SEARCH · Search PubMed

Results for “MACROPHAGES”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 595 records · Page 33Linked to original sources

PubMed1983

Complement (C3)-receptor-mediated phagocytosis of agarose beads by mouse macrophages. II. Extracellular activation of macrophage-derived complement on agarose via the alternative pathway.

Phagocytosis of agarose beads by macrophages cultured under serum-free conditions was studied. 48 h was needed before a plateau in the uptake was reached. The ingested agarose beads were coated extracellularly with macrophage-derived protein before attachment and ingestion of the beads. Intracellularly, the agarose-linked protein was removed from the agarose. If the ingested agarose beads were extracted from the macrophages within 24 h after the plateau in the uptake was reached, a fraction of the beads could attach to new macrophages, demonstrating modification of the agarose beads by opsonin(s). Because of binding of anti-human C3c antibodies to beads extracted from the macrophages after 24 h of phagocytosis and the trypsin sensitivity of the protein on the agarose, we conclude that the main opsonin on the agarose beads is C3bi. Requirements for the stimulatory effect of agarose on macrophages are summarized.

Animals↗

PubMed1987

Macrophages in T and B cell compartments and other tissue macrophages recognized by monoclonal antibody MOMA-2. An immunohistochemical study.

A new monoclonal antibody, MOMA-2, is described, which recognizes monocytes and macrophages in the mouse. The antibody reacts with the majority of mononuclear phagocytes in various tissues as determined by immunohistochemistry. It differs from other macrophage markers that have been described by the strong reaction with macrophages in the lymphoid organs such as the tingible body macrophages and macrophages in T cell-dependent areas. The antibody recognizes predominantly a cytoplasmic component, although a membrane component can also be demonstrated. Isolated Langerhans' cells, interdigitating cells and dendritic cells, members of the mononuclear phagocyte system that are involved in antigen presenting, stain weakly with the antibody. Because of the intense staining the antibody is very useful for defining tissue macrophages by immunohistochemistry.

Animals↗

PubMed2006

Macrophages but not smooth muscle cells undergo benzyloxycarbonyl-Val-Ala-DL-Asp(O-Methyl)-fluoromethylketone-induced nonapoptotic cell death depending on receptor-interacting protein 1 expression: implications for the stabilization of macrophage-rich atherosclerotic plaques.

Several lines of evidence suggest that macrophages play a key role in atherosclerotic plaque destabilization and rupture. Therefore, selective removal of macrophages from plaques via pharmacological therapy could represent a promising approach to stabilize "vulnerable," rupture-prone lesions. Yet, how macrophages can be eliminated from plaques without influencing other cell types, including smooth muscle cells (SMCs), is unknown. In the present study, we report that benzyloxycarbonyl-Val-Ala-DL-Asp(O-methyl)-fluoromethylketone (z-VAD-fmk), a caspase inhibitor with broad specificity, induces nonapoptotic cell death of J774A.1 and RAW264.7 macrophages but not of SMCs. Cell death was characterized by bulk degradation of long-lived proteins, processing of microtubule-associated protein light chain 3, and cytoplasmic vacuolization, which are all markers of autophagy. However, necrosis also occurred, and the number of necrotic cells rapidly increased during z-VAD-fmk treatment. Primary mouse peritoneal macrophages were resistant to z-VAD-fmk-mediated cell death, but unlike SMCs, they underwent z-VAD-fmk-mediated necrosis after pretreatment with interferon-gamma. Further evidence indicated that the expression level of receptor-interacting protein 1 (RIP1) mediates the sensitivity to z-VAD-fmk. Importantly, upon z-VAD-fmk treatment, J774A.1 macrophages overexpressed and secreted several chemokines and cytokines, including tumor necrosis factor (TNF) alpha. The combination of z-VAD-fmk and TNFalpha, but not TNFalpha alone, induced SMCs necrosis via a mechanism that required RIP1 expression. These results suggest that z-VAD-fmk, despite its selective cell death inducing capacity, would be detrimental for the stability of atherosclerotic plaques due to enlargement of the necrotic core, stimulation of inflammatory responses, and indirect induction of SMC death.

Amino Acid Chloromethyl Ketones↗

PubMed1982

Macrophages in resistance to rickettsial infection: strains of mice susceptible to the lethal effects of Rickettsia akari show defective macrophage Rickettsicidal activity in vitro.

Activation of macrophages was assessed in strains of mice inoculated intraperitoneally with 1,000 times the 50% lethal dose of Rickettsia akari. Macrophages from mice resistant to R. akari infection (C3H/HeN, C57BL/10J, and BALB/cN) were nonspecifically tumoricidal 2 to 4 days after rickettsial inoculation. Moreover, these macrophages were microbial for R. akari in vitro; cells were resistant to infection with the bacterium and were capable of killing intracellular rickettsiae. In contrast, macrophages from strains of mice susceptible to R. akari (C3H/HeJ, C57BL/10SnCR, and A/J) failed to develop nonspecific tumoricidal activity over the course of lethal disease and became infected with R. akari in vivo within 2 days of rickettsial inoculation. Macrophages from uninfected mice of strains susceptible to R. akari also could not be activated for rickettsicidal or tumoricidal activities by treatment with macrophage-activating agents (Mycobacterium bovis BCG) in vivo or by treatment with lymphokines in vitro.

Animals↗

PubMed1986

Effect of acute nutritional deprivation on macrophage colony-stimulating factor and macrophage progenitor cells in mice.

The effect of short-term nutritional deprivation on host defenses and on the parameters of macrophage production was determined in outbred mice. Confirming previous data from this laboratory, initial experiments demonstrated that starved mice were relatively resistant to infection by Listeria monocytogenes as determined by spleen and liver bacterial counts. The number of macrophage progenitor cells in bone marrow rose slightly during a 72-h starvation period and returned to normal during refeeding. By contrast, the number of progenitor cells in spleens fell to 12% of the base line during starvation. The concentration of the macrophage colony-stimulating factor in serum decreased during starvation and returned to normal during refeeding. Additional experiments were performed to determine whether starved mice had increased parameters of macrophage production during listerial infection. The number of progenitor cells in the bone marrow and spleens of starved mice had increased compared with that of fed mice early in infection. Macrophage colony-stimulating factor levels in starved mice rose early and remained elevated during infection but were not as high as in fed mice. These data document the changes in the parameters of monocyte production during starvation and suggest that the number of macrophage progenitor cells may be related to increased resistance to L. monocytogenes.

Animals↗

PubMed1997

Role of CCR5 in infection of primary macrophages and lymphocytes by macrophage-tropic strains of human immunodeficiency virus: resistance to patient-derived and prototype isolates resulting from the delta ccr5 mutation.

The alpha-chemokine receptor fusin (CXCR-4) and beta-chemokine receptor CCR5 serve as entry cofactors for T-cell (T)-tropic and macrophage (M)-tropic human immunodeficiency virus type 1 (HIV-1) strains, respectively, when expressed with CD4 in otherwise nonpermissive cells. Some M-tropic and dual-tropic strains can also utilize other beta-chemokine receptors, such as CCR2b and CCR3. A mutation of CCR5 (delta ccr5) was recently found to be common in certain populations and appears to confer protection against HIV-1 in vivo. Here, we show that this mutation results in a protein that is expressed intracellularly but not on the cell surface. Primary CD4 T cells from delta ccr5 homozygous individuals were highly resistant to infection with prototype M-tropic HIV-1 strains, including an isolate (YU-2) that uses CCR5 and CCR3, but were permissive for both a T-tropic strain (3B) and a dual-tropic variant (89.6) that uses CXCR-4, CCR5, CCR3, or CCR2b. These cells were also resistant to M-tropic patient isolates but were readily infected by T-tropic patient isolates. Primary macrophages from delta ccr5 homozygous individuals were also resistant to infection with M-tropic strains, including YU-2, but the dual-tropic strain 89.6 was able to replicate in them even though macrophages are highly resistant to CXCR-4-dependent T-tropic isolates. These data show that CCR5 is the essential cofactor for infection of both primary macrophages and T lymphocytes by most M-tropic strains of HIV-1. They also suggest that CCR3 does not function for HIV-1 entry in primary lymphocytes or macrophages, but that a molecule(s) other than CCR5 can support entry into macrophages by certain virus isolates. These studies further define the cellular basis for the resistance to HIV-1 infection of individuals lacking functional CCR5.

CD4 Antigens↗

PubMed2001

Use of helper-free replication-defective simian immunodeficiency virus-based vectors to study macrophage and T tropism: evidence for distinct levels of restriction in primary macrophages and a T-cell line.

Cell tropism of human and simian immunodeficiency viruses (HIV and SIV, respectively) is governed in part by interactions between the viral envelope protein and the cellular receptors. However, there is evidence that envelope-host cell interactions also affect postentry steps in viral replication. We used a helper-free replication-defective SIV macaque (SIVmac)-based retroviral vector carrying the enhanced jellyfish green fluorescent protein inserted into the nef region (V1EGFP) to examine SIV tropism in a single cycle of infection. Vector stocks containing envelope proteins from three different SIVmac clones, namely, SIVmac239 (T-lymphocyte tropic [T-tropic]), SIVmac316 (macrophage tropic [M-tropic]), and SIVmac1A11 (dualtropic), were tested. SIVmac239 replicates efficiently in many human T-cell lines, but it does not efficiently infect primary rhesus macrophages. Conversely, SIVmac316 efficiently infects primary macrophages, but it does not replicate in Molt4-Clone8 (M4C8) T cells. SIVmac1A11 replicates efficiently in both cell types. When primary macrophages were infected with V1EGFP pseudotyped by SIVmac316 or SIVmac1A11 envelopes, the infection was substantially (ca. 200- to 300-fold) more efficient than for the SIVmac239 pseudotype. Thus, in primary macrophages, a major component of M versus T tropism involves relatively early events in the infection cycle. Quantitative PCR studies indicated that synthesis and transport of vector DNA into the nucleus were similar for macrophages infected with the clone 239 and 316 pseudotypes, suggesting that the restriction for SIVmac239 infection is after reverse transcription and nuclear import of viral DNA. When the same vector pseudotypes were used to infect M4C8 cells, they all showed approximately equivalent infectivities, even though replication-competent SIVmac316 does not continue to replicate in these cells. Therefore, in M4C8 cells, restriction involves a late step in the infection cycle (after proviral integration and expression). Thus, depending on the cell type infected, envelope-dependent cell interactions that govern SIV M and T tropism may involve different steps in infection.

Animals↗

PubMed1992

CFU-rAM, the origin of lung macrophages, and the macrophage lineage.

Macrophage precursors and their progeny have been identified in early rat embryos with the use of a peroxidase-coupled marker, isolectin B4 of Griffonia simplicifolia (GSA I-B4). The macrophage lineage can be traced back to actively dividing GSA-positive angular cells present in the mesenchyme of late neurulas. These increase in number and establish residence successively in rudiments of the central nervous system, liver, and lungs. In organ-cultured fetal lungs they transform directly into a self-replicating population of macrophages responsive to colony-stimulating factors. The angular cell therefore can be seen as the source of lung macrophages during prenatal life. The extent to which this manner of production continues in postnatal life is unclear, but it appears that central hematopoietic tissues (bone marrow, spleen) may generate macrophages by a direct pathway from early-committed progenitors as well as indirectly through a series of intermediate stem cells. Considering the wealth of new information available from diverse studies in specialized culture environments and to a lesser extent from studies in vivo, it is time to integrate these findings into a more comprehensive theory of macrophage origin and fate than we have at present.

Animals↗

PubMed1999

Macrophage activation and programming and its role for macrophage function in glomerular inflammation.

Macrophages have a central role in the control of inflammation because, depending on the local microenvironment, they can develop into cells that cause further injury or facilitate tissue repair. Understanding what signals determine whether macrophages develop into cells that promote injury or facilitate repair is one of the most important issues in inflammatory cell biology, not least because of the opportunities for developing novel therapies. This is highly relevant to glomerulonephritis because of the prominence of the macrophage infiltrate in all types of severe or progressive nephritis, and the present unsatisfactory nature of treatments for these diseases. This review will focuses on how macrophages are activated in vitro and in normal and inflamed glomeruli. The new concept of 'macrophage programming' is introduced and novel strategies to alter macrophage function within nephritic glomeruli that could be used for the treatment of glomerular inflammation are highlighted.

Animals↗

PubMed1999

Transcriptional inhibition by interleukin-6 of the class A macrophage scavenger receptor in macrophages derived from human peripheral monocytes and the THP-1 monocytic cell line.

Expression of the class A macrophage scavenger receptor (MSR) contributes to the uptake of modified low density lipoproteins (LDL) by macrophages and transformation of these cells into lipid-laden foam cells, which characterize atherosclerosis. Many environmental factors, in particular, proinflammatory cytokines and growth factors, can exert regulatory effects on MSR expression, whereas intracellular accumulation of cholesterol itself does not influence MSR levels to any considerable extent. In the present study, by using an in vitro model, we examined whether stimulation with interleukin-6 (IL-6), an immunoregulatory, multipotential cytokine, modulates the expression and activities of the MSR in macrophages. When treated with IL-6, macrophages derived from peripheral monocytes and phorbol 12-myristate 13-acetate (PMA)-differentiated THP-1 monocytic cells showed significantly reduced uptake and/or binding of the MSR ligand, acetylated LDL. This effect was paralleled by a reduction in the expression of MSR protein and mRNA. Analysis of MSR promoter activity in THP-1 cells transfected with an MSR promoter-reporter gene construct demonstrated decreased activity of the MSR promoter in IL-6-treated THP-1 macrophages. Electrophoretic mobility gel shift assay also showed a reduction in the binding of a transcription factor to the MSR promoter AP-1/ets elements in IL-6-treated cells. Thus, exposure to IL-6 may inhibit expression of the class A MSR in differentiated macrophages at transcriptional levels. This result suggests that this cytokine may modulate foam cell formation during atherogenesis.

Carbocyanines↗

PubMed1993

A study of macrophages, macrophage-related cells, and endothelial adhesion molecules in recurrent aphthous ulcers in HIV-positive patients.

The purpose of this immunohistochemical study was to investigate the presence and distribution of macrophages (CD11c+ and CD68+) and macrophage-related dendritic cells (factor XIIIa+ and CD36+) in early and late aphthous ulcers associated with HIV infection. To substantiate a mechanism by which these cells may move from the vascular compartment to tissue spaces, we also investigated expression of ELAM (endothelial leukocyte adhesion molecule), ICAM-1 (intercellular adhesion molecule), and CD18 (leukocyte function antigen). Numerous CD11c+ and CD68+ macrophages were seen in early lesions, though larger numbers of CD68+ cells were present in older lesions. No significant increases in factor XIIIa+ dendrocytes were seen in either early or late lesions, though dendrocytes appeared enlarged. CD36+ cells and CD18+ leukocytes were more numerous in early than in late aphthous ulcers. ELAM and ICAM expression was most intense on endothelial cells in early aphthous ulcers, with staining intensity fading toward the lesion periphery. Control specimens showed weaker ELAM and ICAM staining than did the ulcer specimens. Keratinocytes did not express ICAM. By virtue of their numbers, macrophages and macrophage subtypes appear to have a significant role in both the early and late stages of this disease. Although factor XIIIa-expressing dendrocytes may not have been more numerous in the ulcers, they appeared to be "activated" because of their prominence in the lesions and their occasional co-expression of CD68 antigen (KP1+). They may have a minor role in antigen processing, phagocytosis, and fibroplasia. ELAM and ICAM expression by endothelial cells provides a mechanism by which macrophages and other leukocytes can be recruited to the site of the lesion.(ABSTRACT TRUNCATED AT 250 WORDS)

Antigens, CD↗

PubMed1986

Experimental study on the fine structure of chicken liver parenchyme with special references to extrasinusoidal macrophages and sinusoidal blood cells. Part 1. Sinusoidal cells and macrophages in the normal and India ink-perfused livers.

The chicken livers were electron microscopically observed under a normal condition and after an intravenous India ink perfusion. Kupffer cells and sinusoidal endothelial cells commenced to endocytose India ink particles in the earliest stages (15 min) after perfusion. The attachment of the particles to the cell surface occurred only in the Kupffer cells, which actively took up the particles with coated caveolae. In the endothelial cells the particles were ingested by pinocytosis in the perikaryon and deposited in the macropinocytic vacuoles of Wisse. In Kupffer and endothelial cells, the particles were stored most abundantly at 30 min and 4 hr after perfusion, respectively. At 48 hr, the vacuoles containing the particles were decreased in number and size, while mitotic figures were revealed in the Kupffer cells. Ito cells occasionally ingested in later stages (4 and 48 hr) a few carbon particles; they underwent no mitotic division. Extrasinusoidal macrophages scattered in the parenchyme and phagocytic reticular cells (macrophages) in the lymphoid tissues exhibited phagocytic activity only in later stages (1-4 hr). In 48 hr after the perfusion both cells began to store amounts of the particles in their vacuoles. This delayed phagocytic activity may be ascribed to the location of the cells separated from the sinusoid by the endothelium. Some solitary macrophages projecting a long process into the sinusoid took up the particles at earlier stages. At 48 hr, several mitotic divisions took place in the phagocytic reticular cells of the lymphoid tissue, while no mitotic divisions were found in the solitary macrophages in the parenchyme. After the ink perfusion, migration of solitary macrophages into the sinusoid was accelerated and images indicating their transformation into Kupffer cells were frequently detected. It was concluded that the Kupffer cells maintain their necessary number not only by their self-proliferation but also by replenishment from the extrasinusoidal solitary macrophages scattered in the hepatic parenchyme, which in turn are replenished from the phagocytic reticular cells in the lymphoid tissue capable of mitotic proliferation.

Animals↗

PubMed1988

Distinct macrophage subpopulations in pancreas of prediabetic BB/E rats. Possible role for macrophages in pathogenesis of IDDM.

Use of monoclonal antibodies directed against rat macrophages and serial pancreatic biopsy in the prediabetic period have enabled us to document the involvement of macrophages in the pancreatic events leading to onset of diabetes in the spontaneously diabetic BB/E rat. A few weeks before onset of disease, there is marked recruitment and accumulation of ED1+ macrophages at periductal and perivascular locations adjacent to noninfiltrated islets. These recruited cells, distinct from the resident ED2+ tissue macrophages, then infiltrate the islets. Infiltration of the pancreas by ED1+ macrophages is therefore a very early event in the prediabetic period and suggests a possible role for macrophages in the pathogenesis of insulin-dependent diabetes mellitus (IDDM) in this animal model.

Animals↗

PubMed2002

Cocaine increases intracellular calcium in the interferon-gamma-primed macrophages but not in the LPS-primed-macrophages.

Calcium is required for antigen presentation. In the past study, we found that cocaine increased macrophage antigen-presenting activity. To investigate whether cocaine induces a calcium influx into macrophage cytosol, we used Fura2-AM to directly test the macrophage intracellular calcium concentration [Ca2+]i under the influence of different concentrations of cocaine after macrophages were primed by IFN-gamma or LPS. We report here that cocaine increases the IFN-gamma-primed macrophage [Ca2+]i, but it does not affect the LPS-primed macrophage [Ca2+]i. Furthermore, calcium blocker, nifedipine, blocks the effect of cocaine, suggesting that extracellular calcium enters the cytosol through the L-channel.

Animals↗

PubMed1991

[The role of peritoneal macrophages in realizing the growth inhibiting effect of glucocorticoids on reinoculated murine hepatoma 22 cells: the effect of hydrocortisone on the cytotoxic activity and metabolism of phospholipids by macrophages].

A single injection of hydrocortisone to rats with ascite hepatoma 22 had practically no effect on tumour growth. Inhibition of tumour growth was observed only after reinoculation of ascite hepatoma to mice that had received no less than 8 daily injections of the hormone. A single injection of hydrocortisone induced inhibition of the cytotoxic activity and decreased phospholipid metabolism in peritoneal macrophages. Contrariwise, long-term administration of the hormone caused marked activation of macrophage cytotoxicity. In this case incorporation of 32P into macrophage phospholipids was restored up to the control level. It is concluded that one of mechanisms underlying the inhibitory effect of glucocorticoids on macrophages is inhibition of phospholipid turnover. Presumably, long-term administration of the hormone promotes the formation of a new population of macrophages insensitive to the inhibitory effect of glucocorticoids and possessing a high cytostatic activity. The appearance of such activated macrophages may account for the enhancement of hydrocortisone effect on tumour cells upon prolonged administration of the hormone.

Animals↗

PubMed1989

[The roles of macrophage on the mechanism of development of periapical lesion. The response of macrophage stimulated with bacteria isolated from infected root canals].

It has been proposed that bacteria in infected root canals are most important agents to pathogenesis of the periapical lesion. The aim of the present study was to examine the roles of macrophage on the mechanism of development of periapical lesion. Therefore the influences of bacteria isolated from infected root canals to macrophage functions and the effects of products from macrophage stimulated with bacterial components to periodontal tissue were investigated. In this study, sonic extracts prepared from Bacteroides buccae predominantly isolated from root canals were tested for its capacity of induction of chemotaxis and production of prostaglandin E2 and collagenase from human peripheral monocyte. Furthermore prostaglandin E2, collagenase production and alkaline phosphatase activity of fibroblasts from human periodontal ligament (HPLF), pulp (HPF) and gingiva (Gin 1) stimulated with macrophage conditioned medium (MCM) stimulated with B. buccae sonic extracts were examined. The results obtained were as follows. The sonic extract of B. buccae showed capacity to induce macrophage chemotaxis directly and by activation of serum complement, and the serum activated with sonic extract of B. buccae was more active than the serum activated with LPS of Salmonella typhimurium. Prostaglandin E2 production of macrophage was increased when the cells were stimulated by sonic extracts of B. buccae, but collagenase activity. toas not increased. MCM stimulated with sonic extracts of B. buccae fot 48 hours strongly induced PGE2 and collagenase production from HPLF and HPF, at the same time sonic extract showed the similar capacity of induction of the PGE2 production of MCM. But, HPF stimulated with sonic extract showed the low activity of induction of the PGE2 production. On the other hand, Gin 1 cell produced a few amount of the PGE2 when it was stimulated with MCM, but not produced collagenase. Alkaline phosphatase activity of HPLF and HPF had been inhibited by addition of MCM stimulated with B. buccae sonic extract.

Macrophage Activation↗

PubMedDate not supplied

Regulation of lung fibroblast proliferation and collagen synthesis by alveolar macrophages in experimental silicosis. I: Effect of macrophage conditioned medium from silica instilled rats.

Alveolar macrophages were lavaged from silica or saline instilled rats 0, 3, 7 and 14 days after exposure. Macrophages were cultured for twenty-four hours and the conditioned media assayed for the ability to stimulate rat lung fibroblast proliferation and collagen synthesis. Macrophages remained viable throughout the culture period. DNA synthesis was significantly elevated by macrophage conditioned media (MCM) from silica instilled rats (S-MCM) compared to untreated fibroblasts or fibroblasts exposed to MCM from saline instilled control animals (C-MCM). Stimulation of DNA synthesis was not observed when S-MCM was exposed to non-proliferating fibroblasts. Collagen synthesis quantitated as 3H-hydroxyproline accumulation or percent collagen synthesis was also increased by day 3 and day 7 S-MCM. Specific activity measurements of intracellular 3H-proline minimized the possibility that the increase in 3H-proline incorporation into collagen was a reflection of increased proline transport. Non-collagen protein synthesis was also increased in fibroblasts exposed to day 14 S-MCM. These results suggest that alveolar macrophages elaborate factors following silica exposure capable of altering the DNA and protein synthetic activity of lung fibroblasts. These changes in fibroblast DNA and protein metabolism are similar to those observed for lung tissue in vivo and lend further support to the hypothesis of macrophage mediation of the pulmonary response following silica exposure.

Animals↗

PubMed1988

The interaction of infant formula with macrophages: effect on phagocytic activity, relationship to expression of class II MHC antigen and survival of orally administered macrophages in the neonatal gut.

The effect of infant formula on human peritoneal and breast milk macrophages has been investigated. The ability of peritoneal macrophages to subsequently ingest and degrade immune complexes was slightly impaired, but breast milk cells were not affected. However, the cells were found to have bound antigenically intact casein and beta-lactoglobulin, although little, if any, alpha-lactalbumin was bound. Furthermore, a positive correlation was found between binding of these proteins and expression of HLA-DR antigen. Labelled macrophages fed to newborn mice survived for at least 4 hr in the gastrointestinal tract and, in some cases, localized in the mucosal tissue. In one case a labelled cell was found in the spleen. These findings indicate that breast milk macrophages may be able to perform immunological functions in the gut, and suggest that binding of cows' milk proteins by macrophages may constitute a first step in the sensitization of the neonate to cow's milk proteins. Human milk macrophages may also play a protective role by acting as antigen-presenting cells in the local immune response of the gut.

Animals↗