Examples of these non-specific defences are given below:. An immune response is triggered when the immune system is alerted that something foreign has entered the body. Triggers include the release of chemicals by damaged cells and inflammation, and changes in blood supply to an area of damage which attract white blood cells. White blood cells destroy the infection or convey chemical messages to other parts of the immune system.
As blood and tissue fluids circulate around the body, various components of the immune system are continually surveying for potential sources of attack or abnormal cells. Antigens are usually either proteins or polysaccharides long chains of sugar molecules that make up the cell wall of certain bacteria. Viruses can contain as few as three antigens to more than as for herpes and pox viruses; whereas protozoa, fungi and bacteria are larger, more complex organisms and contain hundreds to thousands of antigens.
An immune response initially involves the production of antibodies that can bind to a particular antigen and the activation of antigen-specific white blood cells. Antibodies immunoglobulins; Ig are protein molecules that bind specifically to a particular part of an antigen, so called antigenic site or epitope. They are found in the blood and tissue fluids, including mucus secretions, saliva and breast milk.
Normally, low levels of antibodies circulate in the body tissue fluids. However, when an immune response is activated greater quantities are produced to specifically target the foreign material. Vaccination increases the levels of circulating antibodies against a certain antigen. Antibodies are produced by a type of white blood cell lymphocyte called B cells. Each B cell can only produce antibodies against one specific epitope. When activated, a B cell will multiply to produce more clones able secrete that particular antibody.
The class of antibody produced is determined by other cells in the immune system, this is known as cell-mediated immunity. Upon exposure to a pathogen, the body will attempt to isolate and destroy it. Chemicals released by inflammation increase blood flow and attract white blood cells to the area of infection.
Specialist cells, known as phagocytes, engulf the target and dismantle it. This response leads to the production of antigen-specific antibodies.
Circulating antibodies then find the organism and bind to its surface antigens. In this way it is labelled as the target. This specific response is also called the adaptive or cell-mediated immune response, since the immune system adapts to suit the type of invader. When the body is first exposed to an antigen, several days pass before this adaptive response becomes active.
Infants have passive immunity because they are born with antibodies that are transferred through the placenta from their mother. These antibodies disappear between ages 6 and 12 months. Passive immunization may also be due to injection of antiserum, which contains antibodies that are formed by another person or animal.
It provides immediate protection against an antigen, but does not provide long-lasting protection. Immune serum globulin given for hepatitis exposure and tetanus antitoxin are examples of passive immunization. The immune system includes certain types of white blood cells.
It also includes chemicals and proteins in the blood, such as antibodies, complement proteins, and interferon. Some of these directly attack foreign substances in the body, and others work together to help the immune system cells.
As lymphocytes develop, they normally learn to tell the difference between your own body tissues and substances that are not normally found in your body. Once B cells and T cells are formed, a few of those cells will multiply and provide "memory" for your immune system. This allows your immune system to respond faster and more efficiently the next time you are exposed to the same antigen. In many cases, it will prevent you from getting sick. For example, a person who has had chickenpox or has been immunized against chickenpox is immune from getting chickenpox again.
The inflammatory response inflammation occurs when tissues are injured by bacteria, trauma, toxins, heat, or any other cause. The damaged cells release chemicals including histamine, bradykinin, and prostaglandins.
These chemicals cause blood vessels to leak fluid into the tissues, causing swelling. This helps isolate the foreign substance from further contact with body tissues.
The chemicals also attract white blood cells called phagocytes that "eat" germs and dead or damaged cells. This process is called phagocytosis. Phagocytes eventually die. Pus is formed from a collection of dead tissue, dead bacteria, and live and dead phagocytes. Immune system disorders occur when the immune response is directed against body tissue, is excessive, or is lacking.
Allergies involve an immune response to a substance that most people's bodies perceive as harmless. Vaccination immunization is a way to trigger the immune response. Small doses of an antigen, such as dead or weakened live viruses, are given to activate immune system "memory" activated B cells and sensitized T cells. Memory allows your body to react quickly and efficiently to future exposures. An efficient immune response protects against many diseases and disorders.
Once activated, Th cells release cytokines that influence the activity of many cell types, including the APCs that activate them. Th1-derived cytokines also contribute to the differentiation of B cells to make opsonizing antibodies that enhance the efficiency of phagocytes. An inappropriate Th1 response is associated with certain autoimmune diseases.
The Th2 response is characterized by the release of cytokines IL-4, 5 and 13 which are involved in the development of immunoglobulin E IgE antibody-producing B cells, as well as the development and recruitment of mast cells and eosinophils that are essential for effective responses against many parasites.
In addition, they enhance the production of certain forms of IgG that aid in combatting bacterial infection. As mentioned earlier, mast cells and eosinophils are instrumental in the initiation of acute inflammatory responses, such as those seen in allergy and asthma.
IgE antibodies are also associated with allergic reactions see Table 2. Therefore, an imbalance of Th2 cytokine production is associated with the development of atopic allergic conditions. Th17 cells have been more recently described. They are characterized by the production of cytokines of the IL family, and are associated with ongoing inflammatory responses, particularly in chronic infection and disease.
Like cytotoxic T cells, most Th cells will die upon resolution of infection, with a few remaining as Th memory cells [ 2 , 3 ]. T reg cells limit and suppress immune responses and, thereby, may function to control aberrant responses to self-antigens and the development of autoimmune disease. T reg cells may also help in the resolution of normal immune responses, as pathogens or antigens are eliminated. B cells arise from hematopoietic stem cells in the bone marrow and, following maturation, leave the marrow expressing a unique antigen-binding receptor on their membrane.
Unlike T cells, B cells can recognize antigens directly, without the need for APCs, through unique antibodies expressed on their cell surface. The principal function of B cells is the production of antibodies against foreign antigens which requires their further differentiation [ 2 , 3 ]. Under certain circumstances, B cells can also act as APCs. When activated by foreign antigens to which they have an appropriate antigen specific receptor, B cells undergo proliferation and differentiate into antibody-secreting plasma cells or memory B cells see Fig.
These cells can be called upon to respond quickly by producing antibodies and eliminating an antigen upon re-exposure. Plasma cells, on the other hand, are relatively short-lived cells that often undergo apoptosis when the inciting agent that induced the immune response is eliminated.
However, these cells produce large amounts of antibody that enter the circulation and tissues providing effective protection against pathogens. Given their function in antibody production, B cells play a major role in the humoral or antibody-mediated immune response as opposed to the cell-mediated immune response, which is governed primarily by T cells [ 2 , 3 ].
Antibody-mediated immunity is the branch of the acquired immune system that is mediated by B-cell-antibody production. Local Th cells secrete cytokines that help the B cell multiply and direct the type of antibody that will be subsequently produced. Some cytokines, such as IL-6, help B-cells to mature into antibody-secreting plasma cells.
The secreted antibodies bind to antigens on the surface of pathogens, flagging them for destruction through complement activation, opsonin promotion of phagocytosis and pathogen elimination by immune effector cells. Upon elimination of the pathogen, the antigen—antibody complexes are cleared by the complement cascade see Fig. IgG antibodies can be further subdivided into structurally distinct subclasses with differing abilities to fix complement, act as opsonins, etc.
The major classes of antibodies have substantially different biological functions and recognize and neutralize specific pathogens. Table 2 summarizes the various functions of the five Ig antibodies [ 5 ]. Antibodies play an important role in containing virus proliferation during the acute phase of infection.
However, they are not generally capable of eliminating a virus once infection has occurred. Once an infection is established, cell-mediated immune mechanisms are most important in host defense against most intracellular pathogens. Cell-mediated immunity does not involve antibodies, but rather protects an organism through [ 2 ]:. The activation of antigen-specific cytotoxic T cells that induce apoptosis of cells displaying foreign antigens or derived peptides on their surface, such as virus-infected cells, cells with intracellular bacteria, and cancer cells displaying tumour antigens;.
The activation of macrophages and NK cells, enabling them to destroy intracellular pathogens; and. Cell-mediated immunity is directed primarily at microbes that survive in phagocytes as well as those that infect non-phagocytic cells.
This type of immunity is most effective in eliminating virus-infected cells and cancer cells, but can also participate in defending against fungi, protozoa, cancers, and intracellular bacteria.
Cell-mediated immunity also plays a major role in transplant rejection. Acquired immunity is attained through either passive or active immunization. It can occur naturally by transplacental transfer of maternal antibodies to the developing fetus, or it can be induced artificially by injecting a recipient with exogenous antibodies that are usually manufactured for this purpose and that are targeted to a specific pathogen or toxin.
The latter is used when there is a high risk of infection and insufficient time for the body to develop its own immune response, or to reduce the symptoms of chronic or immunosuppressive diseases.
Active immunization refers to the production of antibodies against a specific antigen or pathogen after exposure to the antigen. It can be acquired through either natural infection with a microbe or through administration of a vaccine that can consist of attenuated weakened pathogens, inactivated organisms or specific proteins or carbohydrates known to induce immunity.
As mentioned earlier, defects or malfunctions in either the innate or adaptive immune response can provoke illness or disease. Such disorders are generally caused by an overactive immune response known as hypersensitivity reactions , an inappropriate reaction to self known as autoimmunity or ineffective immune responses known as immunodeficiency. Hypersensitivity reactions refer to undesirable responses produced by the normal immune system.
There are four types of hypersensitivity reactions [ 6 , 7 ]:. Type I hypersensitivity is the most common type of hypersensitivity reaction.
It is an allergic reaction provoked by re-exposure to a specific type of antigen, referred to as an allergen. Unlike the normal immune response, the type I hypersensitivity response is characterized by the secretion of IgE by plasma cells. Later exposure to the same allergen cross-links the bound IgE on sensitized cells resulting in degranulation and the secretion of active mediators such as histamine, leukotrienes, and prostaglandins that cause vasodilation and smooth-muscle contraction of the surrounding tissue.
Common environmental allergens inducing IgE-mediated allergies include pet e. Food allergens are also a common cause of type I hypersensitivity reactions, however, these types of reactions are more frequently seen in children than adults. Treatment of type I reactions generally involves trigger avoidance, and in the case of inhaled allergens, pharmacological intervention with bronchodilators, antihistamines and anti-inflammatory agents.
Some types of allergic disease can be treated with immunotherapy see Allergen-specific Immunotherapy article in this supplement. Severe cases of type 1 hypersensitivity anaphylaxis may require immediate treatment with epinephrine. Type II hypersensitivity reactions are rare and take anywhere from 2 to 24 h to develop. Some examples of type II hypersensitivity reactions include: erythroblastosis fetalis, Goodpasture syndrome, and autoimmune anemias. Type III hypersensitivity reactions occur when IgG and IgM antibodies bind to soluble proteins rather than cell surface molecules as in type II hypersensitivity reactions forming immune complexes that can deposit in tissues, leading to complement activation, inflammation, neutrophil influx and mast cell degranulation.
This type of reaction can take days, or even weeks, to develop and treatment generally involves anti-inflammatory agents and corticosteroids. Examples of type III hypersensitivity reactions include systemic lupus erythematosus SLE , serum sickness and reactive arthritis.
Unlike the other types of hypersensitivity reactions, type IV reactions are cell-mediated and antibody-independent.
They are the second most common type of hypersensitivity reaction and usually take 2 or more days to develop. In general, these reactions are easily resolvable through trigger avoidance and the use of topical corticosteroids.
An example of this is the skin response to poison ivy. A brief summary of the four types of hypersensitivity reactions is provided in Table 3.
Autoimmunity involves the loss of normal immune homeostasis such that the organism produces an abnormal response to its own tissue. The hallmark of autoimmunity is the presence of self-reactive T cells, auto-antibodies, and inflammation. Poorly regulated inflammatory responses and tissue damage as a result of inflammation are often immunopathological features.
Defects in immune regulation are associated with many chronic inflammatory diseases, including: rheumatoid arthritis, psoriasis, inflammatory bowel disease and asthma. Classical features of inflammation are heat, redness, swelling and pain. Inflammation can be part of the normal host response to infection and a required process to rid the body of pathogens, or it may become uncontrolled and lead to chronic inflammatory disease.
The overproduction of inflammatory cytokines such as TNF, IL-1 and IL-6 as well as the recruitment of inflammatory cells such as neutrophils and monocytes through the function of chemokines are important drivers of the inflammatory process. Additional mediators produced by recruited and activated immune cells induce changes in vascular permeability and pain sensitivity. Immunodeficiency disorders may result from a primary genetic defect primary immunodeficiency—see Primary Immunodeficiency article in this supplement which can effect either innate or acquired immune function through inhibition of selected immune cells or pathways, or it may be acquired from a secondary cause secondary immunodeficiency , such as viral or bacterial infections, malnutrition, autoimmunity or treatment with drugs that induce immunosuppression.
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