What is meant by specific defense

The hemagglutinen and neuraminidase proteins are potential antigens, but there are only specific portions of these molecules that might be "recognized" by our immune system.

The illustration on the right is an enlarged image of a hemagglutinen protein, and the portion of the molecule circled in red might represent a specific shape, i. When influenza virus infects our cells e. However, as noted above, samples of internally synthesized proteins including viral proteins are broken down in proteosomes, and the fragments are complexed with MHC Class I molecules in the endoplasmic reticulum. The MHC Class I and attached fragments are then inserted into the cell membrane where the fragments are "presented" to cells of the immune system.

These events are depicted in the figure below. Helper T cells with matching receptors would become activated and recruit additional lymphocytes, and cytotoxic T cells with matching receptors would bind to the cell and secrete cytotoxic molecules that penetrate the infected cell and kill it, effectively ending the production of more virus particles. It then sheds its protein coat and begins to replicate viral RNA and proteins uses the cells organelles and substrates.

Some of the viral proteins are transported from the endoplasmic reticulum to proteosomes which break them into fragments which are bound to MHC Class I molecules. These are then transported to the cell membrane and inserted with the protein fragments "presented" to the exterior of the cell where T cells with matching receptors can bind to the fragments and become activated.

B lymphocytes can become activated by direct contact with a pathogen or foreign protein if they have a receptor that is complementary to an epitope on the foreign agent. Helper T cells that have become activated by antigen presentation will further stimulate the activated B cell to replicate over and over and to transform into a large clone of plasma cells that produce antibodies specific for that epitope. These antibodies are widely distributed in the circulation and can bind to the epitopes, tagging the foreign agents to facilitate its identification and destruction by phagocytic cells.

The image below shows an antibody binding to a specific epitope on two virus particles. Keep in mind, however, that antibodies can similarly participate in defense against any agent or substance that has matching epitopes. The graph below depicts the sequence of events that occur during infection with hepatitis A virus HAV. Note, first, that the presence of virus in blood viremia and in stool occurs well before the onset of symptoms, making it easy for a victim to transmit the virus to others.

Also, note that levels of IgM antibodies in blood rise early and then begin to decline. IgG levels rise somewhat later, but they persist for a much longer time. By measuring the titers concentrations of both IgM and IgG antibodies against HAV, it is possible to determine whether an individual was recently infected, or if they were infected some time ago. This information could be important in determining whether a particular food handler, for example, was responsible for an outbreak of hepatitis A.

Immunization primes the adaptive immune system to produce an immune response without actually being infected. Weakened or killed pathogens or antigenic components of a pathogen are administered to evoke a primary immune response of the adaptive immune system. This initial exposure to the antigens of an infectious agent trigger a typical immune response. Most of the immune response rapidly diminishes after a vaccination, but some lymphocytes persist with an immunologic memory.

As a result, if the same pathogen infects a vaccinated person at a later date, the memory cells rapidly spring into action and trigger a much more rapid adaptive immune response than occurred with the primary exposure. The Chinese used "variolation" - exposing uninfected individuals to matter from smallpox lesions — to prevent smallpox. Pus from a smallpox lesion could be placed under the skin with a needle.

Dried, powdered scabs from smallpox lesions could be inhaled or placed in a vein with a needle. Lady Mary Wortley Montagu, wife of the British Ambassador to Turkey, observed this method in the early s and brought it back to England. Edward Jenner was interested when a milkmaid told him she could not catch smallpox because she had had cowpox; he noted that many of the milk maids did not get smallpox.

They were renowned for their unblemished skin. In he infected a young boy with cowpox, allowed him to fully recover, and then intentionally injected the boy with pus from a smallpox lesion. The boy did not become ill. Jenner published a book and people began intentionally infecting themselves with cowpox. It was called "vaccination," after "vacca," the Latin word for cow, and the substance used to vaccinate was called a "vaccine.

Most of the lymphocytes produced in a primary immune response are involved in fighting the pathogens, but as the clone of lymphocytes expands a few thousand of them differentiate into memory cells which persist for months or years. If the same pathogen invades the organism again, the memory cells will again bind to the pathogen and begin to replicate, but memory cells can replicate more quickly. As a result, a secondary exposure to a given antigen triggers an immune response that is much more rapid and more vigorous than that seen with the first exposure.

Active immunity occurs when an individual is infected with a pathogen or if they are vaccinated. Exposure to the pathogen's antigens by either of these will result in a primary immune response and immunologic memory. However, it is also possible in some circumstances to protect a susceptible person by giving them the antibodies produced by another person.

For example, if we were to take serum from people who had previously been infected with hepatitis A virus HAV , it would contain significant concentrations of IgG against HAV. It is possible to pool serum from previously infected individuals and then inject this immunoglobulin G into individuals who may have been recently been exposed to HAV in order to thwart the infection and prevent them from becoming a clinically active case.

In essence, passive immunization:gives antibodies made by others e. However, this passive form of protection bypasses the steps in primary exposure, and it does not produce immunologic memory. Moreover, the protection afforded by this passive form of immunity only lasts as long as the exogenous antibodies, about months. After the exogenous antibodies disappear, the individual is just as susceptible as a person who had never been exposed. The guidelines vary by age and health status:.

IgG is able to cross the placenta from mother to fetus. As a result, newborn infants receive some passive immunity from antigens to which their mother has been exposed. However, this passive protection disappears over a period of months, so it is important for the infant to develop active immunity through vaccinations or by being infected and developing clinical disease. The decline in passive immunity in an infant is what dictates the recommended schedule of immunizations for infants.

Each lymphocyte has only one type of epitope receptor, but pathogens have many potential antigenic molecules, each of which may have several epitopes. In addition, the epitopes for some pathogens, such as those on influenza's hemagglutinen protein, change from year to year as a result of mutations. Consequently, the number of possible foreign epitopes is enormous, but the human genome only has about 30, genes.

Specificity and memory are achieved by essentially programming certain cells involved in the immune response to respond rapidly to subsequent exposures of the pathogen. This programming occurs as a result of the first exposure to a pathogen or vaccine, which triggers a primary response. This secondary response, however, is specific to the pathogen in question. For example, exposure to one virus e.

Adaptive specific immunity involves the actions of two distinct cell types: B lymphocytes B cells and T lymphocytes T cells. Although B cells and T cells arise from a common hematopoietic stem cell differentiation pathway see Figure 1 in Cellular Defenses , their sites of maturation and their roles in adaptive immunity are very different.

B cells mature in the bone marrow and are responsible for the production of glycoproteins called antibodies , or immunoglobulins. Mechanisms of adaptive specific immunity that involve B cells and antibody production are referred to as humoral immunity.

The maturation of T cells occurs in the thymus. T cells function as the central orchestrator of both innate and adaptive immune responses. They are also responsible for destruction of cells infected with intracellular pathogens. The targeting and destruction of intracellular pathogens by T cells is called cell-mediated immunity, or cellular immunity.

Activation of the adaptive immune defenses is triggered by pathogen-specific molecular structures called antigens. Antigens are similar to the pathogen-associated molecular patterns PAMPs discussed in Pathogen Recognition and Phagocytosis ; however, whereas PAMPs are molecular structures found on numerous pathogens, antigens are unique to a specific pathogen.

The antigens that stimulate adaptive immunity to chickenpox, for example, are unique to the varicella-zoster virus but significantly different from the antigens associated with other viral pathogens.

The term antigen was initially used to describe molecules that stimulate the production of antibodies; in fact, the term comes from a combination of the words anti body and gen erator, and a molecule that stimulates antibody production is said to be antigenic. However, the role of antigens is not limited to humoral immunity and the production of antibodies; antigens also play an essential role in stimulating cellular immunity, and for this reason antigens are sometimes more accurately referred to as immunogens.

In this text, however, we will typically refer to them as antigens. Pathogens possess a variety of structures that may contain antigens. For example, antigens from bacterial cells may be associated with their capsules, cell walls, fimbriae, flagella, or pili. Bacterial antigens may also be associated with extracellular toxins and enzymes that they secrete.

Viruses possess a variety of antigens associated with their capsids, envelopes, and the spike structures they use for attachment to cells. Figure 2. An antigen is a macromolecule that reacts with components of the immune system. A given antigen may contain several motifs that are recognized by immune cells.

Antigens may belong to any number of molecular classes, including carbohydrates, lipids, nucleic acids, proteins, and combinations of these molecules. Antigens of different classes vary in their ability to stimulate adaptive immune defenses as well as in the type of response they stimulate humoral or cellular.

The structural complexity of an antigenic molecule is an important factor in its antigenic potential. In general, more complex molecules are more effective as antigens. For example, the three-dimensional complex structure of proteins make them the most effective and potent antigens, capable of stimulating both humoral and cellular immunity. In comparison, carbohydrates are less complex in structure and therefore less effective as antigens; they can only stimulate humoral immune defenses.

Lipids and nucleic acids are the least antigenic molecules, and in some cases may only become antigenic when combined with proteins or carbohydrates to form glycolipids, lipoproteins, or nucleoproteins. Figured 3. A typical protein antigen has multiple epitopes, shown by the ability of three different antibodies to bind to different epitopes of the same antigen.

One reason the three-dimensional complexity of antigens is so important is that antibodies and T cells do not recognize and interact with an entire antigen but with smaller exposed regions on the surface of antigens called epitopes. A single antigen may possess several different epitopes Figure 2 , and different antibodies may bind to different epitopes on the same antigen Figure 3. For example, the bacterial flagellum is a large, complex protein structure that can possess hundreds or even thousands of epitopes with unique three-dimensional structures.

Moreover, flagella from different bacterial species or even strains of the same species contain unique epitopes that can only be bound by specific antibodies. Whereas large antigenic structures like flagella possess multiple epitopes, some molecules are too small to be antigenic by themselves. Such molecules, called haptens , are essentially free epitopes that are not part of the complex three-dimensional structure of a larger antigen.

For a hapten to become antigenic, it must first attach to a larger carrier molecule usually a protein to produce a conjugate antigen. However, the effect of the adaptive immune response is long-lasting, highly specific, and is sustained long-term by memory T cells. Natural killer cells, macrophages, neutrophils, dendritic cells, mast cells, basophils, eosinophils. Tell us what you think about Healio.

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Visit Healio. Your Module Progress. 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. An inefficient immune response allows diseases to develop.

Too much, too little, or the wrong immune response causes immune system disorders. An overactive immune response can lead to the development of autoimmune diseases , in which antibodies form against the body's own tissues. Innate immunity; Humoral immunity; Cellular immunity; Immunity; Inflammatory response; Acquired adaptive immunity.