The largest of all is the skin which acts as a strong, waterproof, physical barrier and very few organisms are able to penetrate undamaged skin. There are other physical barriers and a variety of chemical defences. 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.
The advantages of subunit vaccines are the same as toxoid vaccines with the added benefit that one can distinguish vaccinated people from infected people—for example with hepatitis B vaccination, only an adaptive immune response to the surface antigen is possible whereas with infection core and e responses occur.
Subunit vaccines share the same disadvantages as toxoid vaccines, namely the need for an adjuvant and often multiple doses , together with the frequent occurrence of local reactions at the injection site. There are several approaches to attenuating a viral pathogen for use in humans.
One involves growing the virus in a foreign host—for example, measles virus is cultivated in chick egg fibroblasts—viral replication in such circumstances results in the appearance of a number of mutant types: those mutants with enhanced virulence for the foreign host are then selected as potential vaccine strains since they generally show reduced virulence for the human host and this is a particularly useful approach for RNA viruses which have a high mutation rate.
The molecular basis of attenuation in these circumstances is not known since the process is largely empiric and it is not possible to determine which of the observed genomic nucleotide changes are associated with diminished virulence. An alternative approach is to grow the wild virus in an artificial growth medium at a temperature lower than that found in the human body—over time a strain may emerge which grows well at this lower temperature but multiplies so slowly in humans that adaptive immune responses are able to eliminate it before the virus is able to spread and cause infection—the cold-adapted live attenuated influenza vaccine is an example of this.
Live attenuated vaccines that might be used in the occupational setting include measles, mumps, rubella and chickenpox. Within the cytosol, proteolytic degradation of viral proteins occurs; the peptides produced are then loaded onto major histocompatibility complex type I molecules and the complex is displayed on the cell surface. Circulating cytotoxic T cells Tc with the appropriate high-specificity TCRs are able to recognize the complex and release cytokines that instruct the infected cell to undergo programmed suicide apoptosis [ 12 ].
It appears that some Tc become memory cells but the basis of this is incompletely understood. Additionally, immature dendritic cells will phagocytose virus vaccine initiating the same process previously described for protein antigens that leads to the production of plasma cells, neutralizing IgG antibodies and memory B cells. In an adequately immunized individual, when wild measles virus is inhaled, then both mechanisms of protection work—thus for virus multiplying locally at the site of infection, Tc are able to kill infected cells; for virus that evades this and spreads through the blood stream IgG antibody there will bind it and prevent disease by neutralizing attachment to the target cell [ 9 ].
One disadvantage to live attenuated vaccines is the possibility that they may cause the illness they are designed to protect against either because they revert to virulence or because for some individuals for example, those who are immunosuppressed they are insufficiently attenuated. T-independent antigens generally polysaccharides can be converted to effective T-dependent vaccines by conjugating the polysaccharide molecule to a carrier protein.
Varicella-Zoster and hepatitis B gammaglobulin IgG preparations are examples of passive immunity which have considerable applications to the occupational health situation. Google Scholar. Google Preview. Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide.
Sign In or Create an Account. Sign In. Advanced Search. Search Menu. Article Navigation. Close mobile search navigation Article Navigation. Volume Article Contents Abstract. Active and passive immunity. Vaccine types. Conflicts of interest. Active and passive immunity, vaccine types, excipients and licensing.
David Baxter David Baxter. Oxford Academic. Select Format Select format. Permissions Icon Permissions. Passive Immunity - antibodies given to a person to prevent disease or to treat disease after the body is exposed to an antigen.
Passive immunity is given from mother to child through the placenta before birth, and through breast milk after birth.
It can also be given medically through blood products that contain antibodies, such as immune globulin. This type of immunity is fast acting but lasts only a few weeks or months.
How vaccines work with the immune system Vaccines provide active immunity to disease. Here is how a vaccination works: The vaccine is administered. It contains antigens to a specific disease. The immune system identifies the antigens in the vaccine as foreign invaders. The immune system then develops antibodies to neutralize the antigens. The immune system stores these antibodies for future use in case the person is ever exposed to the disease. NIH: Vaccine Benefits. Although these attempts were successful in providing immunity, the underlying processes required to produce this immunity were unknown.
From a literature review of the current literature, this article will provide an introduction to vaccine immunology including a primer on the components of the immune system, passive vs. Both the innate system and the adaptive system continually interact with each other to provide an effective immune response.
The innate immune system or general resistance includes a variety of protective measures which are continually functioning and provides a first-line of defense against pathogenic agents. However, these responses are not specific to a particular pathogenic agent. Instead, the innate immune cells are specific for conserved molecular patterns found on all microorganisms. This prevents the innate immune system from inadvertently recognizing host cells and attacking them.
However, this prevents the innate immune responses from improving their reactions with repeated exposure to the same pathogenic agent. In other words, the innate immune system does not have memory. The protective defenses of the innate immune system begin with the anatomic barriers such as intact skin and mucous membranes which prevent the entrance of many microorganisms and toxic agents. The skin also has an acidic environment of pH which retards the growth of microorganisms. In addition, the normal microorganisms or flora, which inhabit the skin and mucous membranes compete with other microorganisms for nutrients and attachment sites.
Further, the mucus and cilia on the mucous membranes aid in trapping microorganisms and propelling them out of the body. Next, the innate immune system includes such physiologic barriers as the normal body temperature, fever, gastric acidity, lysozyme, interferon, and collectins. The normal body temperature range inhibits a variety of microorganisms; and, the development of a fever can further inhibit many of these pathogenic organisms. The gastric acidity of the stomach is also quite effective in eliminating many ingested microorganisms.
Lysozyme, which is a hydrolytic enzyme found in tears and mucous secretions, can cleave the peptidoglycan layer of the bacterial cell wall thus lysing the microorganism. They can directly kill certain pathogenic microorganisms by disrupting their lipid membranes or indirectly by clumping microorganisms to enhance their susceptibility to phagocytosis.
The complement pathways are also a part of the defensive measures of the innate immune system. There are three complement pathways. The alternative or properdin pathway is triggered by the deposition of complement protein, C3b, onto microbial surfaces and does not require antibodies for activation.
The third pathway, the lectin pathway, is triggered by the attachment of plasma mannose-binding lectin MBL to microbes and does not require antibodies for activation. These three pathways merge into a common pathway which leads to the formation of the membrane attack complex that can form pores in the membrane of targeted cells. The complement pathways are also integral in the opsonization or increased susceptibility of particulate antigens to phagocytosis and in triggering a localized inflammatory response.
The inflammatory response is another essential part of the innate immune response. The inflammatory response is the body's reaction to invasion by an infectious agent, antigenic challenge, or any type of physical damage. The inflammatory response allows products of immune system into area of infection or damage and is characterized by the cardinal signs of redness, heat, pain, swelling, and loss of function.
In addition to the anatomic and physiologic mechanisms, there are also Pattern recognition receptors or PRRs which contribute to the innate immune response. Pattern recognition receptors are not specific for any given pathogen or antigen, but can provide a rapid response to antigens. PRRs are classified as membrane proteins because they are associated with the cell membrane; and, they can be found in all the membranes of the cells in the innate immune system. Although there are several hundred varieties, all the genes of the PRRs are encoded in the germline to ensure limited variability in their molecular structures.
These antigens are produced by microbal cells and not by human cells. Finally, the mononuclear phagocytes and granulocytic cells are also important to the innate response and help link the innate immune response to the adaptive immune response.
Mononuclear phagocytes include monocytes which circulate in the blood and macrophages which are in the tissues. Monocytes and macrophages are highly important in antigen presentation, phagocytosis, cytokine production, and antimicrobial and cytotoxic activities.
Upon maturity of the monocytes, the monocytes circulate in the blood for approximately 8 h, then migrate into the tissues and differentiate into specific tissue macrophages or into dendritic cells. There are several types of dendritic cells which are involved in different aspects of immune functions.
Many dendritic cells are important in presenting antigen to T-helper cells. However, follicular dendritic cells are found only in lymph follicles and are involved in the binding of antigen—antibody complexes in lymph nodes. Neutrophils are highly active phagocytic cells and generally arrive first at a site of inflammation.
Eosinophils are also phagocytic cells; however, they are more important in resistance to parasites. Basophils in the blood and mast cells in the tissues release histamine and other substances and are important in the development of allergies.
The innate system may be able to eradicate the pathogenic agent without further assistance from the adaptive system; or, the innate system may stimulate the adaptive immune system to become involved in eradicating the pathogenic agent. In contrast to the innate immune system, the actions of adaptive immune system are specific to the particular pathogenic agent. This response will take longer to occur than the innate response.
However, the adaptive immune system has memory which means that the adaptive immune system will respond more rapidly to that particular pathogen with each successive exposure. These are the two arms of the adaptive immune system. The B—cells and antibodies compose humoral immunity or antibody-mediated immunity; and, the T-cells compose cell-mediated immunity. As a note, natural killer cells are also from the lymphocyte lineage like B—cells and T-cells; however, natural killer cells are only involved in innate immune responses.
The first arm of the adaptive immune system is humoral immunity, functions against extracellular pathogenic agents and toxins.
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