Which cells engulf and digest antigens

A macrophage is the first cell to recognize and engulf foreign substances antigens. Macrophages break down these substances and present the smaller proteins to the T lymphocytes. T cells are programmed to recognize, respond to and remember antigens.

Macrophages also produce substances called cytokines that help to regulate the activity of lymphocytes. Dendritic cells are known as the most efficient antigen-presenting cell type with the ability to interact with T cells and initiate an immune response. Dendritic cells are receiving increasing scientific and clinical interest due to their key role in the immune response and potential use with tumor vaccines.

There are different types of white blood cells that are part of the immune response. Neutrophils or granulocytes are the most common immune cells in the body.

A cytokine is a chemical messenger that regulates cell differentiation form and function , proliferation production , and gene expression to affect immune responses.

At least 40 types of cytokines exist in humans that differ in terms of the cell type that produces them, the cell type that responds to them, and the changes they produce. One type cytokine, interferon, is illustrated in Figure One subclass of cytokines is the interleukin IL , so named because they mediate interactions between leukocytes white blood cells.

Interleukins are involved in bridging the innate and adaptive immune responses. In addition to being released from cells after PAMP recognition, cytokines are released by the infected cells which bind to nearby uninfected cells and induce those cells to release cytokines, which results in a cytokine burst. A second class of early-acting cytokines is interferons, which are released by infected cells as a warning to nearby uninfected cells.

One of the functions of an interferon is to inhibit viral replication. They also have other important functions, such as tumor surveillance. Interferons work by signaling neighboring uninfected cells to destroy RNA and reduce protein synthesis, signaling neighboring infected cells to undergo apoptosis programmed cell death , and activating immune cells.

One effect of interferon-induced gene expression is a sharply reduced cellular protein synthesis. Virally infected cells produce more viruses by synthesizing large quantities of viral proteins. Thus, by reducing protein synthesis, a cell becomes resistant to viral infection. The first cytokines to be produced are pro-inflammatory; that is, they encourage inflammation , the localized redness, swelling, heat, and pain that result from the movement of leukocytes and fluid through increasingly permeable capillaries to a site of infection.

The population of leukocytes that arrives at an infection site depends on the nature of the infecting pathogen. Both macrophages and dendritic cells engulf pathogens and cellular debris through phagocytosis.

A neutrophil is also a phagocytic leukocyte that engulfs and digests pathogens. Neutrophils, shown in Figure Neutrophils have a nucleus with two to five lobes, and they contain organelles, called lysosomes, that digest engulfed pathogens. An eosinophil is a leukocyte that works with other eosinophils to surround a parasite; it is involved in the allergic response and in protection against helminthes parasitic worms.

Neutrophils and eosinophils are particularly important leukocytes that engulf large pathogens, such as bacteria and fungi. A mast cell is a leukocyte that produces inflammatory molecules, such as histamine, in response to large pathogens. A basophil is a leukocyte that, like a neutrophil, releases chemicals to stimulate the inflammatory response as illustrated in Figure Basophils are also involved in allergy and hypersensitivity responses and induce specific types of inflammatory responses.

Eosinophils and basophils produce additional inflammatory mediators to recruit more leukocytes. Your own MHC molecules define your tissue type which is the major barrier to successful organ transplantation, and the reason we keep records of the tissue type of potential donors.

Even an individual with the commonest set of HLA genes found in the U. This is also why your best chance of finding a compatible donor is searching among your close relatives, with whom you share genes. Of course, the complexity of this system did not arise to frustrate transplant surgeons.

The immune system uses it, because each of these many different MHC molecules presents a unique selection of antigens processed from the same underlying proteins. For example, the antigens that are presented from the liver of one person will be different from the antigens presented from the liver of an unrelated person.

In this way, the representation of self established by an individual's MHC, presenting its self-proteins to its own lymphocytes, is a very private system of identification that is difficult to copy, allowing the immune system to discriminate between foreign tissue transplants, invading infections and cancerous cells.

This receptor is part of a complicated structure called the TCR complex it is formed by the combination of six different protein chains in four pairs. They are often omitted from cartoons that show the TCR at the cell surface.

In essence, each TCR measures the affinity of this interaction and provides a read-out to the T-cell which determines the subsequent response of that cell. An activated TCR sends signals across the cytoplasm of the cell to the nucleus where it initiates programmes that change the pattern of genes that are being expressed and therefore some of the proteins made by the cell.

The peptide antigen can just be seen at the interface between the two receptors. Complementing the wide variety of possible MHC molecules, TCRs need a comparable level of diversity to ensure the availability of suitable receptors.

This is achieved through a modular approach to building up the receptor. These are joined together in a process that also adds random mutation. This means that at any time there are many more possible ways and individual can make TCRs that there are T-cells in the body. Each T-cell carries multiple copies of a single unique TCR. Because making a TCR involves random recombination, this is quite a wasteful process, and only a small fraction of the T-cells produced will have TCRs with optimal biochemical properties.

To test for these characteristics, T-cells first pass through a specialized organ called the thymus which gives T-cells their name, T for thymus. For the T-cell to survive selection, the TCR must be useful. It must be able to ignore self-antigens in MHC complexes, but must still bind the MHC molecule strongly enough to interact with the peptide antigen. If this binding is too weak, the cell is discarded. TCRs that produce strong activation by self-antigens are dangerous and they are also removed by screening Figure 6.

To match these stringent requirements, the immune system is prepared to throw away more than 19 out of 20 of the T-cells that it makes.

The result is a population of T-cells with a repertoire of TCRs that recognize self-antigen weakly, have the potential to recognize non-self-antigen strongly, and can safely be exported from the thymus. The code for the part of the TCR that recognizes antigen are selected at random from these sequences.

Different structural elements are combined to make the final TCR. The resulting receptor is expressed at the cell surface and tested in the thymus. B Cells bearing each TCR are put through a number of screening tests. If it passes these tests, it is exported from the thymus. In a healthy person, these exported T-cells move continuously between lymph nodes and the blood, testing APCs for signs of infection. Usually they do not encounter activation signals and they move on.

After several weeks, they will be replaced by younger cells, newly exported from the thymus, carrying their own unique TCRs. But when an individual develops an infection, and antigens from this infection begin to be displayed on APCs that are scanned by T-cells, a few of the millions of different T-cells will have TCRs that trigger activation of the T-cell. First this stimulates the cell to divide, producing daughter cells with the same TCR. Instead of the blood only holding a handful of infection-specific T-cells, this expansion leads to it having first thousands and then millions.

These cells also acquire an ability to act Figure 2. As the infection progresses, responding cells become more specialized, developing different effector functions that optimize how the immune system attacks it. The other crucial recognition system of the adaptive immune response, antibodies that are produced by B-cells , go through a process of maturation and selection that serves to greatly increase the strength with which they bind their target antigen.

Antibodies are very different from T-cells because, although they start as a cell-surface receptor [the B-cell receptor BCR ], they are later secreted and can function well in many places that T-cells do not. Once they have been produced, they are an efficient early defence in cases of reinfection, able to bind to pathogens that breach external barriers. They can also neutralize soluble poisons toxins that some organisms produce, which is very important, for example, in the response to diphtheria.

Antibodies circulate in the blood, are found within the mucus that lines our gastrointestinal organs and also in interstitial tissue fluids. Mothers pass antibodies to their children through their breast milk. Like TCRs, antibodies are adapted to specific infections by selection from a pool of randomly generated candidates, through a series of selection steps called affinity maturation that promote optimal function Figure 7.

But, unlike TCRs, antibodies can recognize whole proteins before they have been broken down into peptides. The majority of antibodies recognize proteins in their native state, folded up, with different chains and loops contributing to a patch on their surface to which the antibody binds. Because of this antibodies often focus on the outside of pathogens.

And, as a defence, some pathogens, from the influenza virus to the malaria parasite, have developed processes that continuously change how they look at the surface, as a way to escape the immune system. Antibodies that fit quite well are selected early in the immune response.

The antibody receptor BCR is mutated within daughter cells. Many of these mutations bind the antigen worse than the parent antibody, and cells producing these antibodies die. Some antibodies bind the antigen better than the parent, and these cells live. Antibody production starts in specialized immune system tissues.

When a pathogen invades, antigens from it are carried to areas inside lymph nodes or the spleen by APCs. B-cells that have a BCR that can bind to these antigens are activated, take in and process antigen and load it into their MHC molecules.

This prepares them to receive signals that stimulate growth and affinity maturation from T-cells that recognize these same antigens.

B-cells and T-cells attract each other and this mutual attraction facilitates encounters between rare antigen-specific B- and T-cells. The help that T-cells provide to the B-cell promotes secretion of antibody, changes in the isotype of antibody that is secreted, and stimulates mutation of the genes that code for the BCR.

Because the mutations occur at random, most of them actually impair the ability of the BCR to bind antigen, another expensive process in which the immune system is prepared to throw away many cells to select the best one. A fraction of the mutations improve the binding affinity of the BCR, making it stronger.

Cells with BCRs of a higher affinity compete better for reducing amounts of antigen and are selected to live, whereas their less effective siblings die. By repeating this process several times, the affinity of the antibodies that are being made can increase by many orders of magnitude.

The high specificity that antibodies offer have made them an extremely flexible and effective medical technology.

Isotype switching permits antibodies to be directed into different roles. By rearranging the genes that specify the heavy chain of the antibody, Igs can be optimized for different environments and functions.

Because the antigen-recognizing domains of the antibodies do not change when a molecule with a new heavy chain is produced, each clone of B-cells maintains its specificity. A summary of the functions of different isotypes is given in Table 2.

Discrimination is also a key aspect of the innate immune system. This is an area of research that has grown explosively since studies at the close of the 20th Century identified families of receptors that sampled the environment for the presence of molecules associated with pathogens called pathogen-associated molecular patterns; PAMPs.

One of the first pathways of this kind to be worked out in detail exploited the discovery that a receptor cloned from insects, and implicated in their sensitivity to infection, was related to the gene for a similar protein that could be found in mammalian cells. This molecule, called Toll-like receptor 4 TLR4 is a key mediator of the effects of sepsis in patients critically sick with infections.

When it binds to bacteria, TLR4 triggers the release of cytokines that stimulate the whole immune system producing fever and, in the seriously ill, shock. TLR4 signalling can trigger the activation and recruitment of neutrophils and macrophages that can kill or limit the spread of infection at an early stage, allowing time for the adaptive immune response to develop. Receptors that recognize PAMPs are found both outside and inside cells.

As a group, these innate immune system receptors survey the environment for everything from viruses to fungal infections. The scope of this sensing network is an indication of the importance that an early reaction to infection plays in the survival of its victim. Innate immune responses slow infections down, giving the rest of the immune system time to catch up. The discrimination of appropriate targets that require an immune response from those that do not is the key to immunity.

Unleashing the immune system is a risky business. If the reaction is too strong, it can kill its host. If it is not strong enough, the infection may do the same. To carry out this difficult balancing act, the immune system comes with many checks that operate as the response to a pathogen progresses. The need for co-stimulation was deduced once it was understood that the immune system could generate antigen-specific receptors at random and throughout life.

By continuously making new and unique T-cells and B-cells, there is a constant risk of producing an autoreactive antigen-specific cell that targets self-antigens.

To explain how receptors that recognize self-antigens could be turned off rather than on, if they bound a self-antigen, it was suggested that full activation of immunity required two signals, one from the antigen-specific receptor and a second from a hypothetical co-stimulatory pathway.

This insight, developed ahead of the description of the receptor pathways by which it operated, was very fruitful in explaining how antigen-specific signalling could have two apparently opposite effects, one shutting down the cell, the other spurring full activation. By adding a checking mechanism to the activation process, the immune system increases its discriminatory power, reducing the risk of errors.

As these mechanisms became elucidated down to the level of individual signalling pathways, it was possible to uncover how this strategy has been applied to a number of different types of immune cell interaction.

Another important check is provided by antigen-specific T-cells that shut down responses. These are called T regulatory cells. This population is devoted to negative feedback, limiting dangerous responses to autoantigens.

In summary, immune discrimination is distributed across many cell types. It depends on recognizing the molecular signatures of the diverse world of pathogens. By using a highly variable family of MHC molecules that are essentially unique for each individual, every immune system sees the world of pathogens differently, making it difficult for infection to develop an effective disguise.

By constant surveillance, the immune system provides a safe space to carry out normal functions of life. And, as a bonus, the immune system can carry on learning, so that long-lived animals that are exposed to new rapidly dividing infections, have recourse to real-time evolution of immune memory that can defeat infection.

The most desirable immune response is one that stops an infection in its tracks, before it has established a foothold in the body. Phagocytosis of bacteria in the tissues and antibody-mediated blockade of virus entry into cells work this way.

But if, once an infection was established within a cell, the immune system did no more, or if a cell that had turned into a cancer was ignored, viruses and cancers would be unstoppable. To deal with these eventualities, cells of the immune system control powerful lethal weapons. This ability is so striking that the cells that specialize in execution are known as cytotoxic killer cells. Killers discriminate by using recognition receptors.

In this way, they can interrogate any nucleated cell in the body. When cytotoxic T-cells recognize an infected target cell, they kill it rapidly and move on to the next cell. Natural killer cells , part of the innate response, use a different approach to selecting their targets. These cells patrol the body asking themselves whether the tissues that they survey express MHC I molecules. If the cells that are being examined do, then they move on, but if not, they will become activated and kill.

This provides an alternative method of surveillance, which does not depend on specific antigen, and frustrates a strategy that some pathogens employ, of inhibiting the surface expression of MHC I. By insisting that nucleated cells report on their protein production, the window of opportunity that viruses have to squeeze through to be successful is narrowed further.

Cell killing is a specialized function that occurs in a series of steps. First the cytotoxic cells make close contact with the target and mobilizes intracellular granules to this area of contact. Then these granules fuse with the cell membrane of the cytotoxic cell and release a number of proteins. One, called perforin , forms a pore in the cell membrane of the target. This pore allows the entry of other proteins called granzymes that trigger rapid cell death. A second pathway, that probably plays a minor role in cytotoxicity, is that involving a receptor on the cytotoxic cells called FasL binding to its partner on the target cell called Fas.

This interaction triggers a suicide signal within the target cell. All cells are able to commit suicide and this type of cell death is called apoptosis ; it is very important in development and in the immune system. In the thymus, where, as explained above, most of the lymphocytes that audition for a role as useful effector cells die, it is through the process of apoptosis that this occurs. Apoptosis also frustrates some viral infections and protects individual cells from becoming cancerous.

Cancers only develop if they have mutations that block the activation of apoptosis, and viruses produce proteins to stop apoptosis switching on. In this way, the transformed or infected cell can survive signals that would otherwise lead to it killing itself. The final common pathway of apoptosis is a proteolytic cascade which digests the contents of the cell and fragments its genetic material; the cell shrivels up and exposes signals at its surface that tell neighbouring phagocytes to eat it.

The enzymes that carry out this process come from a family called caspases cysteine proteases that cleave proteins after aspartic acid residues.

There are several different ways to initiate this process, but they share a common final pathway. This means that cells can die without initiating an effector immune response. In contrast, in an aggressive infection, where cells death occurs alongside signals that stimulate innate immune activation, accompanying adaptive responses will also occur. Successful immune responses reach an appropriate match between the threat and the response, producing enough killing to manage infection, but not so much that the host is compromised.

If this is not achieved, the outcome may be disastrous in the short-term, because an infection is not controlled, or because the immune response is so aggressive that the body collapses. Or dangerous in the long-term because a chronic infection becomes established or because the immune system over-reacts and develops specific responses that attack healthy tissue.

Developing precisely targeted adaptive immunity is a core capacity of the immune response, but there are many other important and interlocking effector functions which are essential to successfully overcoming colonization by a pathogen, or adapting to live with long-term infection.

As our understanding of them continues to grow, we learn how to exploit these mechanisms to treat disease. But we can also look back at the beginning of immunology and see how many of the themes were established early in the history of the science. In , a Russian refugee called Elie Metchnikoff carried out an experiment on starfish larvae. He put small thorns into them and when he returned the next morning to study the result microscopically, he discovered that the thorns were surrounded by cells.

This experiment changed the course of his research, alerting him to the importance of cellular function in immune responses. In subsequent decades, following this discovery, there was a fierce debate weighing up the relative importance of such cells.

We now understand that they are a crucial element that functions alongside antibodies and complement activation fighting infection. Phagocytes are part of the first wave of response to many kinds of infection. Two types of cell, called neutrophils and monocytes, are produced and stored in reservoirs in the bone marrow. Early soluble signals, released into the blood in response to infection, stimulate increased cell production in the bone marrow and the release of phagocytes into the circulation, where they can be detected as a sign of infection by blood tests measuring white cell numbers.

This early mobilization can slow down the spread of pathogens, trapping them locally and hindering their growth. Macrophages and neutrophils also produce toxic chemicals that kill, and enzymes that disrupt tissue.

For the individual cells, this is a suicidal strategy: they are sacrificed to end infection. This destruction can result in the formation of an abscess; a collection of dead immune cells and dead bacteria. Such a focus of infection can be relatively benign, if it is localized to peripheral soft tissues and heals quickly.

The same kind of response in a more vulnerable tissue, such as the kidney or the eye, can cause irreversible damage. It may eliminate the infection, but destroy the function of the organ that has been affected. Healing that is delayed or incomplete, because the infection cannot be cleared, can produce chronic damage and long-term disability. Antibiotic therapy is some help, but chronic infection of this kind continues to be a cause of illness and disability worldwide.

Eating infections is not without risk for the phagocyte. Following engulfment, the target is surrounded in a structure a phagosome that fuses with a second organelle called a lysosome, which provides enzymes to digest the bacteria. These enzymes are activated by lowering the pH of the environment. Certain infections, such as tuberculosis caused by Mycobacterium tuberculosis and Legionnaire's disease cause by Legionella pneumophila resist this process, inhibit the fusion of the phagosome with the lysosome, and use this route as a way to hide from adaptive immune responses and to disseminate throughout the body.

Here the adaptive and innate immune responses can be seen to be co-operating to destroy an infection that is hidden within cells. Adaptive immune responses can also be very important in interrupting the development of disease.

It takes time to produce specific antibodies, because they only develop naturally during and after an episode of infectious disease. Getting the immune system to generate them, without suffering from the disease, can be brought about by vaccination as discussed below.

If they are present, antibodies activate the immune system with speed and specificity. Their exceptional sensitivity facilitates a rapid and targeted response, which can halt an infection before it provokes any symptoms. Antibodies interrupt the transmission of viruses by binding to surface proteins needed for cell entry. The different strategies that viruses use to enter cells all depend on specific molecular recognition. Interfering with this specific binding process will stop the virus in its tracks.

This kind of neutralization is also effective against protein toxins, such as the diphtheria toxin, that bind to a receptor at the cell surface as the first step in their attack. Specific antibody that binds the molecules needed for cell entry by a virus or by a toxin prevents disease developing.

Antibodies do not just interfere with entry into cells. Natural antibodies are all bifunctional Figure 1. At one end is the structure that mediates specific recognition called the Fab fragment , but at the other is a tail called the Fc fragment that engages directly with other elements of the immune system.

Some Fc tails bind and activate complement protein that are present in the blood. This starts a powerful proteolytic cascade that forms pores on the surface of bacteria and punch through their tough cell walls, killing them and leaving them for disposal by phagocytes.

Another type of Fc tail produces an isotype called IgE, attaches antibodies to the surface of granulocyte cells. If they encounter an antigen that they recognize they signal the granulocytes to release inflammatory mediators such as histamines and leukotrienes.

These responses are especially relevant in immunity to parasites and in diseases such as asthma and allergy. The Fc part of an antibody molecule is also used as a signal to transport it across cell barriers. The majority of new antibody that a healthy human produces ends up outside the body in the intestines and in the lungs.

Once in these mucosal locations, such antibodies can bind and neutralize pathogens and toxins, before they have the opportunity to cross into the circulation. Because all antibodies facilitate specific recognition but have tails that deliver different functions, they are named on the basis of their tails Table 2.

The path that immune responses follow does not always lead to the complete elimination of infection. Cold sores caused by herpesviruses and tuberculosis are two examples of pathogens that achieve long-term colonization in susceptible individuals. When we study antigen-specific immune cells in these circumstances, they appear to be very different from both naive cells and effector cells. Aggressive immune responses are shut down in two ways.

The first is intrinsic to the cells that have been attacking the infection, and depends on the up-regulation of co-inhibitory receptors on the cell surface. Signals from these co-inhibitory receptors switch off attacking functions, such as cell killing, and terminate local destruction of tissue and of pathogen-infected cells. This is a trade-off between continuing damage and tolerating the presence of infected cells. The extrinsic type of regulation is the expansion of the antigen-specific T-regulatory cells, which secrete anti-inflammatory cytokines that limit immunity and promote tissue healing.

Regulatory cells, which are stimulated by tissue antigens, play a very important role in managing the immune system. Mutations that cripple them cause severe autoimmune disease in animals and people, showing how crucial the control of immune responses is to health. These regulating pathways are meant to be beneficial, but they can be exploited by disease.

This is particularly significant in cancer. Tumours are commonly infiltrated by many different types of immune cell. But although these cells can often respond to cancer antigens, they do not succeed in killing the tumour, and this is because successful cancers produce signals that drive the immune system towards self-regulation, shutting off aggressive potentially tumour-destroying effector mechanisms.

Reviewing how the immune system manages an infection, there is a clear pattern. In the beginning, signals attract early non-specific cells that can kill and limit spread, then there is an explosive adaptive immune response that recruits antigen-specific cells and produces high-affinity antibodies that can block key molecular signals that the pathogen need to thrive.

Finally, either there is a successful resolution that eliminates the danger or the immune cells negotiate a truce through a delicately adjusted process of regulation that preserves the function of the whole, even at the expense of tolerating ongoing colonization see Appendix 1 for a summary. Memory is the signature attribute of the immune system. Individuals who recover from a specific pathogen resist reinfection with the same disease. This striking outcome is the key to vaccination, so it may be a surprise there is still a great deal to learn about how immunological memory develops.

The benefits of an immune system that can fight off measles more effectively the second time it tries to attack is obvious. But the ability of the immune system to learn is also critical for a more subtle reason. One advantage that pathogens have over mammals is that they can evolve much faster than their hosts. An adaptive immune system that can learn to recognize a new infection in a few weeks, rather than having to wait a lifetime to develop an effective defence, provides a bulwark against emerging diseases that have never been encountered before.

The classical measurement of immune memory focuses on the antibody response. Following an infection or a vaccination , specific antibody levels rise, with a lag of about a week, to a peak around 10 days, and then fall off with time to lower levels that are not as low as in the naive state Figure 8.

Re-challenge with the same stimulus produces a faster 1—3 days , larger more antibody is produced and higher-avidity as a result of the evolution and selection of higher affinity antibodies; Figure 7 response. Other changes are also apparent, particularly that the predominant isotype of the antibody response will usually have shifted to IgG and sometimes IgA or IgE.

Following the first immunization, increases in specific antibody can be detected. The levels of this fall but do not return to baseline. Following the boost, the secondary response is greater and the baseline is higher.

Kinetics and levels vary between individuals and between different vaccines. These well-documented and robustly replicable responses are clearly a necessary part of immune memory, but they are not the whole story.

In parallel with changes that are occurring in the antibody response and can be measured in the serum, other important developments occur in different populations of antigen-specific lymphocytes. B-cells develop into two kinds of immune memory cell. Plasma cells localize in bone marrow or mucosal tissues and produce high-affinity antibodies, for many years.

The T cells are grown and modified in a lab to include special receptors chimeric antigen receptor that can recognize and attack cancer cells. Activated cytotoxic T cells can migrate through blood vessel walls and non-lymphoid tissues.

They can also travel across the blood brain barrier. Derived from activated cytotoxic T cells, memory T cells are long-lived and antigen-experienced. One memory T cell can produce multiple cytotoxic T cells.

After activated cytotoxic T cells attack the pathogen, the memory T cells hang around to mitigate any recurrence. Helper T cells secrete cytokines that help B cells differentiate into plasma cells.

These cells also help to activate cytotoxic T cells and macrophages. Lymphocytes are immune cells found in the blood and lymph tissue. T and B lymphocytes are the two main types. Macrophages are large white blood cells that reside in tissues that specialize in engulfing and digesting cellular debris, pathogens and other foreign substances in the body.

Large white blood cells that reside in the blood stream that specialize in engulfing and digesting cellular debris, pathogens and other foreign substances in the body. Monocytes become macrophages. When immature myeloid cells cannot differentiate into mature myeloid cells, due to conditions like cancer, expansion of myeloid-derived suppressor cells occurs, and the T-cell response can be suppressed.

A type of white blood cell, granulocyte, and phagocyte that aids in fighting infection. Neutrophils kill pathogens by ingesting them. Phagocytes eat up pathogens by attaching to and wrapping around the pathogen to engulf it. Once the pathogen is trapped inside the phagocyte, it is in a compartment called a phagosome.

The phagosome will then merge with a lysosome or granule to form a phagolysosome, where the pathogen is killed by toxic materials, such as antimicrobial agents, enzymes, nitrogen oxides or other proteins. Tell us what you think about Healio. Begin your journey with Learn Immuno-Oncology. Test your knowledge and determine where to start. Combination Immunotherapies References. Visit Healio. Your Module Progress. Module 1. Module Content. Thank you for participating in this module.