From Wikipedia, the free encyclopedia
Jump to navigation Jump to search

Phagocytes are cells that protect the body by ingesting harmful foreign particles, bacteria, and dead or dying cells. Their name comes from the Greek phagein, "to eat" or "devour", and "-cyte", the suffix in biology denoting "cell", from the Greek kutos, "hollow vessel",[1] they are essential for fighting infections and for subsequent immunity.[2] Phagocytes are important throughout the animal kingdom[3] and are highly developed within vertebrates.[4] One litre of human blood contains about six billion phagocytes,[5] they were discovered in 1882 by Ilya Ilyich Mechnikov while he was studying starfish larvae.[6] Mechnikov was awarded the 1908 Nobel Prize in Physiology or Medicine for his discovery.[7] Phagocytes occur in many species; some amoebae behave like macrophage phagocytes, which suggests that phagocytes appeared early in the evolution of life.[8]


During an infection, chemical signals attract phagocytes to places where the pathogen has invaded the body; these chemicals may come from bacteria or from other phagocytes already present. The phagocytes move by a method called chemotaxis; when phagocytes come into contact with bacteria, the receptors on the phagocyte's surface will bind to them. This binding will lead to the engulfing of the bacteria by the phagocyte;[13] some phagocytes kill the ingested pathogen with oxidants and nitric oxide.[14] After phagocytosis, macrophages and dendritic cells can also participate in antigen presentation, a process in which a phagocyte moves parts of the ingested material back to its surface; this material is then displayed to other cells of the immune system. Some phagocytes then travel to the body's lymph nodes and display the material to white blood cells called lymphocytes; this process is important in building immunity,[15] and many pathogens have evolved methods to evade attacks by phagocytes.[2]


A bearded old man holding up a test tube. He is sitting at a table by a window; the table is covered with many small bottles and test tubes.
Ilya Ilyich Mechnikov in his laboratory







Phagocytosis is the process of taking in particles such as bacteria, parasites, dead host cells, and cellular and foreign debris by a cell,[21] it involves a chain of molecular processes.[22] Phagocytosis occurs after the foreign body, a bacterial cell, for example, has bound to molecules called "receptors" that are on the surface of the phagocyte; the phagocyte then stretches itself around the bacterium and engulfs it. Phagocytosis of bacteria by human neutrophils takes on average nine minutes.[23] Once inside this phagocyte, the bacterium is trapped in a compartment called a phagosome. Within one minute the phagosome merges with either a lysosome or a granule to form a phagolysosome; the bacterium is then subjected to an overwhelming array of killing mechanisms[24] and is dead a few minutes later.[23] Dendritic cells and macrophages are not so fast, and phagocytosis can take many hours in these cells. Macrophages are slow and untidy eaters; they engulf huge quantities of material and frequently release some undigested back into the tissues; this debris serves as a signal to recruit more phagocytes from the blood.[25] Phagocytes have voracious appetites; scientists have even fed macrophages with iron filings and then used a small magnet to separate them from other cells.[26]

Macrophages have special receptors that enhance phagocytosis (not to scale)


Methods of killing[edit]

Simplified diagram of the phagocytosis and destruction of a bacterial cell


Oxygen-dependent intracellular[edit]

When a phagocyte ingests bacteria (or any material), its oxygen consumption increases; the increase in oxygen consumption, called a respiratory burst, produces reactive oxygen-containing molecules that are anti-microbial.[29] The oxygen compounds are toxic to both the invader and the cell itself, so they are kept in compartments inside the cell; this method of killing invading microbes by using the reactive oxygen-containing molecules is referred to as oxygen-dependent intracellular killing, of which there are two types.[14]

The first type is the oxygen-dependent production of a superoxide,[2] which is an oxygen-rich bacteria-killing substance;[30] the superoxide is converted to hydrogen peroxide and singlet oxygen by an enzyme called superoxide dismutase. Superoxides also react with the hydrogen peroxide to produce hydroxyl radicals, which assist in killing the invading microbe.[2]

The second type involves the use of the enzyme myeloperoxidase from neutrophil granules;[31] when granules fuse with a phagosome, myeloperoxidase is released into the phagolysosome, and this enzyme uses hydrogen peroxide and chlorine to create hypochlorite, a substance used in domestic bleach. Hypochlorite is extremely toxic to bacteria.[2] Myeloperoxidase contains a heme pigment, which accounts for the green color of secretions rich in neutrophils, such as pus and infected sputum.[32]

Oxygen-independent intracellular[edit]


Phagocytes can also kill microbes by oxygen-independent methods, but these are not as effective as the oxygen-dependent ones. There are four main types; the first uses electrically charged proteins that damage the bacterium's membrane. The second type uses lysozymes; these enzymes break down the bacterial cell wall; the third type uses lactoferrins, which are present in neutrophil granules and remove essential iron from bacteria.[33] The fourth type uses proteases and hydrolytic enzymes; these enzymes are used to digest the proteins of destroyed bacteria.[34]


Interferon-gamma—which was once called macrophage activating factor—stimulates macrophages to produce nitric oxide; the source of interferon-gamma can be CD4+ T cells, CD8+ T cells, natural killer cells, B cells, natural killer T cells, monocytes, macrophages, or dendritic cells.[35] Nitric oxide is then released from the macrophage and, because of its toxicity, kills microbes near the macrophage.[2] Activated macrophages produce and secrete tumor necrosis factor; this cytokine—a class of signaling molecule[36]—kills cancer cells and cells infected by viruses, and helps to activate the other cells of the immune system.[37]

In some diseases, e.g., the rare chronic granulomatous disease, the efficiency of phagocytes is impaired, and recurrent bacterial infections are a problem.[38] In this disease there is an abnormality affecting different elements of oxygen-dependent killing. Other rare congenital abnormalities, such as Chédiak–Higashi syndrome, are also associated with defective killing of ingested microbes.[39]



Role in apoptosis[edit]

Apoptosis—phagocytes clear fragments of dead cells from the body



Interactions with other cells[edit]


Antigen presentation[edit]


Antigen presentation is a process in which some phagocytes move parts of engulfed materials back to the surface of their cells and "present" them to other cells of the immune system.[53] There are two "professional" antigen-presenting cells: macrophages and dendritic cells.[54] After engulfment, foreign proteins (the antigens) are broken down into peptides inside dendritic cells and macrophages; these peptides are then bound to the cell's major histocompatibility complex (MHC) glycoproteins, which carry the peptides back to the phagocyte's surface where they can be "presented" to lymphocytes.[15] Mature macrophages do not travel far from the site of infection, but dendritic cells can reach the body's lymph nodes, where there are millions of lymphocytes;[55] this enhances immunity because the lymphocytes respond to the antigens presented by the dendritic cells just as they would at the site of the original infection.[56] But dendritic cells can also destroy or pacify lymphocytes if they recognize components of the host body; this is necessary to prevent autoimmune reactions; this process is called tolerance.[57]

Immunological tolerance[edit]

Dendritic cells also promote immunological tolerance,[58] which stops the body from attacking itself; the first type of tolerance is central tolerance, that occurs in the thymus. T cells that bind (via their T cell receptor) to self antigen (presented by dendritic cells on MHC molecules) too strongly are induced to die; the second type of immunological tolerance is peripheral tolerance. Some self reactive T cells escape the thymus for a number of reasons, mainly due to the lack of expression of some self antigens in the thymus. Another type of T cell; T regulatory cells can down regulate self reactive T cells in the periphery;[59] when immunological tolerance fails, autoimmune diseases can follow.[60]

Professional phagocytes[edit]

Phagocytes derive from stem cells in the bone marrow

Phagocytes of humans and other jawed vertebrates are divided into "professional" and "non-professional" groups based on the efficiency with which they participate in phagocytosis;[9] the professional phagocytes are the monocytes, macrophages, neutrophils, tissue dendritic cells and mast cells.[10] One litre of human blood contains about six billion phagocytes.[5]



In the blood, neutrophils are inactive but are swept along at high speed; when they receive signals from macrophages at the sites of inflammation, they slow down and leave the blood. In the tissues, they are activated by cytokines and arrive at the battle scene ready to kill.[62]


A cartoon depicting a blood vessel and its surrounding tissue cells. There are three similar white blood cells, one in the blood and two among the tissue cells; the ones in the tissue are producing granules that can destroy bacteria.
Neutrophils move from the blood to the site of infection

When an infection occurs, a chemical "SOS" signal is given off to attract phagocytes to the site;[63] these chemical signals may include proteins from invading bacteria, clotting system peptides, complement products, and cytokines that have been given off by macrophages located in the tissue near the infection site.[2] Another group of chemical attractants are cytokines that recruit neutrophils and monocytes from the blood.[13]





Mature macrophages do not travel far but stand guard over those areas of the body that are exposed to the outside world. There they act as garbage collectors, antigen presenting cells, or ferocious killers, depending on the signals they receive,[68] they derive from monocytes, granulocyte stem cells, or the cell division of pre-existing macrophages.[69] Human macrophages are about 21 micrometers in diameter.[70]






Dendritic cells[edit]


Mast cells[edit]


Professional Phagocytes[95]
Main location Variety of phenotypes
Blood neutrophils, monocytes
Bone marrow macrophages, monocytes, sinusoidal cells, lining cells
Bone tissue osteoclasts
Gut and intestinal Peyer's patches macrophages
Connective tissue histiocytes, macrophages, monocytes, dendritic cells
Liver Kupffer cells, monocytes
Lymphoid tissue free and fixed macrophages and monocytes, dendritic cells
Nervous tissue microglial cells (CD4+)
Spleen free and fixed macrophages, monocytes, sinusoidal cells
Thymus free and fixed macrophages and monocytes

Non-professional phagocytes[edit]

Dying cells and foreign organisms are consumed by cells other than the "professional" phagocytes;[96] these cells include epithelial cells, endothelial cells, fibroblasts, and mesenchymal cells. They are called non-professional phagocytes, to emphasize that, in contrast to professional phagocytes, phagocytosis is not their principal function.[97] Fibroblasts, for example, which can phagocytose collagen in the process of remolding scars, will also make some attempt to ingest foreign particles.[98]

Non-professional phagocytes are more limited than professional phagocytes in the type of particles they can take up; this is due to their lack of efficient phagocytic receptors, in particular opsonins—which are antibodies and complement attached to invaders by the immune system.[11] Additionally, most nonprofessional phagocytes do not produce reactive oxygen-containing molecules in response to phagocytosis.[99]

Non-professional Phagocytes[95]
Main location Variety of phenotypes
Blood, lymph and lymph nodes Lymphocytes
Blood Eosinophils and Basophils[100]
Skin Epithelial cells
Blood vessels Endothelial cells
Connective tissue Fibroblasts

Pathogen evasion and resistance[edit]


Avoiding contact[edit]

There are several ways bacteria avoid contact with phagocytes. First, they can grow in sites that phagocytes are not capable of traveling to (e.g., the surface of unbroken skin). Second, bacteria can suppress the inflammatory response; without this response to infection phagocytes cannot respond adequately. Third, some species of bacteria can inhibit the ability of phagocytes to travel to the site of infection by interfering with chemotaxis.[101] Fourth, some bacteria can avoid contact with phagocytes by tricking the immune system into "thinking" that the bacteria are "self". Treponema pallidum—the bacterium that causes syphilis—hides from phagocytes by coating its surface with fibronectin,[103] which is produced naturally by the body and plays a crucial role in wound healing.[104]

Avoiding engulfment[edit]

Bacteria often produce proteins or sugars that coat their cells and interfere with phagocytosis; these are called capsules;[101] some examples are the K5 capsule and O75 O antigen found on the surface of Escherichia coli,[105] and the exopolysaccharide capsules of Staphylococcus epidermidis.[106] Streptococcus pneumoniae produces several types of capsule that provide different levels of protection,[107] and group A streptococci produce proteins such as M protein and fimbrial proteins to block engulfment; some proteins hinder opsonin-related ingestion; Staphylococcus aureus produces Protein A to block antibody receptors, which decreases the effectiveness of opsonins.[108] Enteropathogenic species of the genus Yersinia bind with the use of the virulence factor YopH to receptors of phagocytes from which they influence the cells capability to exert phagocytosis.[109]

Survival inside the phagocyte[edit]

Bacteria have developed ways to survive inside phagocytes, where they continue to evade the immune system.[110] To get safely inside the phagocyte they express proteins called invasins; when inside the cell they remain in the cytoplasm and avoid toxic chemicals contained in the phagolysosomes.[111] Some bacteria prevent the fusion of a phagosome and lysosome, to form the phagolysosome.[101] Other pathogens, such as Leishmania, create a highly modified vacuole inside the phagocyte, which helps them persist and replicate;[112] some bacteria are capable of living inside of the phagolysosome. Staphylococcus aureus, for example, produces the enzymes catalase and superoxide dismutase, which break down chemicals—such as hydrogen peroxide—produced by phagocytes to kill bacteria.[113] Bacteria may escape from the phagosome before the formation of the phagolysosome: Listeria monocytogenes can make a hole in the phagosome wall using enzymes called listeriolysin O and phospholipase C.[114]


Bacteria have developed several ways of killing phagocytes;[108] these include cytolysins, which form pores in the phagocyte's cell membranes, streptolysins and leukocidins, which cause neutrophils' granules to rupture and release toxic substances,[115][116] and exotoxins that reduce the supply of a phagocyte's ATP, needed for phagocytosis. After a bacterium is ingested, it may kill the phagocyte by releasing toxins that travel through the phagosome or phagolysosome membrane to target other parts of the cell.[101]

Disruption of cell signaling[edit]

Some survival strategies often involve disrupting cytokines and other methods of cell signaling to prevent the phagocyte's responding to invasion;[117] the protozoan parasites Toxoplasma gondii, Trypanosoma cruzi, and Leishmania infect macrophages, and each has a unique way of taming them.[117] Some species of Leishmania alter the infected macrophage's signalling, repress the production of cytokines and microbicidal molecules—nitric oxide and reactive oxygen species—and compromise antigen presentation.[118]

Host damage by phagocytes[edit]



Neutrophils also play a key role in the development of most forms of acute lung injury.[121] Here, activated neutrophils release the contents of their toxic granules into the lung environment.[122] Experiments have shown that a reduction in the number of neutrophils lessens the effects of acute lung injury,[123] but treatment by inhibiting neutrophils is not clinically realistic, as it would leave the host vulnerable to infection.[122] In the liver, damage by neutrophils can contribute to dysfunction and injury in response to the release of endotoxins produced by bacteria, sepsis, trauma, alcoholic hepatitis, ischemia, and hypovolemic shock resulting from acute hemorrhage.[124]


Evolutionary origins[edit]

Phagocytosis is common and probably appeared early in evolution,[126] evolving first in unicellular eukaryotes.[127] Amoebae are unicellular protists that separated from the tree leading to metazoa shortly after the divergence of plants, and they share many specific functions with mammalian phagocytic cells.[127] Dictyostelium discoideum, for example, is an amoeba that lives in the soil and feeds on bacteria. Like animal phagocytes, it engulfs bacteria by phagocytosis mainly through Toll-like receptors, and it has other biological functions in common with macrophages.[128] Dictyostelium discoideum is social; it aggregates when starved to form a migrating pseudoplasmodium or slug; this multicellular organism eventually will produce a fruiting body with spores that are resistant to environmental dangers. Before the formation of fruiting bodies, the cells will migrate as a slug-like organism for several days. During this time, exposure to toxins or bacterial pathogens has the potential to compromise survival of the species by limiting spore production; some of the amoebae engulf bacteria and absorb toxins while circulating within the slug, and these amoebae eventually die. They are genetically identical to the other amoebae in the slug; their self-sacrifice to protect the other amoebae from bacteria is similar to the self-sacrifice of phagocytes seen in the immune system of higher vertebrates; this ancient immune function in social amoebae suggests an evolutionarily conserved cellular foraging mechanism that might have been adapted to defense functions well before the diversification of amoebae into higher forms.[129] However, a common ancestry with mammalian phagocytes has not been proven. Phagocytes occur throughout the animal kingdom,[3] from marine sponges to insects and lower and higher vertebrates;[130][131] the ability of amoebae to distinguish between self and non-self is a pivotal one, and is the root of the immune system of many species of amoeba.[8]


  1. ^ a b Little, C., Fowler H.W., Coulson J. (1983). The Shorter Oxford English Dictionary. Oxford University Press (Guild Publishing). pp. 1566–67.CS1 maint: uses authors parameter (link)
  4. ^ Delves et al. 2006, p. 251
  16. ^ Delves et al. 2006, p. 3
  17. ^ Aterman K (April 1, 1998). "Medals, memoirs—and Metchnikoff". J. Leukoc. Biol. 63 (4): 515–17. doi:10.1002/jlb.63.4.515. PMID 9544583. Archived from the original on December 9, 2012. Retrieved December 19, 2014. Cite uses deprecated parameter |dead-url= (help)
  18. ^ "Ilya Mechnikov". The Nobel Foundation. Retrieved December 19, 2014.
  19. ^ Delves et al. 2006, p. 263
  20. ^ Robinson & Babcock 1998, p. vii
  21. ^ Ernst & Stendahl 2006, p. 4
  22. ^ Ernst & Stendahl 2006, p. 78
  23. ^ a b Hampton MB, Vissers MC, Winterbourn CC; Vissers; Winterbourn (February 1994). "A single assay for measuring the rates of phagocytosis and bacterial killing by neutrophils". J. Leukoc. Biol. 55 (2): 147–52. doi:10.1002/jlb.55.2.147. PMID 8301210. Archived from the original on December 28, 2012. Retrieved December 19, 2014. Cite uses deprecated parameter |dead-url= (help)CS1 maint: multiple names: authors list (link)
  25. ^ Sompayrac 2008, p. 3
  26. ^ Sompayrac 2008, p. 2
  27. ^ Sompayrac 2008, pp. 13–16
  28. ^ Dale DC, Boxer L, Liles WC; Boxer; Liles (August 2008). "The phagocytes: neutrophils and monocytes". Blood. 112 (4): 935–45. doi:10.1182/blood-2007-12-077917. PMID 18684880.CS1 maint: multiple names: authors list (link)
  30. ^ Shatwell, KP; AW Segal (1996). "NADPH oxidase". The International Journal of Biochemistry & Cell Biology. 28 (11): 1191–95. doi:10.1016/S1357-2725(96)00084-2. PMID 9022278.
  31. ^ Klebanoff SJ (1999). "Myeloperoxidase". Proc. Assoc. Am. Physicians. 111 (5): 383–89. doi:10.1111/paa.1999.111.5.383. PMID 10519157.
  35. ^ Schroder K, Hertzog PJ, Ravasi T, Hume DA; Hertzog; Ravasi; Hume (February 2004). "Interferon-gamma: an overview of signals, mechanisms and functions". J. Leukoc. Biol. 75 (2): 163–89. doi:10.1189/jlb.0603252. PMID 14525967. Archived from the original on July 3, 2010. Retrieved December 19, 2014. Cite uses deprecated parameter |deadurl= (help)CS1 maint: multiple names: authors list (link)
  36. ^ Delves et al. 2006, p. 188
  37. ^ a b Sompayrac 2008, p. 17
  38. ^ Lipu HN, Ahmed TA, Ali S, Ahmed D, Waqar MA; Ahmed; Ali; Ahmed; Waqar (September 2008). "Chronic granulomatous disease". J Pak Med Assoc. 58 (9): 516–18. PMID 18846805.CS1 maint: multiple names: authors list (link)
  39. ^ Kaplan J, De Domenico I, Ward DM; De Domenico; Ward (January 2008). "Chediak-Higashi syndrome". Curr. Opin. Hematol. 15 (1): 22–29. doi:10.1097/MOH.0b013e3282f2bcce. PMID 18043242. Retrieved December 19, 2014.CS1 maint: multiple names: authors list (link)
  40. ^ Sompayrac 2008, p. 7
  42. ^ Sompayrac 2008, p. 22
  43. ^ Sompayrac 2008, p. 63
  44. ^ "Apoptosis". Merriam-Webster Online Dictionary. Retrieved December 19, 2014.
  45. ^ Li MO, Sarkisian MR, Mehal WZ, Rakic P, Flavell RA; Sarkisian; Mehal; Rakic; Flavell (November 2003). "Phosphatidylserine receptor is required for clearance of apoptotic cells". Science. 302 (5650): 1560–63. doi:10.1126/science.1087621. PMID 14645847.CS1 maint: multiple names: authors list (link) (Free registration required for online access)
  49. ^ Sompayrac 2008, p. 44
  50. ^ Sompayrac 2008, p. 4
  51. ^ Sompayrac 2008, pp. 24–35
  53. ^ Delves et al. 2006, pp. 456
  54. ^ Timothy Lee (2004). "Antigen Presenting Cells (APC)". Immunology for 1st Year Medical Students. Dalhousie University. Archived from the original on January 12, 2008. Retrieved December 19, 2014.
  55. ^ Delves et al. 2006, p. 161
  56. ^ Sompayrac 2008, p. 8
  59. ^ Steinman, Ralph M. (2004). "Dendritic Cells and Immune Tolerance". The Rockefeller University. Retrieved December 19, 2014.
  60. ^ Romagnani, S (2006). "Immunological tolerance and autoimmunity". Internal and Emergency Medicine. 1 (3): 187–96. doi:10.1007/BF02934736. PMID 17120464.
  61. ^ Sompayrac 2008, pp. 16–17
  62. ^ Sompayrac 2008, pp. 18–19
  63. ^ Delves et al. 2006, p. 6
  65. ^ Sompayrac 2008, p. 79
  68. ^ Sompayrac 2008, p. 45
  72. ^ Ernst & Stendahl 2006, p. 8
  73. ^ Delves et al. 2006, p. 156
  74. ^ Delves et al. 2006, p. 187
  75. ^ Stvrtinová, Viera; Ján Jakubovský and Ivan Hulín (1995). "Neutrophils, central cells in acute inflammation". Inflammation and Fever from Pathophysiology: Principles of Disease. Computing Centre, Slovak Academy of Sciences: Academic Electronic Press. ISBN 978-80-967366-1-4. Archived from the original on December 31, 2010. Retrieved December 19, 2014. Cite uses deprecated parameter |deadurl= (help)
  76. ^ Delves et al. 2006, p. 4
  77. ^ a b Sompayrac 2008, p. 18
  80. ^ Soehnlein O, Kenne E, Rotzius P, Eriksson EE, Lindbom L; Kenne; Rotzius; Eriksson; Lindbom (January 2008). "Neutrophil secretion products regulate anti-bacterial activity in monocytes and macrophages". Clin. Exp. Immunol. 151 (1): 139–45. doi:10.1111/j.1365-2249.2007.03532.x. PMC 2276935. PMID 17991288.CS1 maint: multiple names: authors list (link)
  83. ^ a b Steinman, Ralph. "Dendritic Cells". The Rockefeller University. Retrieved December 19, 2014.
  87. ^ Sompayrac 2008, pp. 42–46
  94. ^ Urb M, Sheppard DC (2012). "The role of mast cells in the defence against pathogens". PLoS Pathogens. 8 (4): e1002619. doi:10.1371/journal.ppat.1002619. PMC 3343118. PMID 22577358.
  95. ^ a b Paoletti, Notario & Ricevuti 1997, p. 427
  97. ^ Couzinet S, Cejas E, Schittny J, Deplazes P, Weber R, Zimmerli S; Cejas; Schittny; Deplazes; Weber; Zimmerli (December 2000). "Phagocytic uptake of Encephalitozoon cuniculi by nonprofessional phagocytes". Infect. Immun. 68 (12): 6939–45. doi:10.1128/IAI.68.12.6939-6945.2000. PMC 97802. PMID 11083817.CS1 maint: multiple names: authors list (link)
  100. ^ Lin A, Loré K (2017). "Granulocytes: New Members of the Antigen-Presenting Cell Family". Frontiers in Immunology. 8: 1781. doi:10.3389/fimmu.2017.01781. PMC 5732227. PMID 29321780.
  101. ^ a b c d e Todar, Kenneth. "Mechanisms of Bacterial Pathogenicity: Bacterial Defense Against Phagocytes". 2008. Retrieved December 19, 2014.
  102. ^ Alexander J, Satoskar AR, Russell DG; Satoskar; Russell (September 1999). "Leishmania species: models of intracellular parasitism". J. Cell Sci. 112 (18): 2993–3002. PMID 10462516. Retrieved December 19, 2014.CS1 maint: multiple names: authors list (link)
  105. ^ Burns SM, Hull SI; Hull (August 1999). "Loss of resistance to ingestion and phagocytic killing by O(-) and K(-) mutants of a uropathogenic Escherichia coli O75:K5 strain". Infect. Immun. 67 (8): 3757–62. PMC 96650. PMID 10417134. Retrieved December 19, 2014.
  107. ^ Melin M, Jarva H, Siira L, Meri S, Käyhty H, Väkeväinen M; Jarva; Siira; Meri; Käyhty; Väkeväinen (February 2009). "Streptococcus pneumoniae capsular serotype 19F is more resistant to C3 deposition and less sensitive to opsonophagocytosis than serotype 6B". Infect. Immun. 77 (2): 676–84. doi:10.1128/IAI.01186-08. PMC 2632042. PMID 19047408.CS1 maint: multiple names: authors list (link)
  109. ^ Fällman M, Deleuil F, McGee K (February 2002). "Resistance to phagocytosis by Yersinia". International Journal of Medical Microbiology : IJMM. 291 (6–7): 501–9. doi:10.1078/1438-4221-00159. PMID 11890550.
  119. ^ Paoletti pp. 426–30
  125. ^ Charley B, Riffault S, Van Reeth K; Riffault; Van Reeth (October 2006). "Porcine innate and adaptative immune responses to influenza and coronavirus infections". Ann. N. Y. Acad. Sci. 1081: 130–36. doi:10.1196/annals.1373.014. hdl:1854/LU-369324. PMID 17135502.CS1 maint: multiple names: authors list (link)
  126. ^ Sompayrac 2008, p. 1
  128. ^ Bozzaro S, Bucci C, Steinert M; Bucci; Steinert (2008). Phagocytosis and host-pathogen interactions in Dictyostelium with a look at macrophages. Int Rev Cell Mol Biol. International Review of Cell and Molecular Biology. 271. pp. 253–300. doi:10.1016/S1937-6448(08)01206-9. ISBN 9780123747280. PMID 19081545.CS1 maint: multiple names: authors list (link)
  129. ^ Chen G, Zhuchenko O, Kuspa A; Zhuchenko; Kuspa (August 2007). "Immune-like phagocyte activity in the social amoeba". Science. 317 (5838): 678–81. doi:10.1126/science.1143991. PMC 3291017. PMID 17673666.CS1 maint: multiple names: authors list (link)
  130. ^ Delves et al. 2006, pp. 251–252
  • Ernst, J. D.; Stendahl, O., eds. (2006). Phagocytosis of Bacteria and Bacterial Pathogenicity. New York: Cambridge University Press. ISBN 978-0-521-84569-4. Website
  • Paoletti, R.; Notario, A.; Ricevuti, G., eds. (1997). Phagocytes: Biology, Physiology, Pathology, and Pharmacotherapeutics. New York: The New York Academy of Sciences. ISBN 978-1-57331-102-1.
  • Robinson, J. P.; Babcock, G. F., eds. (1998). Phagocyte Function — A guide for research and clinical evaluation. New York: Wiley–Liss. ISBN 978-0-471-12364-4.

External links[edit]