Antibodies are disease-specific. For example, measles antibody will protect a person who is exposed to measles disease but will have no effect if he or she is exposed to mumps. Active Immunity results when exposure to a disease organism triggers the immune system to produce antibodies to that disease. Active immunity can be acquired through natural immunity or vaccine-induced immunity.
Either way, if an immune person comes into contact with that disease in the future, their immune system will recognize it and immediately produce the antibodies needed to fight it. This is also how immunizations vaccines prevent some diseases. An immunization introduces the body to an antigen in a way that doesn't make someone sick.
But it does let the body make antibodies that will protect the person from future attack by the germ. Although antibodies can recognize an antigen and lock onto it, they can't destroy it without help. That's the job of the T cells. They destroy antigens tagged by antibodies or cells that are infected or somehow changed. Some T cells are actually called "killer cells. These specialized cells and parts of the immune system offer the body protection against disease. This protection is called immunity.
The immune system takes a while to develop and needs help from vaccines. Simultaneously, toxoid molecules not taken up by dendritic cells pass along lymph channels to the same draining lymph nodes where they come into contact with B cells, each with their own unique B-cell receptor BCR. Binding to the B cell through the specific immunoglobulin receptor that recognizes tetanus toxoid results in the internalization of toxoid, processing through the endosomal pathway and presentation on the cell surface as an MHC II:toxoid complex as happens in the dendritic cell.
These two processes occur in the same part of the lymph node with the result that the B cell with the MHC II:toxoid complex on its surface now comes into contact with the activated T H 2 whose receptors are specific for this complex. The process, termed linked recognition, results in the T H 2 activating the B cell to become a plasma cell with the production initially of IgM, and then there is an isotype switch to IgG; in addition, a subset of B cells becomes memory cells. The above mechanism describes the adaptive immune response to a protein antigen-like tetanus toxoid; such antigens are termed T-dependent vaccines since the involvement of T helper cells is essential for the immune response generated.
Polysaccharide antigens in contrast generate a somewhat different response as will be described in the section on subunit vaccines. The rationale for tetanus vaccination is thus based on generating antibodies against the toxoid which have an enhanced ability to bind toxin compared with the toxin receptor binding sites on nerve cells; in the event of exposure to C.
Diphtheria and pertussis toxoid in acellular pertussis vaccines are two commercially available toxoid vaccines against which antibodies are produced in an exactly analogous manner as described above. Tetanus and diphtheria vaccines together with inactivated polio should be offered in the occupational setting to workers who have not completed a five-dose programme.
Toxoid vaccines tend not to be highly immunogenic unless large amounts or multiple doses are used: one problem with using larger doses is that tolerance can be induced to the antigen. In order therefore to ensure that the adaptive immune response is sufficiently effective to provide long-lasting immunity, an adjuvant is included in the vaccine.
For diphtheria, tetanus and acellular pertussis vaccines, an aluminium salt either the hydroxide or phosphate is used; this works by forming a depot at the injection site resulting in sustained release of antigen over a longer period of time, activating cells involved in the adaptive immune response. There are three principal advantages of toxoid vaccines. First, they are safe because they cannot cause the disease they prevent and there is no possibility of reversion to virulence. Second, because the vaccine antigens are not actively multiplying, they cannot spread to unimmunized individuals.
Third, they are usually stable and long lasting as they are less susceptible to changes in temperature, humidity and light which can result when vaccines are used out in the community. Toxoid vaccines have two disadvantages. First, they usually need an adjuvant and require several doses for the reasons discussed above. Second, local reactions at the vaccine site are more common—this may be due to the adjuvant or a type III Arthus reaction—the latter generally start as redness and induration at the injection site several hours after the vaccination and resolve usually within 48—72 h.
The reaction results from excess antibody at the site complexing with toxoid molecules and activating complement by the classical pathway causing an acute local inflammatory reaction. The term killed generally refers to bacterial vaccines, whereas inactivated relates to viral vaccines [ 3 , 4 ]. Typhoid was one of the first killed vaccines to be produced and was used among the British troops at the end of the 19th century.
Polio and hepatitis A are currently the principal inactivated vaccines used in the UK—in many countries, whole cell pertussis vaccine continues to be the most widely used killed vaccine. Thus, following injection, the whole organism is phagocytosed by immature dendritic cells; digestion within the phagolysosome produces a number of different antigenic fragments which are presented on the cell surface as separate MHC II:antigenic fragment complexes.
Within the draining lymph node, a number of T H 2, each with a TCR for a separate antigenic fragment, will be activated through presentation by the activated mature dendritic cell. B cells, each with a BCR for a separate antigenic fragment, will bind antigens that drain along lymph channels: the separate antigens will be internalized and presented as an MHC II:antigenic fragment; this will lead to linked recognition with the appropriate T H 2.
This process takes a minimum of 10—14 days but on subsequent exposure to the organism, a secondary response through activation of the various memory B cells is induced which leads to high levels of the different IgG molecules within 24—48 h. Hepatitis A is an example of an inactivated vaccine that might be used by occupational health practitioners.
Vaccination should be considered for laboratory workers working with HAV and sanitation workers in contact with sewage. Additionally, staff working with children who are not toilet trained or in residential situations where hygiene standards are poor may also be offered vaccination. Primary immunization with a booster between 6 and 12 months after the first should provide a minimum 25 years protection [ 3 ]. They usually require several doses because the microbes are unable to multiply in the host and so one dose does not give a strong signal to the adaptive immune system; approaches to overcome this include the use of several doses and giving the vaccine with an adjuvant [ 8 ].
Local reactions at the vaccine site are more common—this is often due to the adjuvant. Using killed microbes for vaccines is inefficient because some of the antibodies will be produced against parts of the pathogen that play no role in causing disease. Some of the antigens contained within the vaccine, particularly proteins on the surface, may actually down-regulate the body's adaptive response—presumably, their presence is an evolutionary development that helps the pathogen overcome the body's defences.
In this article, we will explore active and passive immunity. Active immunity is defined as immunity to a pathogen that occurs following exposure to said pathogen.
When the body is exposed to a novel disease agent, B cells, a type of white blood cell, create antibodies that assist in destroying or neutralizing the disease agent. Antibodies are y-shaped proteins that are capable of binding to sites on toxins or pathogens called antigens. Antibodies are disease-specific, meaning that each antibody protects the body from only one disease agent. For instance, antibodies produced when the body detects the virus that causes mumps will not provide any defense against cold or flu viruses.
A diagram showing the different types of active and passive immunity. When B cells encounter a pathogen, they create memory cells in addition to antibodies. Memory cells are a type of B cell produced following the primary infection that can recognize the pathogen. Memory cells can survive for decades, waiting within the body until the pathogen invades again.
When the body is exposed to the pathogen for a second time, the immune response is more robust, quickly addressing the disease agent. Immunity does not happen immediately upon disease exposure.
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