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PubMed1980

Recognition of heterologous cells by macrophages. I. Species recognition by mouse and guinea pig macrophages in the phagocytosis of heterologous thymocytes.

The ability of macrophages to recognize homologous and various heterologous cells was studied in mice, rats, and guinea pigs, in terms of the in vitro phagocytosis of non-opsonized viable thymocytes by macrophages. Mouse, rat, and guinea pig macrophages were found to phagocytize actively thymocytes from certain heterologous animals, including chickens. For instance, mouse macrophages displayed conspicuous phagocytic activities against chicken and duck thymocytes, moderate activities against guinea pig and frog thymocytes and weak activities against rat and mouse thymocytes. On the other hand, guinea pig macrophages revealed a different behaviour: they ingested only chicken thymocytes. These observations strongly suggested that mammalian macrophages possess some ability to discriminate homologous from certain heterologous thymocytes. The results, however, did not necessarily support the idea that the degree of phagocytosis is simply related to the phylogenetic distance between the animal species from which thymocytes and macrophages originated, because of the apparent exception in the mode of phagocytosis by guinea pig macrophages. Evidence demonstrating that antibodies are not involved in this phenomenon will be presented in the accompanying paper.

Animals↗
PubMed2004

Significance of macrophage chemoattractant protein-1 expression and macrophage infiltration in squamous cell carcinoma of the esophagus.

OBJECTIVES: Macrophage chemoattractant protein-1 (MCP-1) is a chemokine-inducing infiltration of macrophages, which can play several roles in tumor growth and metastasis. We have attempted to clarify the relationship between MCP-1 expression and macrophage infiltration in esophageal squamous cell carcinoma (SCC). METHODS: Paraffin-embedded sections of tissue samples taken from 56 patients with esophageal SCC after curative surgery were immunohistochemically stained for MCP-1, CC chemokine receptor 2 (CCR-2), and thymidine phosphorylase (TP). Macrophage recruitment in SCC was evaluated by monocytic count based on CD68 immunostaining. Microvessels immunostained for Factor VIII-related antigen were counted in SCC, and microvessel density (MVD) was determined. Ki-67 labeling index was calculated based on Ki-67 immunostaining, and an apoptotic index was calculated based on the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate biotin nick end labeling. RESULTS: MCP-1 was expressed in cancer cells of 31 SCC (55.4%) and in stromal cells mainly identified as macrophages of 16 SCC (28.6%). CCR-2 was expressed in stromal cells of all SCC and in vascular endothelial cells of 15 SCC (26.8%). There was a significant correlation between the expression of MCP-1 in cancer cells and of CCR-2 in stromal cells. TP was expressed in stromal cells in 76.7% of the SCC. Monocytic count, MVD, and Ki-67 LI in SCC with MCP-1 expression in cancer cells were higher than that without, and apoptotic index in SCC with MCP-1 expression in cancer cells were lower than that without. Furthermore, the monocytic count was positively correlated with MVD, while it was inversely correlated with apoptotic index. Clinicopathologically, MCP-1 expression in cancer cells was correlated with venous invasion, distant metastasis, and lymph node metastasis. Monocytic count in SCC with venous invasion, distant metastasis, or lymph node metastasis was higher than that without them. Five-year survival rate in the patients with high monocytic count or MCP-1 expression was worse than that with a low monocytic count or without MCP-1 expression. CONCLUSIONS: These results suggest that MCP-1 expression and macrophage infiltration is associated with angiogenic promotion in esophageal SCC. MCP-1 expression may be interactively associated with macrophage infiltration in esophageal SCC; MCP-1 may play an important role in tumor angiogenesis through production of angiogenic factors, such as TP, by recruited macrophages in esophageal SCC. Furthermore, CCR-2 expression in vascular endothelial cells may participate partially in angiogenesis. Clinicopathologically, esophageal SCC patients with MCP-1 expression have no favorable prognosis.

Angiogenesis Inducing Agents↗
PubMed2002

Interactions between neutrophils and macrophages promote macrophage killing of rat muscle cells in vitro.

Current evidence indicates that the physiological functions of inflammatory cells are highly sensitive to their microenvironment, which is partially determined by the inflammatory cells and their potential targets. In the present investigation, interactions between neutrophils, macrophages and muscle cells that may influence muscle cell death are examined. Findings show that in the absence of macrophages, neutrophils kill muscle cells in vitro by superoxide-dependent mechanisms, and that low concentrations of nitric oxide (NO) protect against neutrophil-mediated killing. In the absence of neutrophils, macrophages kill muscle cells through a NO-dependent mechanism, and the presence of target muscle cells causes a three-fold increase in NO production by macrophages, with no change in the concentration of inducible nitric oxide synthase. Muscle cells that are co-cultured with both neutrophils and macrophages in proportions that are observed in injured muscle show cytotoxicity through a NO-dependent, superoxide-independent mechanism. Furthermore, the concentration of myeloid cells that is necessary for muscle killing is greatly reduced in assays that use mixed myeloid cell populations, rather than uniform populations of neutrophils or macrophages. These findings collectively show that the magnitude and mechanism of muscle cell killing by myeloid cells are modified by interactions between muscle cells and neutrophils, between muscle cells and macrophages and between macrophages and neutrophils.

Animals↗
PubMed1975

Specific macrophage immunity to Sendai virus: macrophage aggregation in vitro with Sendai virus by cytophilic antibodies.

When a 24-h tube culture of rabbit alveolar macrophages was infected with Sendai virus, the rate of infected cells was found to be limited. Even at a multiplicity of infection (MOI) of 500 plaque-forming units per cell, an average of 63% cells was found to synthesize viral antigens stainable by direct immunofluorescence. When the macrophages obtained from rabbits hyperimmunized by an intravenous injection of Sendai virus were infected under the same in vitro conditions, the rate of antigen synthesis averaged a low as 23%. At the time of infection of alveolar macrophages from immunized rabbits (immune macrophages), cell aggregation at an MOI 50 and cell fusion at an MOI 500 were found 24 h after infection, and these reactions were never encountered after the infection of nonimmune macrophages. When the immune macrophages were either pretreated by trypsin or incubated in medium at pH 4.0, the infection no longer caused the aggregation. The supernatant fluid obtained after incubation at pH 4.0 contained neutralizing antibody to Sendai virus. Conversely, when nonimmune macrophages were incubated in the presence of rabbit anti-Sendai virus serum or purified immunoglobulin G, the same aggregation reaction occurred after virus infection. Ultraviolet light-killed Sendai virus could be used as the counterpart of alive virus in the same aggregation reaction. These results suggest that the aggregation reaction of the immune macrophages could be attributed to the presence of specific cytophilic antibodies on their surface.

Antibodies↗
PubMed1985

Survival and growth of Yersinia pestis within macrophages and an effect of the loss of the 47-megadalton plasmid on growth in macrophages.

The survival and growth of Yersinia pestis cells within mouse peritoneal cavities and within mouse peritoneal macrophages maintained in vitro was examined. Two strains were used which differed only in that one (KIM) contained the 47-megadalton plasmid associated with virulence and the second (KIM1) lacked this plasmid. The KIM cells, but not the KIM1 cells, acquired some resistance to phagocytosis during growth at 37 degrees C which was not evident when cells were grown at 26 degrees C. Whether previously grown at 26 or 37 degrees C, however, a substantial portion of the cells of either strain which were phagocytized were apparently killed after phagocytosis in vivo, although this was not observed in vitro. KIM cells which survived phagocytosis proliferated within macrophages in vivo, but no increase in viable cells was seen with the KIM1 cells. Growth of the KIM1 cells within macrophages in vitro required that a complex supportive medium be used in which the bacteria could have grown if extracellular. This was not the case for the KIM cells which proliferated within macrophages supported in medium not permissive to bacterial growth. After phagocytosis of cells of either strain by macrophages maintained in vitro, phagolysosome formation occurred normally, as shown by the acridine orange dye staining technique. KIM and KIM1 cells were equally sensitive to hydrogen peroxide and superoxide anion, although the sensitivity in each case varied with growth temperature. The oxidative burst, as determined by the luminol chemiluminescence assay, was low when compared with that seen after phagocytosis of Escherichia coli cells. Chemiluminescence after phagocytosis of yeast cells by macrophages which had engulfed KIM or KIM1 was also low. We conclude that survival within macrophages is substantially independent of the 47-megadalton plasmid and may be a consequence, as least in part, of blockage of the oxidative burst or rapid removal of the oxidizing compounds formed. The 47-megadalton plasmid is apparently required for subsequent proliferation within the macrophage.

Animals↗
PubMed1972

Specific macrophage immunity to vaccinia virus: macrophage-virus interaction.

Macrophage immunity to vaccinia virus was examined by measuring replication of vaccinia virus in immune and nonimmune rabbit peritoneal macrophages. Vaccinia virus multiplied in macrophages from normal rabbits but failed to replicate in macrophages from immune rabbits. The specificity of vaccinia restriction was demonstrated by the ability of myxoma virus to replicate in nonimmune and vaccinia-immune macrophages. Vaccinia virus absorbed equally well to immune and nonimmune macrophages, but only a small fraction of immune cells supported synthesis of virus antigen. Virus eclipse and infective center neutralization studies suggested that much of the virus remained at the plasma membrane of immune macrophages, even after prolonged incubation in culture. These data support our previous suggestions that macrophages may contribute to specific immunity against vaccinia virus.

Adsorption↗
PubMed2005

Macrophages from patients with SLE and rheumatoid arthritis have defective adhesion in vitro, while only SLE macrophages have impaired uptake of apoptotic cells.

BACKGROUND: It has been suggested that defective handling of apoptotic cells by macrophages plays a key role in the development of systemic lupus erythematosus (SLE). The relative contribution of intrinsic defects and serum factors remains controversial. OBJECTIVE: To compare monocytes from SLE patients, patients with rheumatoid arthritis, and healthy controls for their ability to differentiate in vitro into macrophages and to bind/engulf apoptotic cells. METHODS: Peripheral blood derived monocytes from healthy donors or from patients with SLE or rheumatoid arthritis were allowed to differentiate into macrophages. The in vitro uptake of apoptotic cells by macrophages was evaluated by a flow cytometry assay that allowed discrimination between binding and internalisation. RESULTS: Monocytes from SLE and rheumatoid patients showed a striking defect in adherence to plastic compared with healthy donors. Absence or heat inactivation of serum resulted in a reduction in the binding and engulfment of apoptotic cells by macrophages. Macrophages from rheumatoid and SLE patients had similar percentages of apoptotic cells bound to their surface compared with normal controls. However, macrophages from SLE patients showed a significant defect in the internalisation of apoptotic cells compared with those from healthy controls, even in the presence of normal human serum. CONCLUSIONS: Monocytes from patients with SLE and rheumatoid arthritis have a similar defect in their capacity to adhere to plastic. However, only macrophages from SLE patients showed an impaired ability to engulf apoptotic cells, which indicates that an intrinsic cellular defect may be responsible for this phenomenon.

Adolescent↗
PubMed1993

Scavenger macrophages and central macrophages of erythroblastic islands in liver hemopoiesis of the fetal and early postnatal mouse: a semithin light- and electron-microscopic study.

The livers of 12-day mouse embryos contain many hemopoietic cells in the hepatic cords and macrophages which are laden with large heterophagosomes in the sinusoids. Macrophages, as scavengers, engulfed circulating primitive erythroblasts from the yolk sac, as well as nuclei expelled from erythroblasts. At the 14th day of gestation, scavenger macrophages in mitosis were seen, extending long and thin cytoplasmic projections from their cell surface. At the 13-14 day of gestation, macrophages migrated from sinusoids into hepatic cords, and erythroblasts gathered around them, thus forming cell clusters designated as erythroblastic islets. Central macrophages formed a cell-socket-like structure on their cell surface for surrounding erythroblasts, reflecting the close association between macrophages and erythroblasts. In the erythroblastic islands, contained in late fetal and neonatal livers, erythroblasts have dissociated from the central macrophages having a starfish-shaped cell profile. The macrophage-erythroblastic association in the islands became less marked rapidly after birth.

Animals↗
PubMed1999

Role of matrix metalloproteinases in models of macrophage-dependent acute lung injury. Evidence for alveolar macrophage as source of proteinases.

Matrix metalloproteinases (MMPs) have been implicated in the tissue injury seen in neutrophil-dependent models of acute lung injury. However, the role of MMPs in macrophage-dependent models of lung injury is unknown. To address this issue, the macrophage-dependent immunoglobulin A immune complex-induced lung injury model and the macrophage-dependent portion of the lipopolysaccharide-induced acute lung injury model in the rat were assessed for MMP involvement and for the source of these activities. In both models, injury was inhibited by the recombinant human tissue inhibitor of metalloproteinases-2. Bronchoalveolar lavage fluids (BALFs) from injured animals in both models showed increased levels of MMPs. Characterization of MMP production by isolated lung fibroblasts, endothelial cells, type II epithelial cells, and alveolar macrophages revealed that only the macrophage had the same spectrum of MMP activity as seen in the BALF. Further, isolated alveolar macrophages from injured lungs showed evidence of in vivo activation with the release of the same spectrum of MMP activities. Together these studies show that MMPs are produced during macrophage-dependent lung injury, that these MMPs play a role in the development of the lung injury, and that the alveolar macrophage is the likely source of these MMPs.

Animals↗
PubMed1994

A simple method for the assessment of macrophage scavenger receptor-ligand interaction: adherence of erythrocytes coated with oxidized low density lipoprotein and modified albumin to macrophages.

A simple method is described for the assessment of the binding of macrophage scavenger receptor and its ligands such as oxidized low density lipoprotein (ox-LDL) and maleylated bovine serum albumin (m-BSA). In this method, the binding of ox-LDL or m-BSA to macrophages is observed as the adherence of erythrocytes precoated with ox-LDL or m-BSA under phase-contrast microscopy. Erythrocytes were coated with native LDL or ox-LDL simply by incubating mouse erythrocytes with LDL. The ox-LDL-coated erythrocytes attached to the monolayer of mouse peritoneal macrophages without phagocytosis at 37 degrees C, while native LDL-coated erythrocytes did not. The extent of the adherence of the ox-LDL-coated erythrocytes to the macrophages was conveniently expressed as the proportion of the macrophages binding the coated erythrocytes. An optimal concentration of ox-LDL for erythrocyte coating giving maximum erythrocyte adherence to macrophages was 10 micrograms/ml as protein at an erythrocyte concentration of 2%. The binding of the ox-LDL-coated erythrocytes to the macrophages could be inhibited by ligands for scavenger receptor, and reflected the extent of LDL oxidation. Mouse erythrocytes were successfully coated with m-BSA using chromium(III) ion as adsorbent. The m-BSA-coated erythrocytes attached to the macrophages, while native BSA-coated erythrocytes did not. The adherence was inhibitable with ligands for scavenger receptor, and reflected the extent of maleylation. The method would be useful particularly for measurement of the ligand-binding activity of the receptor, and the receptor-binding activity of the ligands.

Absorption↗
PubMed1978

Electron microscopy of peroxidase and acid phosphatase in leprous and uninfected armadillo macrophages: a macrophage subpopulation contains peroxisomes and lacks bacilli.

Lepromatous tissue from armadillos inoculated 24--36 months earlier with Mycobacterium leprae was obtained for electron microscopic studies. Cytochemically stained lepromas revealed a subpopulation of macrophages containing peroxisomes. These peroxidase reactive macrophages were not infected with bacilli. Acid phosphatase was present in macrophages and many of these were infected with bacilli and contained vacuoles and lipid globules. Within the membrane-bound vacuoles, acid phosphatase surrounded bacilli. However, the reaction product ended abruptly at a 15--40 millimicron thick zone of low electron density surrounding intact bacilli. Acid phosphatase was more intensely reactive and localized less precisely in heavily infected and vacuolated macrophages than in lightly and non-infected cells. The effectiveness of this bacillary barrier and the numerous infected macrophages with substantial acid phosphatase argue against the ability of acid phosphatase to protect host cells from leprosy bacilli. Evidence suggests a protective action of peroxidase or the rapid turnover of macrophages within lepromas. Granular and membranous debris were commonly seen within vacuoles of infected macrophages. A portion of the debris was ultrastructurally similar to bacillary matrix and was nonreactive for peroxidase and acid phosphatase. Following homogenization and centrifugation, similar materials banded with bacilli above 60% sucrose. Another portion of the debris was ultrastructurally similar to host lysosomal matrix and was reactive for acid phosphatase. Results support the concept of dual host and parasitic origins of the debris found in phagolysosomes of infected macrophages. Transparent, oval Epon defects remained eccentric to the majority of intact bacilli in centrifuged fractions. Apparently, an intrinsic property of leprosy produced these Epon defects.

Acid Phosphatase↗
PubMed1999

Adrenomedullin in monocytes and macrophages: possible involvement of macrophage-derived adrenomedullin in atherogenesis.

Macrophages secrete a variety of growth factors, cytokines and vasoactive peptides, which are related to the progression of atherosclerosis. Adrenomedullin (ADM) is a potent vasodilator peptide and inhibits proliferation and migration of vascular smooth muscle cells. In this study, we investigated the production and secretion of ADM by monocytes and macrophages by Northern blot analysis, RIA and immunocytochemistry. Northern blot analysis showed that ADM mRNA was expressed in human monocytes obtained from peripheral blood and monocyte-derived macrophages. The expression level of ADM mRNA in monocyte-derived macrophages was about five times higher than that in monocytes. Treatment with lipopolysaccharide (100 ng/ml) for 24 h increased ADM mRNA expression levels in both monocytes and monocyte-derived macrophages. The levels of immunoreactive ADM in the media of monocyte-derived macrophages were about three times higher than that of monocytes (0. 718+/-0.046 fmol/24 h/10(5) cells, n=8 compared with 0.259+/-0.018 fmol/24 h/10(5) cells, n=8; mean+/-S.E.M., P<0.01). The secretion was also increased by treatment with lipopolysaccharide. Immunocytochemistry showed positive ADM immunostaining in macrophages in atherosclerotic lesions of human aorta obtained at autopsy. ADM secreted from activated macrophages may play an inhibitory role in atherogenesis.

Adrenomedullin↗
PubMed2000

Role of macrophages in experimental malaria: VII--studies on adoptive transfer of macrophages.

Adoptive transfer of purified macrophages harvested from normal, Plasmodium berghei infected and latent/cured mice and also macrophages exposed to parasites in vitro were carried out to see the role of macrophages in transferring immunity against P. berghei infection. Macrophages obtained from mice having high parasitaemia at a dose of one million cells/animal showed significant increase in survival period (SP) and K values, compared to controls. Macrophages exposed to low parasite density conferred significant K values only. There was a decrease in prepatent period (PP) in the animal which received macrophages from animals cured 7-11 months compared to controls. The adoptive transfer studies with macrophages conditioned in vitro to parasite contributed towards increased protection of host against P. berghei as expressed by K values only. These studies showed that the macrophages harvested from infected mice were capable of acting as immunogen against P. berghei infection.

Adoptive Transfer↗
PubMed2001

Neutralization/enhancement of macrophage-tropic SIVmac infection by plasma from macaques infected with macrophage-tropic or lymphocyte-tropic SIVmac.

Plasma from macaques inoculated with macrophage-tropic SIVmac were tested for neutralization/enhancement of macrophage-tropic SIVmac239-17EBR in normal rhesus macrophages. The plasma of a macaque (R71) that developed a highly virulent neuro-tropic (macrophage-tropic) strain of SIVmac in neuro-adaptation studies significantly enhanced infection of SIVmac239-17EBR as well as infection of dual-tropic SIVmac251. Plasma from other macaques that were inoculated with macrophage-tropic virus, neutralized SIVmac239-17EBR. Also, plasma from macaques infected with lymphocyte-tropic SIVmac239 or dual-tropic SIVmac251 neutralized SIVmac251 infection. When the effect of R71 plasma on the early stages of the SIV life cycle was investigated, this plasma significantly increased binding of 35S-methionine labeled SIVmac239-17EBR and increased binding of 35S-SIVmac251 to primary macrophages, unlike plasma from other macaques infected with either macrophage-tropic or lymphocyte-tropic SIV. A single-cycle infection assay showed higher percentages of positive cells and more intense fluorescence in cultures treated with R71 plasma compared with control plasma. By in situ hybridization, SIV RNA transcripts were detected earlier (12 hr post-infection) and in higher percentages, in cultures treated with R71 plasma than in cultures treated with control plasma (18 hr post-infection). These results indicate that enhancing activity in infected macaque plasma may be associated with severe infection by highly virulent macrophage-tropic (neuro-tropic) SIV. The enhancing effect occurs early in infection and results in increased transcription of SIV RNA.

Animals↗
PubMed1977

The role of macrophages in the generation of T helper cells. V. Evidence for differential activation of short-lived T1 and long-lived T2 lymphocytes by the macrophage factors GRF and NMF.

The generation of T helper cells in vitro requires macrophages or macrophage-derived factors such as genetically related macrophage factor (GRF) or nonspecific macrophage factor (NMF). However, there is a basic difference of T helper cell induction when using particulate antigens. The present study demonstrates that this difference is based on the activation of two different T cell subsets. GRF activates short-lived 'T1' cells which amplify the induction of T2 cells, which are the helper cell precursors. Thus, the genetic restriction of T helper cell induction seen with soluble antigen or GRF lies on the level of macrophage or GRF interaction with T1 cells. NMF (or macrophages) and particulate antigens directly activate the helper cell precursor (T2) indicating no requirement for T1-T2 cooperation. The direct activation of the helper cell precursor with particulate antigens does not require histocompatible macrophages or NMF from histocompatible macrophages. The present results may explain some of the discrepancies reported in the literature concerning the genetic requirements and specificity of T cell activation.

Animals↗
PubMed1977

Macrophage activation for tumor cytotoxicity: induction of tumoricidal macrophages by supernatants of PPD-stimulated Bacillus Calmette-Guérin-immune spleen cell cultures.

Resident peritoneal macrophages from normal mice were activated for tumor cytotoxicity in vitro by co-cultivation with BCG1-immune spleen cells and PPD and by incubation with supernatants of PPD-stimulated BCG-immune spleen cell cultures (lymphokine supernatants). Lymphokine activation of macrophages occurred in unfractionated PC suspensions as well as in macrophage monolayers depleted of nonadherent PC. Tumor cytotoxicity by lymphokine-activated macrophages was evident by 3 to 4 hr of culture in active supernatants, reached maximal levels by 8 to 12 hr. and was absent by 20 hr. Continued incubation in lymphokines or even re-exposure after washing did not maintain macrophage cytotoxicity. The capacity of normal resident macrophages to be activated by lymphokines in vitro progressively decreased and was absent by 20 hr in culture. This decrease did not necessarily reflect cell death; macrophage viability as estimated by exclusion of trypan blue or by phagocytic responses did not change over the 20-hr culture period. The short lived nature of both macrophage tumoricidal capacity and capacity of precursor cells to be activated by lymphokines may function as negative feedback mechanisms in immune reactions.

Animals↗
PubMed1986

A role for the macrophage in normal hemopoiesis. I. Functional capacity of bone-marrow-derived macrophages to release hemopoietic growth factors.

Almost pure macrophage populations were obtained when mouse bone marrow cells were cultured under low-oxygen tension on hydrophobic Teflon foils. Macrophage content was determined using nonspecific esterase staining and binding of the mouse, macrophage-specific monoclonal antibody directed against the F4/80 antigen. Using both these techniques, the macrophage content present after 14 days in culture was approximately 98%. This represented an approximate two- to fourfold increase over the initial macrophage content present in primary bone marrow cell suspensions. Granulocytes and erythroblasts were found to be the contaminating cell types. No T-lymphocytes were present at 14 days of culture. The activities of three hemopoietic growth factors (erythropoietin, colony-stimulating factor, and a factor enhancing early erythroid progenitor cells [BFU-E] and stimulating in vitro multipotential stem cells) present in the supernatant were shown to increase in parallel with macrophage content. The results demonstrate that bone-marrow-derived macrophage populations are functionally capable of producing and secreting hemopoietic growth factors. These results form the basis of a hypothesis in which the macrophage is perceived as a regulator cell for hemopoiesis.

Animals↗
PubMed1984

Slow virus-macrophage interactions. Characterization of a transformed cell line of sheep alveolar macrophages that express a marker for susceptibility to ovine-caprine lentivirus infections.

Visna-maedi of sheep and arthritis encephalitis of goats are slowly progressive diseases caused by serologically related lentiviruses. Lesions are inflammatory and can occur at one or many sites including the central nervous system, lungs, joints, and mammary glands. The viruses replicate in macrophages, and in the animal large numbers of infected macrophages can be obtained from inflamed tissues. To study virus-macrophage interactions we transformed sheep alveolar macrophages, which are natural virus target cells, with simian virus 40 and produced a macrophage cell line. The transformed cells grew into density-dependent monolayers and were subcultured after trypsin dissociation. They maintained histochemical and physiologic properties of macrophages as well as the ability to support replication of the lentiviruses. Rabbit antisera to these cells reacted with blood monocytes and only selected populations of tissue macrophages, including those in lung, synovium, mammary gland, and spleen. Microglia, Kupffer cells, and connective tissue histiocytes were not recognized by the sera. Since the tissues in which virus localizes in infected animals are the same as those recognized by the sera, the antimacrophage serum may provide an immunologic marker for virus-susceptible macrophages in the animal.

Animals↗