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For the ecological classification, see Macrophage (ecology). Macrophage_sentence_0


PronunciationMacrophage_header_cell_0_2_0 /ˈmakrə(ʊ)feɪdʒ/Macrophage_cell_0_2_1
SystemMacrophage_header_cell_0_3_0 Immune systemMacrophage_cell_0_3_1
FunctionMacrophage_header_cell_0_4_0 PhagocytosisMacrophage_cell_0_4_1
LatinMacrophage_header_cell_0_6_0 MacrophagocytusMacrophage_cell_0_6_1
Acronym(s)Macrophage_header_cell_0_7_0 Mφ, MΦMacrophage_cell_0_7_1
MeSHMacrophage_header_cell_0_8_0 Macrophage_cell_0_8_1
THMacrophage_header_cell_0_9_0 Macrophage_cell_0_9_1
FMAMacrophage_header_cell_0_10_0 Macrophage_cell_0_10_1

Macrophages (abbreviated as Mφ, MΦ or MP) (Greek: large eaters, from Greek μακρός (makrós) = large, φαγεῖν (phagein) = to eat) are a type of white blood cell of the immune system that engulfs and digests cellular debris, foreign substances, microbes, cancer cells, and anything else that does not have the type of proteins specific to healthy body cells on its surface in a process called phagocytosis. Macrophage_sentence_1

These large phagocytes are found in essentially all tissues, where they patrol for potential pathogens by amoeboid movement. Macrophage_sentence_2

They take various forms (with various names) throughout the body (e.g., histiocytes, Kupffer cells, alveolar macrophages, microglia, and others), but all are part of the mononuclear phagocyte system. Macrophage_sentence_3

Besides phagocytosis, they play a critical role in nonspecific defense (innate immunity) and also help initiate specific defense mechanisms (adaptive immunity) by recruiting other immune cells such as lymphocytes. Macrophage_sentence_4

For example, they are important as antigen presenters to T cells. Macrophage_sentence_5

In humans, dysfunctional macrophages cause severe diseases such as chronic granulomatous disease that result in frequent infections. Macrophage_sentence_6

Beyond increasing inflammation and stimulating the immune system, macrophages also play an important anti-inflammatory role and can decrease immune reactions through the release of cytokines. Macrophage_sentence_7

Macrophages that encourage inflammation are called M1 macrophages, whereas those that decrease inflammation and encourage tissue repair are called M2 macrophages. Macrophage_sentence_8

This difference is reflected in their metabolism; M1 macrophages have the unique ability to metabolize arginine to the "killer" molecule nitric oxide, whereas rodent M2 macrophages have the unique ability to metabolize arginine to the "repair" molecule ornithine. Macrophage_sentence_9

However, this dichotomy has been recently questioned as further complexity has been discovered. Macrophage_sentence_10

Human macrophages are about 21 micrometres (0.00083 in) in diameter and are produced by the differentiation of monocytes in tissues. Macrophage_sentence_11

They can be identified using flow cytometry or immunohistochemical staining by their specific expression of proteins such as CD14, CD40, CD11b, CD64, F4/80 (mice)/EMR1 (human), lysozyme M, MAC-1/MAC-3 and CD68. Macrophage_sentence_12

Macrophages were first discovered by Élie Metchnikoff, a Russian zoologist, in 1884. Macrophage_sentence_13

Structure Macrophage_section_0

Types Macrophage_section_1

Main article: Mononuclear phagocyte system Macrophage_sentence_14

A majority of macrophages are stationed at strategic points where microbial invasion or accumulation of foreign particles is likely to occur. Macrophage_sentence_15

These cells together as a group are known as the mononuclear phagocyte system and were previously known as the reticuloendothelial system. Macrophage_sentence_16

Each type of macrophage, determined by its location, has a specific name: Macrophage_sentence_17


Cell NameMacrophage_cell_1_0_0 Anatomical LocationMacrophage_cell_1_0_1
Adipose tissue macrophagesMacrophage_cell_1_1_0 Adipose tissue (fat)Macrophage_cell_1_1_1
MonocytesMacrophage_cell_1_2_0 Bone marrow / bloodMacrophage_cell_1_2_1
Kupffer cellsMacrophage_cell_1_3_0 LiverMacrophage_cell_1_3_1
Sinus histiocytesMacrophage_cell_1_4_0 Lymph nodesMacrophage_cell_1_4_1
Alveolar macrophages (dust cells)Macrophage_cell_1_5_0 Pulmonary alveoliMacrophage_cell_1_5_1
Tissue macrophages (histiocytes) leading to giant cellsMacrophage_cell_1_6_0 Connective tissueMacrophage_cell_1_6_1
MicrogliaMacrophage_cell_1_7_0 Central nervous systemMacrophage_cell_1_7_1
Hofbauer cellsMacrophage_cell_1_8_0 PlacentaMacrophage_cell_1_8_1
Intraglomerular mesangial cellsMacrophage_cell_1_9_0 KidneyMacrophage_cell_1_9_1
OsteoclastsMacrophage_cell_1_10_0 BoneMacrophage_cell_1_10_1
Epithelioid cellsMacrophage_cell_1_11_0 GranulomasMacrophage_cell_1_11_1
Red pulp macrophages (sinusoidal lining cells)Macrophage_cell_1_12_0 Red pulp of spleenMacrophage_cell_1_12_1
Peritoneal macrophagesMacrophage_cell_1_13_0 Peritoneal cavityMacrophage_cell_1_13_1
LysoMacMacrophage_cell_1_14_0 Peyer's patchMacrophage_cell_1_14_1

Investigations concerning Kupffer cells are hampered because in humans, Kupffer cells are only accessible for immunohistochemical analysis from biopsies or autopsies. Macrophage_sentence_18

From rats and mice, they are difficult to isolate, and after purification, only approximately 5 million cells can be obtained from one mouse. Macrophage_sentence_19

Macrophages can express paracrine functions within organs that are specific to the function of that organ. Macrophage_sentence_20

In the testis, for example, macrophages have been shown to be able to interact with Leydig cells by secreting 25-hydroxycholesterol, an oxysterol that can be converted to testosterone by neighbouring Leydig cells. Macrophage_sentence_21

Also, testicular macrophages may participate in creating an immune privileged environment in the testis, and in mediating infertility during inflammation of the testis. Macrophage_sentence_22

Cardiac resident macrophages participate in electrical conduction via gap junction communication with cardiac myocytes. Macrophage_sentence_23

Macrophages can be classified on basis of the fundamental function and activation. Macrophage_sentence_24

According to this grouping there are classically-activated (M1) macrophages, wound-healing macrophages (also known as alternatively-activated (M2) macrophages), and regulatory macrophages (Mregs). Macrophage_sentence_25

Development Macrophage_section_2

Macrophages that reside in adult healthy tissues either derive from circulating monocytes or are established before birth and then maintained during adult life independently of monocytes. Macrophage_sentence_26

By contrast, most of the macrophages that accumulate at diseased sites typically derive from circulating monocytes. Macrophage_sentence_27

When a monocyte enters damaged tissue through the endothelium of a blood vessel, a process known as leukocyte extravasation, it undergoes a series of changes to become a macrophage. Macrophage_sentence_28

Monocytes are attracted to a damaged site by chemical substances through chemotaxis, triggered by a range of stimuli including damaged cells, pathogens and cytokines released by macrophages already at the site. Macrophage_sentence_29

At some sites such as the testis, macrophages have been shown to populate the organ through proliferation. Macrophage_sentence_30

Unlike short-lived neutrophils, macrophages survive longer in the body, up to several months. Macrophage_sentence_31

Function Macrophage_section_3

Phagocytosis Macrophage_section_4

Main article: Phagocytosis Macrophage_sentence_32

Macrophages are professional phagocytes and are highly specialized in removal of dying or dead cells and cellular debris. Macrophage_sentence_33

This role is important in chronic inflammation, as the early stages of inflammation are dominated by neutrophils, which are ingested by macrophages if they come of age (see CD31 for a description of this process). Macrophage_sentence_34

The neutrophils are at first attracted to a site, where they perform their function and die, before they are phagocytized by the macrophages. Macrophage_sentence_35

When at the site, the first wave of neutrophils, after the process of aging and after the first 48 hours, stimulate the appearance of the macrophages whereby these macrophages will then ingest the aged neutrophils. Macrophage_sentence_36

The removal of dying cells is, to a greater extent, handled by fixed macrophages, which will stay at strategic locations such as the lungs, liver, neural tissue, bone, spleen and connective tissue, ingesting foreign materials such as pathogens and recruiting additional macrophages if needed. Macrophage_sentence_37

When a macrophage ingests a pathogen, the pathogen becomes trapped in a phagosome, which then fuses with a lysosome. Macrophage_sentence_38

Within the phagolysosome, enzymes and toxic peroxides digest the pathogen. Macrophage_sentence_39

However, some bacteria, such as Mycobacterium tuberculosis, have become resistant to these methods of digestion. Macrophage_sentence_40

Typhoidal Salmonellae induce their own phagocytosis by host macrophages in vivo, and inhibit digestion by lysosomal action, thereby using macrophages for their own replication and causing macrophage apoptosis. Macrophage_sentence_41

Macrophages can digest more than 100 bacteria before they finally die due to their own digestive compounds. Macrophage_sentence_42

Role in adaptive immunity Macrophage_section_5

Role in muscle regeneration Macrophage_section_6

The first step to understanding the importance of macrophages in muscle repair, growth, and regeneration is that there are two "waves" of macrophages with the onset of damageable muscle use – subpopulations that do and do not directly have an influence on repairing muscle. Macrophage_sentence_43

The initial wave is a phagocytic population that comes along during periods of increased muscle use that are sufficient to cause muscle membrane lysis and membrane inflammation, which can enter and degrade the contents of injured muscle fibers. Macrophage_sentence_44

These early-invading, phagocytic macrophages reach their highest concentration about 24 hours following the onset of some form of muscle cell injury or reloading. Macrophage_sentence_45

Their concentration rapidly declines after 48 hours. Macrophage_sentence_46

The second group is the non-phagocytic types that are distributed near regenerative fibers. Macrophage_sentence_47

These peak between two and four days and remain elevated for several days during the hopeful muscle rebuilding. Macrophage_sentence_48

The first subpopulation has no direct benefit to repairing muscle, while the second non-phagocytic group does. Macrophage_sentence_49

It is thought that macrophages release soluble substances that influence the proliferation, differentiation, growth, repair, and regeneration of muscle, but at this time the factor that is produced to mediate these effects is unknown. Macrophage_sentence_50

It is known that macrophages' involvement in promoting tissue repair is not muscle specific; they accumulate in numerous tissues during the healing process phase following injury. Macrophage_sentence_51

Role in wound healing Macrophage_section_7

Macrophages are essential for wound healing. Macrophage_sentence_52

They replace polymorphonuclear neutrophils as the predominant cells in the wound by day two after injury. Macrophage_sentence_53

Attracted to the wound site by growth factors released by platelets and other cells, monocytes from the bloodstream enter the area through blood vessel walls. Macrophage_sentence_54

Numbers of monocytes in the wound peak one to one and a half days after the injury occurs. Macrophage_sentence_55

Once they are in the wound site, monocytes mature into macrophages. Macrophage_sentence_56

The spleen contains half the body's monocytes in reserve ready to be deployed to injured tissue. Macrophage_sentence_57

The macrophage's main role is to phagocytize bacteria and damaged tissue, and they also debride damaged tissue by releasing proteases. Macrophage_sentence_58

Macrophages also secrete a number of factors such as growth factors and other cytokines, especially during the third and fourth post-wound days. Macrophage_sentence_59

These factors attract cells involved in the proliferation stage of healing to the area. Macrophage_sentence_60

Macrophages may also restrain the contraction phase. Macrophage_sentence_61

Macrophages are stimulated by the low oxygen content of their surroundings to produce factors that induce and speed angiogenesis and they also stimulate cells that re-epithelialize the wound, create granulation tissue, and lay down a new extracellular matrix. Macrophage_sentence_62

By secreting these factors, macrophages contribute to pushing the wound healing process into the next phase. Macrophage_sentence_63

Role in limb regeneration Macrophage_section_8

Scientists have elucidated that as well as eating up material debris, macrophages are involved in the typical limb regeneration in the salamander. Macrophage_sentence_64

They found that removing the macrophages from a salamander resulted in failure of limb regeneration and a scarring response. Macrophage_sentence_65

Role in iron homeostasis Macrophage_section_9

Main article: Human iron metabolism Macrophage_sentence_66

As described above, macrophages play a key role in removing dying or dead cells and cellular debris. Macrophage_sentence_67

Erythrocytes have a lifespan on average of 120 days and so are constantly being destroyed by macrophages in the spleen and liver. Macrophage_sentence_68

Macrophages will also engulf macromolecules, and so play a key role in the pharmacokinetics of parenteral irons. Macrophage_sentence_69

The iron that is released from the haemoglobin is either stored internally in ferritin or is released into the circulation via ferroportin. Macrophage_sentence_70

In cases where systemic iron levels are raised, or where inflammation is present, raised levels of hepcidin act on macrophage ferroportin channels, leading to iron remaining within the macrophages. Macrophage_sentence_71

Role in pigment retainment Macrophage_section_10

Melanophages are a subset of tissue-resident macrophages able to absorb pigment, either native to the organism or exogenous (such as tattoos), from extracellular space. Macrophage_sentence_72

In contrast to dendritic juncional melanocytes, which synthesize melanosomes and contain various stages of their development, the melanophages only accumulate phagocytosed melanin in lysosome-like phagosomes. Macrophage_sentence_73

This occurs repeatedly as the pigment from dead dermal macrophages is phagocytosed by their successors, preserving the tattoo in the same place. Macrophage_sentence_74

Role in tissue homeostasis Macrophage_section_11

Every tissue harbors its own specialized population of resident macrophages, which entertain reciprocal interconnections with the stroma and functional tissue. Macrophage_sentence_75

These resident macrophages are sessile (non-migratory), provide essential growth factors to support the physiological function of the tissue (e.g. macrophage-neuronal crosstalk in the guts), and can actively protect the tissue from inflammatory damage. Macrophage_sentence_76

Clinical significance Macrophage_section_12

Due to their role in phagocytosis, macrophages are involved in many diseases of the immune system. Macrophage_sentence_77

For example, they participate in the formation of granulomas, inflammatory lesions that may be caused by a large number of diseases. Macrophage_sentence_78

Some disorders, mostly rare, of ineffective phagocytosis and macrophage function have been described, for example. Macrophage_sentence_79

As a host for intracellular pathogens Macrophage_section_13

In their role as a phagocytic immune cell macrophages are responsible for engulfing pathogens to destroy them. Macrophage_sentence_80

Some pathogens subvert this process and instead live inside the macrophage. Macrophage_sentence_81

This provides an environment in which the pathogen is hidden from the immune system and allows it to replicate. Macrophage_sentence_82

Diseases with this type of behaviour include tuberculosis (caused by Mycobacterium tuberculosis) and leishmaniasis (caused by Leishmania species). Macrophage_sentence_83

In order to minimize the possibility of becoming the host of an intracellular bacteria, macrophages have evolved defense mechanisms such as induction of nitric oxide and reactive oxygen intermediates, which are toxic to microbes. Macrophage_sentence_84

Macrophages have also evolved the ability to restrict the microbe's nutrient supply and induce autophagy. Macrophage_sentence_85

Tuberculosis Macrophage_section_14

Once engulfed by a macrophage, the causative agent of tuberculosis, Mycobacterium tuberculosis, avoids cellular defenses and uses the cell to replicate. Macrophage_sentence_86

Leishmaniasis Macrophage_section_15

Upon phagocytosis by a macrophage, the Leishmania parasite finds itself in a phagocytic vacuole. Macrophage_sentence_87

Under normal circumstances, this phagocytic vacuole would develop into a lysosome and its contents would be digested. Macrophage_sentence_88

Leishmania alter this process and avoid being destroyed; instead, they make a home inside the vacuole. Macrophage_sentence_89

Chikungunya Macrophage_section_16

Infection of macrophages in joints is associated with local inflammation during and after the acute phase of Chikungunya (caused by CHIKV or Chikungunya virus). Macrophage_sentence_90

Others Macrophage_section_17

Adenovirus (most common cause of pink eye) can remain latent in a host macrophage, with continued viral shedding 6–18 months after initial infection. Macrophage_sentence_91

Brucella spp. can remain latent in a macrophage via inhibition of phagosomelysosome fusion; causes brucellosis (undulant fever). Macrophage_sentence_92

Legionella pneumophila, the causative agent of Legionnaires' disease, also establishes residence within macrophages. Macrophage_sentence_93

Heart disease Macrophage_section_18

Macrophages are the predominant cells involved in creating the progressive plaque lesions of atherosclerosis. Macrophage_sentence_94

Focal recruitment of macrophages occurs after the onset of acute myocardial infarction. Macrophage_sentence_95

These macrophages function to remove debris, apoptotic cells and to prepare for tissue regeneration. Macrophage_sentence_96

HIV infection Macrophage_section_19

Macrophages also play a role in human immunodeficiency virus (HIV) infection. Macrophage_sentence_97

Like T cells, macrophages can be infected with HIV, and even become a reservoir of ongoing virus replication throughout the body. Macrophage_sentence_98

HIV can enter the macrophage through binding of gp120 to CD4 and second membrane receptor, CCR5 (a chemokine receptor). Macrophage_sentence_99

Both circulating monocytes and macrophages serve as a reservoir for the virus. Macrophage_sentence_100

Macrophages are better able to resist infection by HIV-1 than CD4+ T cells, although susceptibility to HIV infection differs among macrophage subtypes. Macrophage_sentence_101

Cancer Macrophage_section_20

Macrophages can contribute to tumor growth and progression by promoting tumor cell proliferation and invasion, fostering tumor angiogenesis and suppressing antitumor immune cells. Macrophage_sentence_102

Attracted to oxygen-starved (hypoxic) and necrotic tumor cells they promote chronic inflammation. Macrophage_sentence_103

Inflammatory compounds such as tumor necrosis factor (TNF)-alpha released by the macrophages activate the gene switch nuclear factor-kappa B. Macrophage_sentence_104

NF-κB then enters the nucleus of a tumor cell and turns on production of proteins that stop apoptosis and promote cell proliferation and inflammation. Macrophage_sentence_105

Moreover, macrophages serve as a source for many pro-angiogenic factors including vascular endothelial factor (VEGF), tumor necrosis factor-alpha (TNF-alpha), Macrophage colony-stimulating factor (M-CSF/CSF1) and IL-1 and IL-6 contributing further to the tumor growth. Macrophage_sentence_106

Macrophages have been shown to infiltrate a number of tumors. Macrophage_sentence_107

Their number correlates with poor prognosis in certain cancers including cancers of breast, cervix, bladder, brain and prostate. Macrophage_sentence_108

Tumor-associated macrophages (TAMs) are thought to acquire an M2 phenotype, contributing to tumor growth and progression. Macrophage_sentence_109

Some tumors can also produce factors, including M-CSF/CSF1, MCP-1/CCL2 and Angiotensin II, that trigger the amplification and mobilization of macrophages in tumors. Macrophage_sentence_110

Research in various study models suggests that macrophages can sometimes acquire anti-tumor functions. Macrophage_sentence_111

For example, macrophages may have cytotoxic activity to kill tumor cells directly; also the co-operation of T-cells and macrophages is important to suppress tumors. Macrophage_sentence_112

This co-operation involves not only the direct contact of T-cell and macrophage, with antigen presentation, but also includes the secretion of adequate combinations of cytokines, which enhance T-cell antitumor activity. Macrophage_sentence_113

Recent study findings suggest that by forcing IFN-α expression in tumor-infiltrating macrophages, it is possible to blunt their innate protumoral activity and reprogram the tumor microenvironment toward more effective dendritic cell activation and immune effector cell cytotoxicity. Macrophage_sentence_114

Additionally, subcapsular sinus macrophages in tumor-draining lymph nodes can suppress cancer progression by containing the spread of tumor-derived materials. Macrophage_sentence_115

Cancer therapy Macrophage_section_21

Experimental studies indicate that macrophages can affect all therapeutic modalities, including surgery, chemotherapy, radiotherapy, immunotherapy and targeted therapy. Macrophage_sentence_116

Macrophages can influence treatment outcomes both positively and negatively. Macrophage_sentence_117

Macrophages can be protective in different ways: they can remove dead tumor cells (in a process called phagocytosis) following treatments that kill these cells; they can serve as drug depots for some anticancer drugs; they can also be activated by some therapies to promote antitumor immunity. Macrophage_sentence_118

Macrophages can also be deleterious in several ways: for example they can suppress various chemotherapies, radiotherapies and immunotherapies. Macrophage_sentence_119

Because macrophages can regulate tumor progression, therapeutic strategies to reduce the number of these cells, or to manipulate their phenotypes, are currently being tested in cancer patients. Macrophage_sentence_120

However, macrophages are also involved in antibody mediated cytotoxicity (ADCC)and this mechanism has been proposed to be important for certain cancer immunotherapy antibodies. Macrophage_sentence_121

Obesity Macrophage_section_22

It has been observed that increased number of pro-inflammatory macrophages within obese adipose tissue contributes to obesity complications including insulin resistance and diabetes type 2. Macrophage_sentence_122

Within the fat (adipose) tissue of CCR2 deficient mice, there is an increased number of eosinophils, greater alternative macrophage activation, and a propensity towards type 2 cytokine expression. Macrophage_sentence_123

Furthermore, this effect was exaggerated when the mice became obese from a high fat diet. Macrophage_sentence_124

This is partially caused by a phenotype switch of macrophages induced by necrosis of fat cells (adipocytes). Macrophage_sentence_125

In an obese individual some adipocytes burst and undergo necrotic death, which causes the residential M2 macrophages to switch to M1 phenotype. Macrophage_sentence_126

This is one of the causes of a low-grade systemic chronic inflammatory state associated with obesity. Macrophage_sentence_127

Intestinal macrophages Macrophage_section_23

Though very similar in structure to tissue macrophages, intestinal macrophages have evolved specific characteristics and functions given their natural environment, which is in the digestive tract. Macrophage_sentence_128

Macrophages and intestinal macrophages have high plasticity causing their phenotype to be altered by their environments. Macrophage_sentence_129

Like macrophages, intestinal macrophages are differentiated monocytes, though intestinal macrophages have to coexist with the microbiome in the intestines. Macrophage_sentence_130

This is a challenge considering the bacteria found in the gut are not recognized as "self" and could be potential targets for phagocytosis by the macrophage. Macrophage_sentence_131

To prevent the destruction of the gut bacteria, intestinal macrophages have developed key differences compared to other macrophages. Macrophage_sentence_132

Primarily, intestinal macrophages do not induce inflammatory responses. Macrophage_sentence_133

Whereas tissue macrophages release various inflammatory cytokines, such as IL-1, IL-6 and TNF-α, intestinal macrophages do not produce or secrete inflammatory cytokines. Macrophage_sentence_134

This change is directly caused by the intestinal macrophages environment. Macrophage_sentence_135

Surrounding intestinal epithelial cells release TGF-β, which induces the change from proinflammatory macrophage to noninflammatory macrophage. Macrophage_sentence_136

Even though the inflammatory response is downregulated in intestinal macrophages, phagocytosis is still carried out. Macrophage_sentence_137

There is no drop off in phagocytosis efficiency as intestinal macrophages are able to effectively phagocytize the bacteria,S. Macrophage_sentence_138

typhimurium and E. Macrophage_sentence_139 coli, but intestinal macrophages still do not release cytokines, even after phagocytosis. Macrophage_sentence_140

Also, intestinal macrophages do not express lipoplysaccharide (LPS), IgA, or IgG receptors. Macrophage_sentence_141

The lack of LPS receptors is important for the gut as the intestinal macrophages do not detect the microbe-associated molecular patterns (MAMPS/PAMPS) of the intestinal microbiome. Macrophage_sentence_142

Nor do they express IL-2 and IL-3 growth factor receptors. Macrophage_sentence_143

Role in disease Macrophage_section_24

Intestinal macrophages have been shown to play a role in inflammatory bowel disease (IBD), such as Crohn's disease (CD) and ulcerative colitis (UC). Macrophage_sentence_144

In a healthy gut, intestinal macrophages limit the inflammatory response in the gut, but in a disease-state, intestinal macrophage numbers and diversity are altered. Macrophage_sentence_145

This leads to inflammation of the gut and disease symptoms of IBD. Macrophage_sentence_146

Intestinal macrophages are critical in maintaining gut homeostasis. Macrophage_sentence_147

The presence of inflammation or pathogen alters this homeostasis, and concurrently alters the intestinal macrophages. Macrophage_sentence_148

There has yet to be a determined mechanism for the alteration of the intestinal macrophages by recruitment of new monocytes or changes in the already present intestinal macrophages. Macrophage_sentence_149

Media Macrophage_section_25


  • Macrophage_item_0_0
  • Macrophage_item_0_1

History Macrophage_section_26

See also Macrophage_section_27


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