It is characterised by an abnormal immune response that targets myelin, a fatty material responsible for insulating the nerve fibres in the central nervous system. This causes the disruption of nerve impulses. Healthdirect Australia is not responsible for the content and advertising on the external website you are now entering.
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Your email: is required Error: This is required Error: Not a valid value. Send to: is required Error: This is required Error: Not a valid value. On this page What is the immune system? How does the immune system work?
How can the immune system go wrong? Related information on Australian websites What is the immune system? Parts of the immune system are: skin — the first line of defence bone marrow — helps produce immune cells the thymus, a gland in the upper chest where some immune cells mature lymphatic system, a network of tiny vessels which allows immune cells to travel between tissues and the bloodstream.
The lymphatic system contains lymphocytes white blood cells; mostly T cells and B cells , which try to recognise any bacteria, viruses or other foreign substances in the body and fight them. Haemophilus influenzae type b Hib. Hepatitis A and Hepatitis B. History of Polio Poliomyelitis. Human Papillomavirus Infection. Meningococcal Disease. Pertussis Whooping Cough. Pneumococcal Disease. Shingles Herpes Zoster. Typhoid Fever. Vaccines for Sexually Transmitted Diseases.
Yellow Fever. Common Questions [ ]. Do Vaccines Cause Autism? Have I Been Vaccinated? Misconceptions about Vaccines. Top 20 Questions about Vaccination. Vaccination for Rare Diseases. Why Vaccinate? Which vaccine developer isolated the mumps virus from his daughter? Correct Maurice Hilleman isolated the mumps virus from his daughter Jeryl Lynn while she was ill. Antigen-presenting cells are phagocytes white blood cells that display pieces of antigens to other cells of the immune system.
Killer T cells can find and destroy infected body cells. Non-Specific Innate Immunity The human immune system has two levels of immunity: specific and non-specific immunity.
Specific Immunity While healthy phagocytes are critical to good health, they are unable to address certain infectious threats. T helper cells release chemicals to Help activate B cells to divide into plasma cells Call in phagocytes to destroy microbes Activate killer T cells Once activated, killer T cells recognize infected body cells and destroy them.
Organs and Tissues The cells that make up the specific immune response circulate in the blood, but they are also found in a variety of organs. I nfection and Disease Infection occurs when a pathogen invades body cells and reproduces.
For more on vaccination, see the activity How Vaccines Work. Assessment Questions True or false? Only invertebrates have specific immune responses. True False. This activity is best viewed on larger screens. Literally it means antibody generator. One of the most amazing features of the immune system is that B cells can recognise millions of different antigens.
B cells can recognise antigens that have never entered the body before and even man-made molecules that don't even exist in nature. When a foreign particle enters your body, B cells recognise it, binding to the antigen on its surface. This activates the B cell which then changes into a plasma cell. The plasma cell makes antibodies specific to that antigen. Antibodies can immobilise bacteria, encourage other cells to 'eat' the pathogen and activate other immune defences.
While some B cells become plasma cells, others don't. These cells live on as memory B cells that respond more vigorously should the same antigen invade your body again. T cells directly attack the invading organism; however, they are not able to recognise antigens without the help of other cells. These cells process the antigen and then present them to T cells. T cells are very different from each other. When an antigen enters the body only a few T cells are able to recognise and bind to the antigen.
While T cells also bind to antigens they need a second signal to become activated. Once activated, T cells get bigger and start to divide.
These cells then target the invaders and release chemicals that destroy the pathogen. Like B cells, some of the T cells remain to form memory T cells.
This allows your body to respond quickly if the same antigen enters your body. The lymphatic system is a major part of your body's defence against infection. Lymph nodes are one of the components of this system. These are specialised structures which are found in lymph vessels.
Lymph nodes are a filter for the lymph flowing through the vessels. They contain B and T cells which recognise bacteria and pathogens which have entered your lymph via your bloodstream. When foreign material is detected, other dedicated immune cells are recruited to the node to deal with the infection. This helps to prevent the infection from spreading throughout your body. There are around lymph nodes throughout your body, usually in groups.
Large groups of lymph nodes are found in your groin inguinal nodes , in your armpit axillary nodes and in your neck area cervical nodes. In health they are pea-sized but if you develop an infection you may find that they become enlarged. This is due to a build-up accumulation of lymphocytes and other cells of the immune system.
Lymphoid tissue helps to defend mucosal surfaces, such as the mouth and intestines, from infection. Your tonsils, which are found in the back of your throat, often become enlarged in response to infection.
These tissues help to trap bacteria and other pathogens and activate white blood cells. The thymus is an important lymphatic organ.
It is found in front of your windpipe trachea. Its main role is to teach white blood cells to recognise our own cells. Although most mucosal surfaces are in the interior of the body, some are contiguous with the external skin at various body openings, including the eyes, nose, mouth, urethra, and anus.
Most pathogens are suited to a particular portal of entry. The respiratory and gastrointestinal tracts are particularly vulnerable portals of entry because particles that include microorganisms are constantly inhaled or ingested, respectively. Pathogens can also enter through a breach in the protective barriers of the skin and mucous membranes. Pathogens that enter the body in this way are said to enter by the parenteral route.
For example, the skin is a good natural barrier to pathogens, but breaks in the skin e. In pregnant women, the placenta normally prevents microorganisms from passing from the mother to the fetus.
However, a few pathogens are capable of crossing the blood-placental barrier. The gram-positive bacterium Listeria monocytogenes , which causes the foodborne disease listeriosis, is one example that poses a serious risk to the fetus and can sometimes lead to spontaneous abortion.
Other pathogens that can pass the placental barrier to infect the fetus are known collectively by the acronym TORCH Table 3. Transmission of infectious diseases from mother to baby is also a concern at the time of birth when the baby passes through the birth canal. Babies whose mothers have active chlamydia or gonorrhea infections may be exposed to the causative pathogens in the vagina, which can result in eye infections that lead to blindness.
Fifth disease erythema infectiosum Treponema pallidum bacterium. Upon learning that Pankaj became sick the day after the party, the physician orders a blood test to check for pathogens associated with foodborne diseases. There he is to receive additional intravenous antibiotic therapy and fluids. Following the initial exposure, the pathogen adheres at the portal of entry. The term adhesion refers to the capability of pathogenic microbes to attach to the cells of the body using adhesion factors , and different pathogens use various mechanisms to adhere to the cells of host tissues.
Figure 4. Glycocalyx produced by bacteria in a biofilm allows the cells to adhere to host tissues and to medical devices such as the catheter surface shown here. Molecules either proteins or carbohydrates called adhesins are found on the surface of certain pathogens and bind to specific receptors glycoproteins on host cells.
Adhesins are present on the fimbriae and flagella of bacteria, the cilia of protozoa, and the capsids or membranes of viruses. Protozoans can also use hooks and barbs for adhesion; spike proteins on viruses also enhance viral adhesion. The production of glycocalyces slime layers and capsules Figure 4 , with their high sugar and protein content, can also allow certain bacterial pathogens to attach to cells.
Biofilm growth can also act as an adhesion factor. A biofilm is a community of bacteria that produce a glycocalyx, known as extrapolymeric substance EPS , that allows the biofilm to attach to a surface.
Persistent Pseudomonas aeruginosa infections are common in patients suffering from cystic fibrosis, burn wounds, and middle-ear infections otitis media because P.
The EPS allows the bacteria to adhere to the host cells and makes it harder for the host to physically remove the pathogen. The EPS not only allows for attachment but provides protection against the immune system and antibiotic treatments, preventing antibiotics from reaching the bacterial cells within the biofilm.
In addition, not all bacteria in a biofilm are rapidly growing; some are in stationary phase. Since antibiotics are most effective against rapidly growing bacteria, portions of bacteria in a biofilm are protected against antibiotics.
Once adhesion is successful, invasion can proceed. Invasion involves the dissemination of a pathogen throughout local tissues or the body. Pathogens may produce exoenzymes or toxins, which serve as virulence factors that allow them to colonize and damage host tissues as they spread deeper into the body. Pathogens may also produce virulence factors that protect them against immune system defenses.
Figure 5 shows the invasion of H. Figure 5. Some are obligate intracellular pathogens meaning they can only reproduce inside of host cells and others are facultative intracellular pathogens meaning they can reproduce either inside or outside of host cells. By entering the host cells, intracellular pathogens are able to evade some mechanisms of the immune system while also exploiting the nutrients in the host cell.
Entry to a cell can occur by endocytosis. For most kinds of host cells, pathogens use one of two different mechanisms for endocytosis and entry. One mechanism relies on effector proteins secreted by the pathogen; these effector proteins trigger entry into the host cell. This is the method that Salmonella and Shigella use when invading intestinal epithelial cells. When these pathogens come in contact with epithelial cells in the intestine, they secrete effector molecules that cause protrusions of membrane ruffles that bring the bacterial cell in.
This process is called membrane ruffling. The second mechanism relies on surface proteins expressed on the pathogen that bind to receptors on the host cell, resulting in entry.
For example, Yersinia pseudotuberculosis produces a surface protein known as invasin that binds to beta-1 integrins expressed on the surface of host cells. Some host cells, such as white blood cells and other phagocytes of the immune system, actively endocytose pathogens in a process called phagocytosis. Although phagocytosis allows the pathogen to gain entry to the host cell, in most cases, the host cell kills and degrades the pathogen by using digestive enzymes.
Normally, when a pathogen is ingested by a phagocyte, it is enclosed within a phagosome in the cytoplasm; the phagosome fuses with a lysosome to form a phagolysosome, where digestive enzymes kill the pathogen see Pathogen Recognition and Phagocytosis. However, some intracellular pathogens have the ability to survive and multiply within phagocytes. Bacteria such as Mycobacterium tuberculosis , Legionella pneumophila , and Salmonella species use a slightly different mechanism to evade being digested by the phagocyte.
These bacteria prevent the fusion of the phagosome with the lysosome, thus remaining alive and dividing within the phagosome. Following invasion, successful multiplication of the pathogen leads to infection. Infections can be described as local, focal, or systemic, depending on the extent of the infection.
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