Immunity Chapter 9 PDF

CHAPTER 9 Immunity Examples of pathogens Physical / chemical barriers Innate immunity Adaptive immunity Lymphatic system Immunization Organ donation Problems with the immune system  Examples of potential invaders Viral: Influenza (flu), common cold, chicken pox, HIV/AIDS, COVID 19 Bacte...

CHAPTER 9 Immunity Examples of pathogens Physical / chemical barriers Innate immunity Adaptive immunity Lymphatic system Immunization Organ donation Problems with the immune system  Examples of potential invaders Viral: Influenza (flu), common cold, chicken pox, HIV/AIDS, COVID 19 Bacterial: Tuberculosis, salmonella, cholera, urinary tract infections, gonorrhea Protist: Malaria, amoebic dysentery Fungal: Athlete’s foot, yeast infection Animal: Intestinal fluke, whip worm Whip worm Burrows into the tissue surrounding the large intestine. May cause rectal bleeding  anemia and diarrhea  dehydration Intestinal Fluke Attaches to the inside of the small intestine, causing sores and inflammation. Severe infections can cause nutritional deficiencies.  Defenses against invaders Physical / chemical surface barriers (1st line of defense). Prevent pathogens from entering our bodies. Nonspecific defenses “innate immunity”(2nd line). Attack pathogens that enter the body, but do not recognize specific pathogens, and are not important for long-term immunity Specific defenses “adaptive immunity” (3rd line) Recognize specific pathogens the body has been exposed to before, responsible or long-term immunity Physical / chemical barriers: Skin The epidermis consists of many layers of tightly- packed cells, providing a good physical barrier preventing pathogens from entering the body. pH of skin = 5-6: too acidic for many microorganisms Resident, harmless bacteria on the skin’s surface may out-compete pathogens White blood cells to kill pathogens that get past the epidermis Other physical / chemical barriers Other protection where skin cannot be: Tears, saliva, mucus (contain lysozymes that kill bacteria) Earwax Digestive acids Resident bacteria produce vaginal acids Urination Vomiting Defecation/ diarrhea Innate immunity: Neutrophil WBC’s Neutrophils 2/3 of our WBC’s are neutrophils. Attracted by chemicals released by bacterially infected or damaged tissue, they leave capillaries, phagocytize (engulf) bacteria and digest them with lysosomes. Dead neutrophils contribute to pus.  Innate immunity: macrophage WBC’s Monocyte WBC’s become macrophages. Also leave capillaries (like neutrophils), that phagocytize (engulf) bacteria, dead bacterial and tissue cells and dead neutrophils. Macrophages release cytokine chemicals (pyrogens) that trigger fevers. Macrophages also function as antigen-presenting cells. Macrophages with engulfed cells  Innate immunity: fever Raising the body temperature can create an unfavorable temperature for bacteria, so mild fevers (up to 39 degrees C) can be useful Increases activity of white blood cells and cells healing damaged tissue. High, sustained fevers can be dangerous, as they may lead to important proteins being denatured.  Innate immunity: eosinophil WBC’s Attacks invaders that are large (parasites like worms) by surrounding them and releasing digestive enzymes on them. Innate immunity: natural killer cell WBC’s Recognizes our own cells that have become infected with viruses, and our own cells that have become cancerous and kills them. Natural killer cells attacking a cancerous cell Innate immunity: complement proteins Present in blood and tissue fluids. Activated complement proteins: -Attach themselves to pathogens -They attract neutrophils and macrophages to engulf and destroy pathogens -They help neutrophils and macrophages attach to pathogens to phagocytize (engulf) them. Innate immunity: complement proteins Complement proteins form membrane attack complexes that “punch holes” in bacterial cell membranes. The water rushes through these holes into the bacteria (osmosis) and they rupture. Innate immunity: inflammatory response Inflammatory response caused by mast cells in connective tissue and basophils WBC’s, both of which release histamine chemicals that cause inflammation. Signs: Redness Warmth Swelling (edema) Pain Innate immunity: inflammatory response 1) Tissue damage  histamine released by basophils and mast cells (in connective tissue) 2) Histamine causes arterioles to dilate, so more blood flows through them, thus the inflamed area becomes more red and warmer. Increased temperature makes white blood cells, and cells involved in tissue repair, more active. More blood flow to the area means more nutrients and oxygen to white blood cells and cells involved with tissue repair. 3) Histamines also cause the spaces between capillary cells to become wider. “Leaky” capillaries  more nutrients, clotting proteins, complement proteins, phagocytic white blood cells escape capillaries into surrounding tissues (swelling). Clotting proteins “wall off” injured area. 4) Swelling puts pressure on pain receptors. Also damaged tissue releases chemicals that stimulate pain receptors. Pain is useful: you know something is wrong, so you take care of yourself. Innate immunity: inflammatory response Adaptive immunity: lymphocyte WBC’s B cells: produce protein antibodies that bind to foreign antigens (surface proteins of viruses, bacteria, etc.) Cytotoxic T cells: “touch kill” foreign cells, or our own cells that are virus- infected or cancerous Helper T cells: coordinate the immune response, by causing the cell division of the cytotoxic T and B lymphocytes. All are mostly found in the lymphatic system, especially lymph nodes. Adaptive immunity: key features 1) Targets specific foreign antigens (that you’ve been exposed to before): each B or T cell has proteins for 1 specific antigen (each B cell and each T cell produces different proteins). 2) We have over 1 billion different B lymphocytes and T lymphocytes (high diversity), each of which is unique and targets a different antigen. So any foreign antigen that enters our body will have a B and T cell with matching proteins. 3) During initial exposure to an antigen, we produce memory B and T cells. These lie in wait in our bodies, so that if we encounter the same pathogen in the future, we can mount a quick and overwhelming response, so we do not get sick again. This is the basis of long-term immunity Adaptive immunity: B cells and antibodies Each B lymphocyte cell produces one unique protein antibody. We have millions of different B lymphocytes. Each different antibody type can bind to a different antigen. So we have B cells that produce an antibody that will bind to any foreign antigen that enters our body. Adaptive immunity: B cells and antibodies If one B lymphocyte binds to an antigen it multiplies rapidly, forming effector B cells and memory cells just like it (same antibodies). Effector B cells secrete antibodies into lymph (one cell can make 2,000 antibodies / sec.!), to bind to other pathogens with the same antigen. Lymph vessels joined to blood vessels, so they circulate there too. Memory B cells: remain in the body for a quick, overwhelming response to future attack by the same pathogen (so you do not get sick again).  What antibodies do Activate complement proteins Immobilize bacteria or viral pathogens (prevent viruses from entering our cells, for example) Signal phagocytes to engulf the pathogen Adaptive immunity: T cells Each helper T and cytotoxic T lymphocyte cell produces one unique protein receptor. We have millions of different T lymphocytes. Each different protein receptor type can bind to a different antigen. So we have T cells that produce protein receptors that will bind to any foreign antigen that enters our body. Adaptive immunity: Cytotoxic T cells Macrophages engulf bacteria, virus, protist or cancerous cells and presents the cell’s antigens to T cells (helper T and cytotoxic T). Virally-infected cells present antigens too. Cytotoxic T cells If there is a match between the antigen and the protein receptor of a cytotoxic T cell, that T cell divides repeatedly, producing many copies of itself with the same protein receptor. Some of these copies become effector cytotoxic T cells that touch kill anything with that antigen, others form memory cells to wait for future attacks. Antigen presented to a T cell (by a macrophage, or virally-infected cell). If there is a match between the protein receptors of the T cell and the antigen, the T cells divide into more effector cytotoxic T and memory T cells with that receptor. Adaptive immunity: Cytotoxic T cells Cytotoxic T cell recognizes a cell with specific foreign antigens, releases perforin proteins that “punch holes” in the foreign, virus-infected or cancerous cell. They also release chemicals that lead to cell death by fragmenting the cell’s DNA (among other things) It then moves on to kill other cells (with the same foreign antigens it recognizes). Adaptive immunity: Helper T cells Helper T cells stimulate other immune cells: Stimulates cell division of macrophages, cytotoxic T cells and B lymphocyte cells. Without helper T cells the rapid division of effector B cells and effector cytotoxic T cells would not occur. Therefore they are crucial to the overall immune response (HIV infects helper T cells, and disables the immune system). Memory cytotoxic T and helper T cells: remain in the body for a quick, overwhelming response to future attack by the same pathogen (so you do not get sick again).  1st exposure to a pathogen There is a lot of time between when a pathogen first enters the body, and when antibodies are produced in large amounts, and effector cytotoxic T cells are produced. During this time, you will be sick Characteristics: lag time of 3-6 days for antibody production as more B and T cells develop into effector cells, peak antibody concentration at 10-12 days. Memory B and T cells created for faster secondary response when exposed again.  2nd exposure to the same pathogen The second (and third, etc.) time you are exposed to the same pathogen, with the same antigens, memory cells encounter the pathogen quickly, and mount a quick overwhelming response that kills the pathogens before you feel sick. Characteristics: lag time in hours, peak in days. Much greater antibody response  Compare first and later responses Secondary immune responses occur much faster, and result in much higher antibody production  Why can you get sick from the flu year after year? Flu virus mutates  new antigens = old memory cells do not work. COVID is similar to this as well. Why can you get a cold year after year? Common cold caused by over 200 different viruses Lymphatic system: immune function Take up bacteria and other pathogens, transport them to lymph nodes. At lymph nodes, macrophages engulf and destroy pathogens, present antigens to T cells. B and T lymphocytes also in high density in lymph nodes, produce effector B cells, cytotoxic T cells, helper T cells, and memory T and B cells. Lymph system joins with blood system, so antibodies and effector cells enter blood stream as well. Lymphatic system Lymphatic vessels Structure: Blind-ended capillaries, but with larger inter-cellular gaps than blood capillaries (to take in bacteria) Have one-way valves, like veins (not shown). Contain lymph (plasma fluid, white blood cells, fats, fat-soluble vitamins, proteins) Lymphatic system Lymph nodes: Contain macrophages and lymphocytes Spleen: Macrophages and lymphocytes for infections within blood. Macrophages here break down old red blood cells too. Thymus gland: creates mature T lymphocytes Early childhood immunity / breastfeeding Antibodies can cross placenta. Antibodies, phagocytes, B and T lymphocytes are released in breast milk, in the first days after a child is born. These both give the child some of the mother’s immunity. Breast milk also has all the nutrients the baby needs, and is easier to digest than commercial formula / cow’s milk. Breast feeding is a good thing, particularly in the first week after birth. Active immunization (vaccination) Against viruses, like: polio, hepatitis B, the flu, measles, chicken pox, genital warts, COVID – 19, etc. Against bacteria, like: tetanus, whooping cough, pneumococcus, etc. Exposure to dead or weakened pathogens  formation of memory B and T cells. mRNA vaccines cause our cells to make the foreign antigen, then our cells present it formation of memory B and T cells. You gain immunity without getting sick! Mutating flu virus / COVID virus = new vaccine needed each year Mutating HIV virus = no vaccine possible Vaccination has wiped out, or nearly wiped out some diseases: small pox, polio and it saved many people’s lives during COVID Be sure to follow your doctor’s recommendations for your child’s vaccination. Vaccinations save lives! Note: there is NO link between vaccination and autism. Vaccination is safe. Not vaccinating your child against potentially fatal diseases is definitely NOT safe.  Passive immunization Passive immunization: against existing infections, such as tetanus, hepatitis B, rabies. Inject antibodies that are artificially produced and help fight the existing infection. No long-term immunity for you (memory cells are not produced). Antibiotics Effective only against bacteria! Do not work against viruses, like the flu and common colds. Antibiotic resistance is a problem: take all of your prescription!  Donating organs and tissue rejection Transplanted organs have foreign antigens, so they are attacked by the recipient’s immune system! Test for same blood types / similar antigen proteins: close relatives make good donors. Immunosuppressive drugs: prevent patient’s immune system from attacking transplanted tissue (and any foreign invaders too) Antibiotics needed to fight off infections Techniques are getting better for receiving donations, but many people who need organs don’t get them, as there are not enough donors. UAE law allowing organ donation was passed in 2016.  Allergies Harmless substances cause an immune system response: histamines released  inflammation of mucus membranes: redness, swelling, pain, mucus production. Localized: affect only the area exposed (external) Anaphylactic shock: potentially fatal full-body allergic response. Some people have this in response to bee stings, shellfish and various nuts, as examples. Bronchioles constrict, body capillaries become leaky, and blood plasma leaks into tissue, potentially leading to circulatory system collapse. An epinephrine shot can save their life.  Autoimmune disorders Defective recognition of “self”: Antibodies and cytotoxic T cells target your own cells. Multiple sclerosis: repeated inflammation of central nervous system results in damage to cells protecting neurons. Nerve transmission disrupted / slowed  paralysis, tremors, numbness, loss of vision, speech problems, coordination problems Type I diabetes: cells in pancreas which produce insulin are destroyed. High blood sugar levels can lead to high blood pressure, heart attacks, strokes, blindness, kidney failure and amputations.  Autoimmune Disorders Rheumatoid Arthritis: inflammed synovial membrane that lubricates joints. Scar tissue leads to fused joints. Slide 9.16