The term immunity was derived from the Latin word “ see immunis” (exempt), which originally referred to the protection from legal prosecution offered to the Roman senators during their tenures in office. The same term was later adopted subsequently to designate the naturally acquired protection against diseases by the immune system.
A person or individual can develop lifelong resistance to a certain disease after having contracted it only once. The immune system involves the cells and molecules that are responsible for immunity. The chief function of the immune system is to limit or prevent pathogenic microorganisms such as parasites, bacteria, viruses, and fungi to cause infections. The collective and coordinated response of the Immune system to foreign substances is called the source immune response.
The first event in immune response of a particular host involves the recognition of microorganisms and foreign substances. The body’s defence mechanisms (Immunity) is divided into two types:
|click here Feature||Innate immunity||Acquired immunity|
|Definition||The resistance to infection that an individual possesses by virtue of genetic and constitutional makeup||The resistance that an individual acquires during life|
|Time taken to develop||Hours||Days|
|Types||Nonspecific and specific||Active and passive|
|Specificity||For structures shared by groups of related microbes||For antigens of microbes and for non-microbial antigens|
|Memory||None; repeated exposure brings response like primary response||Yes; secondary response much faster than primary response|
|Physical and chemical barriers||Skin, mucosal epithelia, and antimicrobial chemicals||Lymphocytes in epithelia and antibodies secreted at epithelial surfaces|
|Blood and tissue antimicrobial substances||Complement; leukins from leukocytes, plakins from platelets, lactic acid found in muscle tissue, lactoperoxidase in milk, and interferons (antiviral)||Antibodies|
|Cells||Phagocytes (macrophages and neutrophils) and natural killer cells||Lymphocytes|
It is resistance that an individual possesses by birth and it’s therefore acts as the first line of defence of the host immune system and occurs due to the constitutional and genetic makeup of an individual that is the mechanisms involved in innate immunity are present in place even before exposure to the foreign agent.
Innate immunity is not specific to any infectious agent and do not seem to improve response on repeated exposures. Phagocytic cells such as neutrophils and macrophages, natural barriers like the skin and mucous membrane and a variety of antimicrobial compounds synthesized by the host are all involved in innate immunity. Innate immunity is classified into:
- Individual immunity
- go to link Racial immunity
- Species immunity
What is Species immunity?
Species immunity involves a total or relative resistance to a particular pathogen shown by all members of a particular species. For instance, rats are resistant to Corynebacterium diphtheriae, chickens to Bacillus anthracis meanwhile humans are very susceptible to these bacteria. The exact reason for such type of immunity is not known.
What is Individual immunity?
This is genetically determined and involves resistance to infection, which varies within different individuals in the same race and species. For instance, if one homozygous twin develops tuberculosis, there is a very high probability that the other will also develop tuberculosis. But in heterozygous twins, there is a very low probability of the other twin suffering from tuberculosis.
What is Racial immunity ?
In this case, there’s a difference in resistance or susceptibility to infection among different races within a same species. For instance, races with sickle cell anaemia prevalent in Mediterranean coast are immune to infection caused by malaria parasite Plasmodium falciparum. This difference is due to a genetic abnormality of red cells, resulting in a crescent or sickle shaped red cells that prevent parasitization by Plasmodium falciparum. Another similar case: individuals with a hereditary deficiency of Glucose6-phosphatase dehydrogenase (G6PD) are also less resistant or susceptible to infection by Plasmodium falciparum.
What are those factors influencing innate immunity?
These following factors may influence innate immunity of the host.
Very young children and older individuals are highly susceptible to various infections. This is due to an immature immune system in very young children and waning immunity in older individuals. During pregnancy, the placental barrier naturally protects the foetus from maternal infections. However, rubella virus, human immunodeficiency virus (HIV), toxoplasma gondii and cytomegalovirus are able to cross the placental barrier and causes congenital infections.
Very old people are usually more susceptible to suffer than young people from a disease due to a weaken immune system and have high mortality.
Diseases such as poliomyelitis, measles, mumps and chicken pox are few examples that cause more severe clinical illness in adults than in young children. One of the possible explanation could be due to more active immune response in adult causing greater tissue damage.
Individual with certain hormonal disorders turns to be increasingly susceptible to infection. For instant, individuals suffering from adrenal dysfunction, diabetes mellitus, and hypothyroidism are increasingly susceptible to candidiasis, staphylococcal infection, streptococcal infection, zygomycosis, aspergillosis and many other microbial infections. Similarly, pregnant women are more susceptible to many infections due to higher level of steroid during pregnancy
Nutritional status of the host also plays an important role in innate immunity as it is observed that both cell mediated and humoral immunities are lowered in malnutrition. Examples are:
- Deficiency of folic acid, vitamin A and vitamin C, makes an individual highly susceptible to infection by many microbial pathogens.
- In protein–calorie malnutrition (PCM), interferon response is decreased , Neutrophil activity is reduced and C3 and factor B of the complement are decreased
Mechanisms of innate immunity
The two most important functions of innate immunity of the host is to activate acquired (adaptive) immune processes and kill invading microbes.
Innate immunity unlike adaptive immunity, lack any memory therefore does not improve after re-exposure to the same microorganism.
Innate immunity is primarily dependent on four types of defensive barriers:
- anatomic barriers
- physiologic barriers
- Inflammatory responses.
The anatomic barriers of innate immunity includes the mucous membrane and skin as they are the most important components of innate immunity. They act as mechanical barriers thereby preventing the entry of microorganisms into the body.
The skin acts as an anatomic barrier and is responsible for the prevention of microorganism from entering into the body. For instance, breaks in the skin due to wounds, scratches, or abrasion cause infection. Bites of insects (mosquitoes, mites, ticks, fleas, and sand flies) harbouring pathogenic organisms, introduces the pathogens into the body therefore transmit infection.
The oily sebum secreted by the skin prevents the growth of many microorganisms. Sebum consists of lactic acid and fatty acids that maintain the pH between 3 and 5 of the skin which inhibits the growth of most microorganisms.
Another m anatomic barrier is the mucous membranes form a large part of outer covering of respiratory, gastrointestinal, genitourinary and many other tracts of human host. A number of nonspecific defence mechanisms act to prevent entry of microorganisms especially through mucous membrane.
Tears, mucous secretion and saliva tend to wash away potential invading microorganisms which prevent their attachment to the initial site of infections. These secretions also contain antiviral and antibacterial substances that kill invading pathogens.
- Mucus (a viscous fluid) is originally secreted by the epithelial cells of mucous membranes that entraps invading microorganisms.
- In lower respiratory tract, these mucous membrane are covered by cilia (hair-like protrusions of the epithelial cell membranes). The synchronous movement of cilia propels mucus entrapped microorganisms from these tracts.
- Also, non-pathogenic organisms (normal flora) tend to colonize the epithelial cells of these mucosal surfaces. These non-pathogenic organisms generally compete with pathogens for attachment sites on the epithelial cell surface and for necessary nutrients.
There are certain types of substances or molecules of substances that are unique to microbes that are never found in multicellular organisms. The ability of the host to immediately recognize and combat invaders displaying such molecules is a strong feature of innate immunity.
The following are physiologic barriers contributing to innate:
Gastric acidity: It is an innate physiologic barrier to infection or microorganism causing diseases. Very few ingested microorganisms can survive the low pH of stomach contents.
Interferon, Lysozyme and complement: These are some of the soluble mediators of innate immunity. Lysozyme are enzymes and also have antibacterial effect due to its action on the bacterial cell wall (bacteriostatic).
Interferons are substances secreted by cells in response to products of viral infected cells. These substances have a general antiviral effect by preventing the synthesis of viral structural proteins.
Complement is a group of serum-soluble substances. When activated, they damages the cell membrane of microorganism.
This is another important defence mechanism of the innate immunity. Phagocytosis a process of ingestion of extracellular particulate material by certain specialized cells, such as neutrophils, tissue macrophages and blood monocytes. Phagocytosis a type of endocytosis in which invading microorganisms present in the environment are ingested by the phagocytic cells. In this process, plasma membrane of the cell expands around the foreign or particulate material, which may include whole pathogenic microorganisms or particles to form large vesicles called phagosomes.
Tissue damage caused by a wound or by an invading pathogenic microorganism induces a complex sequence of events collectively known as inflammatory responses. The end result of inflammation may be the activation of a specific immune response to the invasion or clearance of the invader by components of the innate immune system. The four cardinal signs or features of inflammatory responses are calor (rise in temperature), rubor (redness), tumor (swelling) and dolor (pain).
Mediators of inflammatory reactions
The following are important mediator of inflammatory reactions: kinins, defensin, acute phase proteins and histamine.
Histamine is a chemical substance produced by a variety of cells in response to tissue damage or injury. Histamine is one of the principal mediators of the inflammatory response and it binds to receptors on nearby capillaries and venules causing increased permeability and vasodilatation.
These are small peptides and important mediators of inflammatory response. Kinins are normally present in blood plasma but in an inactive form. They are activated by tissue injury, which then causes increased permeability of capillaries and vasodilatation.
Bradykinin is another type of kinins which stimulates pain receptors in the skin. This effect probably serves a protective role because pain normally causes an individual to protect the injured area
- Acute-phase proteins
These include C-reactive proteins (CRP) and mannose-binding proteins that form part of the innate immunity. These proteins are synthesized in the liver in response to pro-inflammatory cytokines like tissue necrosis factor (TNF), interleukin-1 (IL-1) and interleukin-6 (IL6) because they enhance the inflammatory responses.
They are also produced at an increased concentration in plasma during acute-phase reaction, as a nonspecific response to microorganisms and other forms of tissue injury.
Defensins are cationic peptides that kills bacteria by producing pores in membrane of these bacteria. These peptides are mainly present in the lower respiratory tract and gastrointestinal tract. Beta-defensins is found at the level of the respiratory tract, whereas the gastrointestinal tract contains alpha-defensins. Alpha-defensins also exhibit antiviral activity. It binds to the CXCR4 receptors and block entry of HIV virus into the cell.
Adaptive (Acquired) Immunity
This is also called acquired immunity because it is the resistance acquired by an individual during life. Acquired immunity occurs after exposure to an agent and is mediated by antibodies as well as T lymphocytes (helper T cells and cytotoxic T cells).It has immunologic memory and capable of discriminating between self and non-self-antigens. Adaptive immunity is very specific. That is, once an antigen has been recognized by the cells of acquired immune system, the response to it is specific and can be repeated (immunologic memory). In most cases, the acquired immune response improves with repeated exposure.
The immune response to the second invasion or re-exposure is stronger and occurs more quickly than the first. It is often more effective in neutralizing and clearing the pathogen.
Types of acquired immunity
There are two types of acquired immunity: Active immunity and passive immunity.
The immunity induced by exposure to a foreign antigen is called active immunity. It is the resistance developed by an individual after contact with foreign antigens or particles such bacteria, viruses, fungi etc.
Contact with such foreign particles or antigen may be clinical or subclinical, exposure to microbial products such as toxins and toxoids or immunization with a killed or live infectious agents or their antigens.
In all these circumstances, the immune system of the host is stimulated to elicit an immune response consisting of activated helper T (TH) cells, antibodies and cytotoxic T lymphocytes/cells (CTLs).
This type of immunity develops after a latent period, during which immunity of the host is geared up to act against the microorganism. Hence it is slow in onset, especially during this primary response. However, once the active immunity develops, it is long-lasting and this is the major advantage of the active immunity. There are types of active immunity: Natural active immunity and artificial active immunity.
Natural active immunity
Natural active immunity is acquired by natural clinical or subclinical infections. It is long-lasting. For instant, individuals suffering from smallpox become immune to second attack of the disease.
Artificial active immunity
Artificial active immunity is induced in individuals with vaccines. There is a wide range of vaccines available against many microbial pathogens. These may be killed vaccines, vaccines containing bacterial products or live vaccines.
Mediators of active immunity
Active immunity is mediated by cell-mediated immunity and humoral immunity. These two types of immunities are mediated by different components of the immune system thereby functioning in different ways to kill different types of pathogens.
- Humoral immunity: This is the principal defence mechanism against extracellular microbes. It is mediated by antibodies in the blood and mucosal secretions. These antibodies are secreted by B lymphocytes and recognizes microbial antigens then combine specifically with these antigens to neutralize the infectivity of microbes and target microbes for elimination by various effector mechanisms.
- Cell-mediated immunity: It is mediated by both activated T-helper cells and cytotoxic T lymphocytes/cells. Cytokines secreted by T helper cells activate various phagocytic cells which enables them to phagocytose and kill microorganisms. This type of cell-mediated immune response is especially important against a host of bacterial and protozoal pathogens. Cytotoxic T lymphocytes/cells play an important role in killing virus-infected cells and tumour cells. They act by killing altered self-cells.
Differences between cell-mediated and humoral immunity
|Humoral immunity||Cell-mediated immunity|
|Protects against fungi, viruses, and facultative intracellular bacterial pathogens||Protects against extracellular bacterial pathogens and viruses infecting respiratory or intestinal tract; and prevents recurrence of viral infections|
|Immune response mediated by cells||Immune response mediated by antibodies|
|Mediates delayed (type IV) hypersensitivity||Mediates immediate (types I, II, and III) hypersensitivity|
|Only T-cell-dependent antigens lead to cell mediated immunity||B cells directly bind soluble antigens resulting in production of antibodies|
|Both CD4+ and CD8+ T cells are involved||Only T helper cells are involved|
|Participates in rejection of homograft and graft-versus-host reaction||May be involved in early graft rejection due to preformed antibodies|
|Provides immunological surveillance and immunity against cancer||No major role in immunological surveillance|
Antigens, which are generally very large and complex are not recognized in their entirety by T and B lymphocytes. They are instead recognize by discrete sites on the antigens called epitopes or antigenic determinants.
These epitopes are the immunologically active regions found on complex antigen. That is, the regions that actually bind to B-cell or T-cell receptors.
The B and T lymphocytes differ in their mechanisms of antigen recognition. B lymphocytes recognizes the antigen by interacting with the epitope on their own while T lymphocytes recognizes the antigen only when the epitope is presented by one of the specialized antigen-presenting cells. Once the antigen has been recognized, these cells then go on to diversify by several intricate mechanisms. This diversification helps in conferring the specificity which is one of the cardinal characteristics of the immune system.
Major histocompatibility complex (MHC)
MHC is a large genetic complex having multiple loci. The MHC loci encode two major classes of membrane-bound glycoproteins:
- Class I MHC molecules
- Class II MHC molecules.
Class I MHC molecules present antigens to the cytotoxic T lymphocytes/cells while The Class II MHC molecules present antigens to the T helper cells. In order for a foreign protein antigen to be recognized by a T cell, it must be degraded into small antigenic peptides that form complexes with class II MHC molecules or class I MHC molecules. The conversion of proteins into MHC-associated peptide fragments is called antigen processing and presentation.
Passive immunity is the natural or artificial transfer of lymphocytes or serum from a specifically immunized individual to achieve immunization. This method is useful for conferring resistance rapidly i.e. without waiting for the development of an active immune response.
Natural passive immunity
During pregnancy, immunoglobulin G and Immunoglobulin A is passed from mother to foetus through the placenta and during breast feeding to the neonate respectively. This transfer forms the basis of prevention by active immunization of pregnant mothers and natural passive immunization of the foetus or neonate. Therefore, natural passive immunity is the natural passing of already made antibodies from the mother to the foetus or neonate.
The administration of vaccine (Tetanus toxoid) to pregnant mothers during the last trimester of pregnancy induces production of high level of antibodies in mother against tetanus toxin. These antibodies are subsequently transmitted from mother to foetus through placenta. These antibodies subsequently protects the neonates after birth against the risk of infections (tetanus).
Artificial passive immunity
Artificial passive immunity is induced in an individual by the administration of preformed antibodies. This is generally in the form of antiserum raised against an infecting agent. The administration of these antisera makes illicit the production of large amounts of antibodies available in the recipient host to neutralize the action of toxins.
The main advantages of passive immunity is the immediate availability of large amount of antibodies. However, passive immunity has a short lifespan of these antibodies and possibility of hypersensitivity reaction.
Active-passive immunity can be administered together by preparing preformed antibodies (antiserum) and a vaccine. This provide immediate and long-term protection respectively against a disease. This is mostly employed for prevention of certain infectious conditions such as hepatitis, tetanus and rabies.
Differences between passive and active immunity
|Passive immunity||Active immunity|
|Antibodies transferred directly||Antibodies induced by infection or by immunogens|
|No active host participation; received passively||Produced actively by host’s immune system|
|Passive immunity is due to readymade antibodies||Active immunity often involves both the cell-mediated and humoral immunity|
|Natural : transfer of maternal antibodies through placenta; Artificial: injection of immunoglobulins||Natural : clinical or in apparent infection Artificial : induced by vaccines|
|Immediate immunity; no lag period||Immunity effective only after lag period|
|Transient; less effective||Durable; effective protection|
|Subsequent dose less effective due to immune elimination||Booster effect on subsequent dose|
|Applicable even in immunodeficient||Not applicable in immunodeficient|
|No negative phase||Negative phase may occur|
What is Herd Immunity
Herd immunity is the overall level of immunity in a community. The eradication of an infectious disease depends on the development of a high level of herd immunity in a community against the pathogen. Epidemic of a disease will likely occur when herd immunity against that disease is very low which is indicative to the presence of a larger number of susceptible people in the community.
What is Local Immunity?
Local Immunity is refer to as the immunity at a particular site. That is, at the site of invasion and multiplication of a pathogen. It is conferred by secretory Immunoglobulin A (Ig A) antibodies in various body secretions. Ig A antibodies are locally produced by plasma cells present in secretory glands or mucosal surfaces. Natural infection or attenuated live viral vaccines given intranasally or orally induces local immunity at nasal mucosa and gut mucosa, respectively.
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