Created by CK-12 Foundation/Adapted by Christine Miller

The photomicrograph in Figure 17.5.1 shows a group of killer T cells (green and red) surrounding a cancer cell (blue, centre). When a killer T cell makes contact with the cancer cell, it attaches to and spreads over the dangerous target. The killer T cell then uses special chemicals stored in vesicles (red) to deliver the killing blow. This event has thus been nicknamed “the kiss of death.” After the target cell is killed, the killer T cells move on to find the next victim. Killer T cells like these are important players in the adaptive immune system.

The adaptive immune system is a subsystem of the overall immune system. It is composed of highly specialized cells and processes that eliminate specific pathogens and tumor cells. An adaptive immune response is set in motion by antigens that the immune system recognizes as foreign. Unlike an innate immune response, an adaptive immune response is highly specific to a particular pathogen (or its antigen). An important function of the adaptive immune system that is not shared by the innate immune system is the creation of immunological memory — or immunity — which occurs after the initial response to a specific pathogen. It allows for a faster, stronger response on subsequent encounters with the same pathogen, usually before the pathogen can even cause symptoms of illness.

Lymphocytes are the main cells of the adaptive immune system. They are leukocytes that arise and mature in organs of the lymphatic system, including the bone marrow and thymus. The human body normally has about 2 trillion lymphocytes, which constitute about 1/3 of all leukocytes. Most of the lymphocytes are normally sequestered within tissue fluid or organs of the lymphatic system, including the tonsils, spleen, and lymph nodes. Only about 2% of the lymphocytes are normally circulating in the blood. There are two main types of lymphocytes involved in adaptive immune responses, called T cells and B cells. T cells destroy infected cells or release chemicals that regulate immune responses. B cells secrete antibodies that bind with antigens[/pb_glossary] of [pb_glossary id="271"]pathogens so they can be removed by other immune cells or processes.

There are multiple types of T cells, or T lymphocytes. Major types are killer (or cytotoxic) T cells and helper T cells. Both types develop from immature T cells that become activated by exposure to an antigen.

T Cell Activation (or Cell-Mediated Immunity)

T cells must be activated to become either killer T cells or helper T cells. This requires presentation of a foreign antigen by antigen-presenting cells, as shown in Figure 17.5.2. Antigen-presenting cells may be dendritic cells, macrophages, or B cells. Activation occurs when T cells are presented with a foreign antigen coupled with an MHC self antigen. Helper T cells are more easily activated than killer T cells. Activation of killer T cells is strongly regulated and may require additional stimulation from helper T cells.

Killer T Cells

Activated killer T cells induce the death of cells that bear a specific non-self antigen because they are infected with pathogens or are cancerous. The antigen targets the cell for destruction by killer T cells, which travel through the bloodstream searching for target cells to kill. Killer T cells may use various mechanisms to kill target cells. One way is by releasing toxins in granules that enter and kill infected or cancerous cells (see Figure 17.5.3).

Helper T Cells

Activated helper T cells do not kill infected or cancerous cells. Instead, their role is to “manage” both innate and adaptive immune responses by directing other cells to perform these tasks. They control other cells by releasing cytokines, which are proteins that can influence the activity of many cell types, including killer T cells, B cells, and macrophages. Some cytokines released by helper T cells assist with the activation of killer T cells.

B cells, or B lymphocytes, are the major cells involved in the creation of antibodies that circulate in blood plasma and lymph. Antibodies are large, Y-shaped proteins used by the immune system to identify and neutralize foreign invaders. Besides producing antibodies, B cells may also function as antigen-presenting cells, or secrete cytokines that help control other immune cells and responses.

B Cell Activation (or Antibody-Mediated Immunity)

Before B cells can actively function to defend the host, they must be activated. As shown in Figure 17.5.4, B cell activation begins when a B cell engulfs and digests an antigen. The antigen may be either free floating in the lymph, or it may be presented by an antigen-presenting cell, such as a dendritic cell or macrophage. In either case, the B cell then displays antigen fragments bound to its own MHC antigens. The MHC-antigen complex on the B cell attracts helper T cells. The helper T cells, in turn, secrete cytokines that help the B cell to multiply, and the daughter cells to mature into plasma cells.

Plasma Cells

Plasma cells are antibody-secreting cells that form from activated B cells. Each plasma cell is like a tiny antibody factory. It may secrete millions of copies of an antibody, each of which can bind to the specific antigen that activated the original B cell. The specificity of an antibody to a specific antigen is illustrated in Figure 17.5.5. When antibodies bind with antigens, it makes the cells bearing them easier targets for phagocytes to find and destroy. Antibody-antigen complexes may also trigger the complement system of the innate immune system, which destroys the cells in a cascade of protein enzymes. In addition, the complexes are likely to clump together (agglutinate). If this occurs, they are filtered out of the blood in the spleen or liver.

Once a pathogen has been cleared from the body, most activated T cells and B cells die within a few days. A few of the cells, however, survive and remain in the body as memory T cells or memory B cells. These memory cells are ready to activate an immediate response if they are exposed to the same antigen again in the future. This is the basis of immunity.

The earliest known reference to the concept of immunity relates to the bubonic plaque (see Figure 17.5.6). In 430 B.C., a Greek historian and general named Thucydides noted that people who had recovered from a previous bout of the plague could nurse people who were sick with the plague without contracting the illness a second time. We now know that this is true of many diseases, and that it occurs because of active immunity.

Active Immunity

Active immunity is the ability of the adaptive immune system to resist a specific pathogen because it has formed an immunological memory of the pathogen. Active immunity is adaptive, because it occurs during the lifetime of an individual as an adaptation to infection with a specific pathogen, and prepares the immune system for future challenges from that pathogen. Active immunity can come about naturally or artificially.

Naturally Acquired Active Immunity

Active immunity is acquired naturally when a pathogen invades the body and activates the adaptive immune system. When the initial infection is over, memory B cells and memory T cells remain, providing immunological memory of the pathogen. As long as the memory cells are alive, the immune system is ready to mount an immediate response if the same pathogen tries to infect the body again.

Artificially Acquired Active Immunity

Active immunity can also be acquired artificially through immunization. Immunization is the deliberate exposure of a person to a pathogen in order to provoke an adaptive immune response and the formation of memory cells specific to that pathogen. The pathogen is introduced in a vaccine — usually by injection, sometimes by nose or mouth (see Figure 17.5.7) — so immunization is also called vaccination.

Typically, only part of a pathogen, a weakened form of the pathogen, or a dead pathogen is used in a vaccine, which causes an adaptive immune response without making the immunized person sick. This is how you most likely became immune to diseases such as measles, mumps, and chicken pox. Immunizations may last for a lifetime, or they may require periodic booster shots to maintain immunity. While immunization generally has long-lasting effects, it usually takes several weeks to develop full immunity.

Immunization is the most effective method ever discovered of preventing infectious diseases. As many as 3 million deaths are prevented each year because of vaccinations. Widespread immunity from vaccinations is largely responsible for the worldwide eradication of smallpox, and the near elimination of several other infectious diseases from many populations, including polio and measles. Immunization is so successful because it exploits the natural specificity and inducibility of the adaptive immune system.

Passive Immunity

Passive immunity results when pathogen-specific antibodies or activated T cells are transferred to a person who has never been exposed to the pathogen. Passive immunity provides immediate protection from a pathogen, but the adaptive immune system does not develop immunological memory to protect the host from the same pathogen in the future. Unlike active immunity, passive immunity lasts only as long as the transferred antibodies or T cells survive in the blood — usually between a few days and a few months. However, like active immunity, passive immunity can be acquired both naturally and artificially.

Naturally Acquired Passive Immunity

Passive immunity is acquired naturally by a fetus through its mother’s blood. Antibodies are transported from mother to fetus across the placenta, so babies have high levels of antibodies at birth. Their antibodies have the same range of antigen specificities as their mother’s. Passive immunity may also be acquired by an infant through the mother’s breast milk. This gives young infants protection from common pathogens in their environment while their own immune system matures.

Artificially Acquired Passive Immunity

Older children and adults can acquire passive immunity artificially through the injection of antibodies or activated T cells, which may be done when there is a high risk of infection and insufficient time for the body to develop active immunity through vaccination. It may also be done to reduce symptoms of ongoing disease, or to compensate for immunodeficiency diseases.

Many pathogens have been around for a long time, living with human populations for generations. To persist, some have evolved mechanisms to evade the adaptive immune system of human hosts. One way they have done this is by rapidly changing their non-essential antigens. This is called antigenic variation. An example of a pathogen that takes this approach is human immunodeficiency virus (HIV). It mutates rapidly so the proteins on its viral envelope are constantly changing. By the time the adaptive immune system responds, the virus’s antigens have changed. Antigenic variation is the main reason that efforts to develop a vaccine against HIV have not yet been successful.

Another evasion approach that some pathogens may take is to mask pathogen antigens with host molecules so the host’s immune system cannot detect the antigens. HIV takes this approach, as well. The envelope that covers the virus is formed from the outermost membrane of the host cell.

If you think that immunizations are just for kids, think again. There are several vaccines recommended by HealthLinkBC for people over the age of 18. The tables below from HealthLinkBC show the vaccine schedules recommended for infants and children, school-aged children, and adults and senior. Additional vaccines may be recommended for certain adults based on specific travel plans, medical conditions or other indications. Are you up to date with your vaccines? You can check with your doctor to be sure.

Attributions

Figure 17.5.1

Killer_T_cells_surround_a_cancer_cell by Alex Ritter, Jennifer Lippincott Schwartz and Gillian Griffiths at the National Institutes of Health/ Visuals Online on Wikimedia Commons is in the public domain (https://en.wikipedia.org/wiki/Public_domain).

Figure 17.5.2

T_cell_activation.svg by Rehua (derivative work) on Wikimedia Commons is in the public domain (https://en.wikipedia.org/wiki/Public_domain). (Original image: T_cell_activation.png:  from The Immune System - NIH Publication No. 03–5423)

Figure 17.5.3

Cytotoxic T Cell function by CNX OpenStax on Wikimedia Commons is used under a CC BY 4.0 (https://creativecommons.org/licenses/by/4.0) license.

Figure 17.5.4

B_cell_activation.svg by Fred the Oyster on Wikimedia Commons is in the public domain (https://en.wikipedia.org/wiki/Public_domain). (Original from The Immune System - NIH Publication No. 03–5423)

Figure 17.5.5

Antibody.svg by Fvasconcellos  on Wikimedia Commons is in the public domain (https://en.wikipedia.org/wiki/Public_domain). (Original black and white image from the National Human Genome Research Institute's Talking Genetics Glossary)

Figure 17.5.7

immunizations by U.S. Air Force photo by Airman 1st Class Destinee Dougherty from Military Health System website, Health.mil, is in the public domain (https://en.wikipedia.org/wiki/Public_domain).

References

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Mayo Clinic Staff. (n.d.). Mumps [online article]. MayoClinic.org. https://www.mayoclinic.org/diseases-conditions/mumps/symptoms-causes/syc-20375361

Mayo Clinic Staff. (n.d.). Polio [online article]. MayoClinic.org. https://www.mayoclinic.org/diseases-conditions/polio/symptoms-causes/syc-20376512

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OpenStax. (2016, March 23). Figure 4 Naïve CD4⁺ T cells engage MHC II molecules on antigen-presenting cells (APCs) and become activated. Clones of the activated helper T cell, in turn, activate B cells and CD8⁺ T cells, which become cytotoxic T cells. Cytotoxic T cells kill infected cells [digital image]. In OpenStax, Biology (Section 42.2). OpenStax CNX. https://cnx.org/contents/GFy_h8cu@10.53:etZobsU-@6/Adaptive-Immune-Response

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