM, respectively. The molecular weight and dissociation constant for 8-N3-[32P]cAMP of this cAMP receptor protein are similar to what has been known for RII, the regulatory subunit of the type II cAMP-dependent protein kinase. Unlike the human neutrophils, no evidence of RI activity was detected. cAMP-dependent protein kinase activity was identified by using histone as a substrate. Subcellular fractionation studies showed that the cAMP receptor protein and the cAMP-dependent protein kinase activity are most enriched in the cytosol fraction.

Recent studies of the "naturally occurring leprosy-like disease of wild armadillos" establish that the causative bacillus is genetically identical to M. leprae from human sources, and thus the disease is a zoonosis, sylvatic leprosy. A recent survey of 451 wild armadillos from the Texas Gulf Coast demonstrated sylvatic leprosy in 4.66%. This companion study reports the anatomic pathologic changes seen in the 17 leprous and 17 nonleprous armadillos necropsied in that survey. Findings support previous studies on the histopathology and pathogenesis of sylvatic leprosy, but a broader spectrum of histologic changes are noted.