Adaptive immunity is also known as acquired immunity since the efficacy of immune response is only acquired by experience.
Types of acquired immunity
Acquired immunity to a microbe can be caused by either the host’s reaction to the microbe or by the transfer of antibodies or lymphocytes specific for the microbes. There are two forms of immunity: active immunity and passive immunity.
Active immunity refers to immunity caused by foreign antigen exposure. Active immunity is the resistance that a person develops after coming into contact with foreign antigens, such as microorganisms. This contact may take the form of:
- Infection, whether clinical or subclinical
- immunization of infectious agents, live or dead, or their antigens, or
- exposure to microbial products such as toxins and toxoids
In both of these cases, the host’s immune system is stimulated, resulting in an immune response composed of antibodies, activated helper T (TH) cells, and cytotoxic T lymphocytes/cells (CTLs).
After a latent cycle in which the host’s immunity is tuned up to function against the microorganism, active immunity grows. As a result, it has a slow onset, particularly during this primary response. However, once active immunity grows, it is long-lasting, which is the primary benefit of active immunity. There are two forms of active immunity: natural active immunity and artificial active immunity.
Natural active immunity
It is contracted by normal clinical or subclinical infections. This form of natural immunity is long-lasting. Individuals infected with smallpox, for example, develop immunity to the disease’s second attack.
Artificial active immunity
Individuals are exposed to it as a result of vaccines. Vaccines against a wide variety of microbial pathogens are available. There may be live vaccines, killed vaccines, or vaccines that contain bacterial products.
Mediators of active immunity
Humoral immunity and cell-mediated immunity are also involved in active immunity. These two types of immunities are regulated by different immune system components and act in different ways to destroy different types of pathogens.
It is activated by antibodies, which are molecules found in the blood and mucosal secretions. B cells are a form of lymphocyte that secretes antibodies. Antibodies recognize microbial antigens, bind to them specifically, neutralize microbe infectivity, and target microbes for elimination through various effector mechanisms. The primary protective mechanism against extracellular microbes is humoral immunity.
It is mediated by activated TH cells as well as CTLs. Cytokines secreted by T cells stimulate different phagocytic cells, allowing them to phagocytose and destroy microorganisms. This form of cell-mediated immune response is critical against a wide range of bacterial and protozoal pathogens. CTLs play a significant role in the death of virus-infected and tumor cells. They work by annihilating altered self-cells.
|Cell-mediated immunity||Humoral immunity|
|Immune response mediated by cells||Immune response mediated by antibodies|
|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|
|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|
|Provides immunological surveillance and immunity against cancer||No major role in immunological surveillance|
|Participates in rejection of homograft’s and graft versus-host reaction||May be involved in early graft rejection due to preformed antibodies|
Lymphocytes do not identify antigens in their entirety because they are usually very large and complex. Instead, both B and T lymphocytes identify distinct antigenic determinants, or epitopes on antigens. Epitopes are immunologically active regions of a complex antigen that bind to B-cell or T-cell receptors.
The mechanisms of antigen detection used by B cells and T cells vary. Although B cells recognize the antigen by communicating with the epitope on their own, T cells only recognize the antigen when it is “presented” by one of the specialized antigen-presenting cells. If the antigen is detected, these cells diversify into a variety of complex mechanisms. This diversification contributes to the immune system’s specificity, which is one of its defining characteristics.
Major histocompatibility complex (MHC)
It is a massive genetic complex with several loci. MHC loci encode two types of membrane-bound glycoproteins: class I MHC molecules and class II MHC molecules. Class II molecules deliver antigens to TH cells, while class I molecules deliver antigens to CTLs. To be recognized by a T cell, a foreign protein antigen must be degraded into small antigenic peptides that form complexes with class I or class II MHC molecules. Antigen processing and presentation refers to the method of converting proteins into MHC-associated peptide fragments.
Passive immunity occurs when immunity is conferred by the transfer of serum or lymphocytes from a directly immunized organism. This is a useful method for conferring resistance quickly, i.e. without waiting for an active immune response to evolve. Passive immunity may be either natural or artificial.
Natural passive immunity
It is observed during pregnancy as IgG is transferred from mother to fetus. This is the basis for preventing neonatal tetanus in newborns by active immunization of pregnant mothers. It is accomplished by giving tetanus toxoid to pregnant women during the last trimester of their pregnancy. This causes the mother to produce a high level of antibodies against tetanus toxin, which is then passed on to the fetus through the placenta. Following birth, the antibodies protect neonates against the possibility of tetanus. Passage of IgA from mother to infant during breast feeding often results in natural passive immunity.
Artificial passive immunity
It is induced in a person by administering preformed antibodies, usually in the form of antiserum, that have been raised against an infecting agent. When these antisera are administered, significant quantities of antibodies are made available in the recipient host to neutralize the action of toxins.
During the incubation phase, preformed antibodies against rabies and hepatitis A and B viruses, among others, inhibit virus replication and thus alter the path of infection. The biggest benefit of passive immunity is the immediate availability of significant amounts of antibodies. The two noted drawbacks of passive immunity are the short lifetime of these antibodies and the risk of hypersensitivity reaction if antibodies prepared in other animal species are given to individuals who are hypersensitive to these animal globulins (e.g., serum sickness).
Combined passive–active immunity is carried out by giving both preformed antibodies (antiserum) and a vaccine to provide immediate protection and long-term protection, respectively, against a disease. This method is practiced for prevention of certain infectious diseases, including, tetanus, rabies, and hepatitis B
|Passive immunity||Active immunity|
|No active host participation; received passively||Produced actively by host’s immune system|
|Antibodies transferred directly||Antibodies induced by infection or by immunogens|
|Passive immunity is due to readymade antibodies||Active immunity often involves both the cell-mediated and humoral immunity|
|Types: Natural—transfer of maternal antibodies through placenta; Artificial—injection of immunoglobulins||Types: Natural—clinical or inapparent infection; Artificial—induced by vaccines|
|Immediate immunity; no lag period||Immunity effective only after lag period|
|Transient; less effective||Durable; effective protection|
|No immunological memory||Immunological memory present|
|Subsequent dose less effective due to immune elimination||Booster effect on subsequent dose|
|No negative phase||Negative phase may occur|
|Applicable even in immunodeficient||Not applicable in immunodeficient|