Chapter 24: The Immune System

Chapter 24: The Immune SystemNEW AIM: How does the body defend itself against MOs?Nonspecific (innate)

vs. Specific (adaptive/acquired) Immunity

Chapter 24: The Immune SystemNEW AIM: How does the body defend itself against MOs?1. skinI. Nonspecific (innate) vs. Specific (adaptive) Immunity

A. Nonspecific immunityi. 1st line of defenseii. Does not distinguish one pathogen from another- dead, stratified epithelium blocks MOs- acids secreted from skin glands- Lysozyme * Enzyme that breaks down bacterial cell wall* Found in sweat, saliva, tearsiii. Components

Chapter 24: The Immune SystemNEW AIM: How does the body defend itself against MOs?1. skinI. Nonspecific (innate) vs. Specific (adaptive) Immunity

A. Nonspecific immunityi. 1st line of defenseii. Does not distinguish one pathogen from anotheriii. Components- desquamation of skin* Your skin is stratified epithelium (many layers). Only the bottom layers are alive and doing mitosis. The top (outer) layers are constantly falling off along with anything attached to it like bacteria or viruses.

Chapter 24: The Immune SystemNEW AIM: How does the body defend itself against MOs?2. Beating cilia/mucus of respiratory systemI. Nonspecific vs. Specific Immunity

A. Nonspecific immunityi. 1st line of defenseii. Does not distinguish one pathogen from another3. Stomach acid4. Hairs of nostrilsiii. Components

Chapter 24: The Immune SystemNEW AIM: How does the body defend itself against MOs?5. Nonspecific defense cellsI. Nonspecific vs. Specific Immunity

A. Nonspecific immunityi. 1st line of defenseii. Does not distinguish one pathogen from anotheriii. Components- cells that confront microbes that get past skin, digestive and resp. surfacesa. Monocytes (become macrophages = big eaters) and neutrophilsCollectively called phagocytes (cyte = cell; phago = phagocytosis) cells that phagocytoseb. Natural killer cells (do not confuse with killer T-cells)* Attack viral infected body cells

Chapter 24: The Immune SystemNEW AIM: How does the body defend itself against MOs?6. ProteinsI. Nonspecific vs. Specific Immunity

A. Nonspecific immunityiii. Components- interferonsFig. 24.1The infected cell is done for and will become a viral producing factory. However, it will secrete a protein called interferon, which will warn neighboring cells that a virus is in town.

Chapter 24: The Immune SystemNEW AIM: How does the body defend itself against MOs?6. ProteinsI. Nonspecific vs. Specific Immunity

A. Nonspecific immunityiii. Components- complement proteinsFig. 24.11Complement proteins are always in your blood in an inactive form. They are activated by antibodies bound to a foreign cell (cancer cell, bacterium, etc...). When activated, they make a hole in the membrane causing the cell to lyse nutrients, organelles, etc... diffuse out.

Chapter 24: The Immune SystemNEW AIM: How does the body defend itself against MOs?7. Inflammatory response (local)I. Nonspecific vs. Specific Immunity

A. Nonspecific immunityiii. Components- triggered by ANY tissue damageFig. 24.2


A. Nonspecific immunityiii. Components1. Rubor (redness) - due to vasodilation2. Edema (swelling) enhanced leakiness of blood vessesl 3. calor (warmth) both due to enhances leakiness of blood vesselsFig. 24.2Results in:histamine


A. Nonspecific immunityiii. Components- triggered by ANY tissue damage- Rubor, edema, calor - Pus - Coagulation cascade seals off area so bacteria cant get into the blood The dead warriors (white blood cells and bacteria) after the battleA pimple is a bacterial infection of a skin pore, pus is what is left after the battle.

Chapter 24: The Immune SystemNEW AIM: How does the body defend itself against MOs?8. Inflammatory response (systemic entire system)I. Nonspecific vs. Specific Immunity

A. Nonspecific immunityiii. Componentsa. MOs in blood and/orb. toxins from bacteria in blood (recall exo- and endotoxins ch27) c. Bodys Response - increase WBC count- increase body temp. = fever (this is a normal response)- triggered by toxins or chemicals released by WBCs- Higher temps stimulates phagocytes, gives your WBCs and advantage while at the same time inhibits bacterial growth

Chapter 24: The Immune SystemNEW AIM: How does the body defend itself against MOs?8. Inflammatory response (systemic entire system)I. Nonspecific vs. Specific Immunity

A. Nonspecific immunityiii. Componentsd. Septic shock (when the systemic response goes bad)Septic shock is caused by cytokines (cell signaling molecules secreted by one cell to talk to another like hormones, but not secreted into blood) and by the toxins produced by some bacteria.

These substances cause the blood vessels to widen (vasodilate), which results in a drop in blood pressure.

Consequently, blood flow to vital organsparticularly the kidneys and brainis reduced. This reduction in blood flow occurs despite the body's attempts to compensate by increasing both the heart rate and the volume of blood pumped.

Eventually, the toxins and the increased work of pumping weaken the heart, resulting in a decreased output of blood and even poorer blood flow to vital organs. The walls of the blood vessels may leak, allowing fluid to escape from the bloodstream into tissues and causing swelling. Leakage and swelling can develop in the lungs, causing difficulty breathing (respiratory distress).

Chapter 24: The Immune SystemNEW AIM: How does the body defend itself against MOs?9. Lymphatic systemI. Nonspecific vs. Specific Immunity

A. Nonspecific immunityiii. Componentsa. Involved in both nonspecific and specific immunityb. Lymph vessels, lymph nodes, tonsils and adenoids, appendix, spleen, bone marrow, thymus c. Lymph - fluid carried by vessels- similar to IF, less O2 and nutrients


A. Nonspecific immunityiii. Componentsd. functionsi. return IF to circ. system- vessels resemble veins- valves, skeletal muscles propel lymph- vessels are dead-endedii. fight infection- in lymph nodes and other lymph organs- lymph nodes- packed with macrophages and lymphocytes- lymphocytes involved in specific immunity


Fig. 24.39. Lymphatic system


A. Nonspecific immunityiii. ComponentsFig. 24.3


A. Nonspecific immunityiii. ComponentsFig. 24.3-Spleen- destruction of old RBCs- rich in B and T cells for fighting infection- large lymph node for blood- filters pathogens out of blood


A. Nonspecific immunityiii. ComponentsFig. 24.3- Appendix- Thought to be vestigial- Possibly a shrunken cecum since we no longer rely on hard to digest plant material- New studies suggest it harbors and protects bacteria helpful to the colon. - Contain WBCs and may be important in fighting infection- If an infection occurs in the colon, the bacteria living there will be destroyed. Those in the appendix can repopulate the colon.


A. Nonspecific immunityiii. ComponentsFig. 24.3- Appendcitis- Infection of the appendix- Caused by an obstruction of the opening to the appendix- Fills with mucus and swells- Blood flow disrupted, cells begin to die (necrosis = dying cells), walls begin to breakdown and if it breaks, bacteria will enter your body cavity. Infected appendixAppendectomy removal of the appendix


A. Nonspecific immunityiii. ComponentsFig. 24.3- Tonsils and Adenoids- Trap bacteria/viruses as they enter through nose and mouth

Chapter 24: The Immune SystemNEW AIM: How does the body defend itself against MOs?I. Nonspecific vs. Specific Immunity

B. Specific immunity (The Immune System)i. More effective than nonspecificii. Used when nonspec. fails or in combinationiii. antigena. Foreign molecule that elicits immune responseb. Surface molecule of virus, bacteria, mold spores, cancer cells, pollen, transplant, etcWhy must it be a surface molecule?The same reason that when a person is wanted by the FBI they show a picture of their face and not of their heart. The surface of the cells is the part that other cells and antibodies will see.


B. Specific immunity (The Immune System)iv. Lymphocytes (B and T cells)a. Spend time in lymph tissueb. Produce the specific immune responsec. Originate in bone marrow- 2 fates1. Mature in bone marrow = B-cell2. Leave bone marrow and circulate to thymus, mature there and become a T-cell


B. Specific immunity (The Immune System)iv. Lymphocytes (B and T cells)Fig. 24.51. B cells elicit humoral immunity2. T cells elicit Cell-Mediated immunityHumoral implies humors or fluids. This response will involve antibodies (proteins), which will be dissolved in the fluids of the body secretions like saliva and breast milk, the blood plasma, interstitial fluid, lymph fluid, etc - to recognize foreign substances (antigens)In this case cells will be directly involved in recognizing foreign substances (antigens)

Chapter 24: The Immune SystemAIM: How does the body defend itself against MOs?I. Nonspecific vs. Specific Immunity

B. Specific immunity (The Immune System)v. Humoral immunityFig. 24.6a. B-cells make and secrete antibodies (a protein) into bloodb. We have millions of B-cells and each one produces a different antibody, which will bind to a different antigen (one B-cell, one antigen).Antibody structure (quarternary structure)(Epitope)


B. Specific immunity (The Immune System)v. Humoral immunityFig. 24.6a. B-cells make and secrete antibodies (a protein) into bloodThe antigenic determinant (epitope) is the specific part of the antigen that the antibody binds to via hydrogen/ionic/hydrophobic interactions.b. We have million of B-cells and each one produces a different antibody, which will bind to a different antigen (one B-cell, one antigen).


B. Specific immunity (The Immune System)v. Humoral immunityFig. 24.6How can there be millions of B-cells each expressing a unique antibody if we only have 30,000 or so genes?? Wouldnt we need 1,000,000s of genes, one for each antibody?


B. Specific immunity (The Immune System)v. Humoral immunityFig. 24.6How can there be millions of B-cells each expressing a unique antibody if we only have 30,000 or so genes?? Wouldnt we need 1,000,000s of genes, one for each antibody?There are many genes coding for each segment (V, D or J) of the variable region. The genes will undergo recombination in a given B-cell and a unique combination of VDJ will result in both chains (light chain doesnt have a D segment). 1. V(D)J recombination


B. Specific immunity (The Immune System)v. Humoral immunityFig. 24.6How can there be millions of B-cells each expressing a unique antibody if we only have 30,000 or so genes?? Wouldnt we need 1,000,000s of genes, one for each antibody?When a B-cell is activated it begins to rapidly divide. 2. Somatic hypermutationThe VDJ regions have an abnormally high rate of mutation (1 nucleotide change per variable gene [VDL] per division) during S-phase resulting in a slight variations in all daughter cells genetic diversity followed by natural selection!!


B. Specific immunity (The Immune System)There are five major types of antibodies (IgG, IgM, IgA, IgD and IgE or G-MADE), each has a slightly different function in the body. For example: IgG - found in the blood and interstitial fluid and can cross the placenta giving immunity to the fetus

IgA - found in external secretions like saliva and breast milk.Another name for an antibody is an immunoglobulin or Ig for short.


B. Specific immunity (The Immune System)The five antibody (immunoglobulin) types of mammals


B. Specific immunity (The Immune System)v. Humoral immunityFig. 24.5a. B-cells make and secrete antibodies (a protein) into bloodc. B-cells display the antibody they make (~100,000 of them) on their surface as an antigen receptor and wait in the lymph system and spleen for an antigen that will bind the antibody it makesb. We have million of B-cells and each one produces a different antibody, which will bind to a different antigen (one B-cell, one antigen).


B. Specific immunity (The Immune System) - OVERVIEWMemory T-cells are also made form T-cells activated by Helper T-cells. For a future encounter with the same antigen carrying pathogen.


B. Specific immunity (The Immune System)v. Humoral immunityd. Clonal selection- The single activated B-cell will undergo mitosis resulting in the formation of plasma cells (antibody secreting cells) and memory B cells- Why are plasma cells shown with a lot of ER?Fig. 24.9Now what do these antibodies do?- If the antigen does come along one day, it will bind to the B-cells antibody and activate the B-cell.(Activation actually requires a second signal by a helper T-cell that we will discuss shortly)They are secreting incredible amounts of protein (antibodies) and the ER/Golgi are required to do this recall endomembrane system.


B. Specific immunity (The Immune System)v. Humoral immunityAntibodies bind to antigens (surface molecules), flagging them for phagocytosis by phagocytes or activating complement. Fig. 24.11http://catalog.nucleusinc.com/generateexhibit.php?ID=15529&ExhibitKeywordsRaw=&TL=1&A=2What about those memory B-cells?Know all the terms like neutralization, agglutination, precipitation

Chapter 24: The Immune SystemAIM: How does the body defend itself against MOs?


B. Specific immunity (The Immune System)v. Humoral immunityFig. 24.91. Memory B-cells are soldiers that will wait in reserve for the return of the same antigen.2.These cells with memory T-cells are what gives you immunity.STORY: You are infected with the virus Varicella zoster, which causes chicken pox. A B-cell will recognize the virus somewhere in your spleen or lymph nodes and be activated with the help of a helper-T cell (discussed shortly). The B-cell will undergo mitosis forming plasma and memory B-cells, which all make the same antibody (it is mitosis so they are all ALMOST genetically identical clones). Plasma cells will make and secrete antibodies to fight the current virus, while many, many memory B-cells will sit in lymph nodes and the spleen for the rest of your life possibly, with the same antibody on their surface awaiting the return of the virus/antigen. Initially there was only a handful of B-cells activated, the second response will activate 10,000s!!


B. Specific immunity (The Immune System)v. Humoral immunityFig. 24.9Why not make Memory B-cells for all 100+ million antibodies?A. You do not have enough room in your lymph and spleen and B. You would spend a huge amount of ATP to do this. You would need to eat incredible amounts of food to maintain such a system.


B. Specific immunity (The Immune System)vi. Cell-mediated immunitya. B-cells fight the battle outside our cells, but what about when the pathogen has gotten in like a virus that has turned your cell into a virus producing factory?

- T-cells fight this oneb. We have million of T-cells in our lymph nodes and spleen and each one produces a slightly different antigen receptor called a T-cell receptor (this is the antibody of the T-cell although it well never secrete it).


B. Specific immunity (The Immune System)vi. Cell-mediated immunityFig. 24.13c. STORY1. It all starts when some kind microorganism (microbe) gets engulfed by a macrophage (a mature monocyte) of the innate immune system.The macrophage needs to warn the specific immune system as to what is going on!!The phagocytosed microbe will be in a vesicle which will fuse with a lysosome thereby partially digesting the microbe. 2 and 3. The pieces of the microbe will then bind to MHC-II receptors of the macrophage and be displayed on the surface the macrophage is now called an Antigen Presenting Cell (APC).(MHC-II)


B. Specific immunity (The Immune System)vi. Cell-mediated immunityFig. 24.13c. STORY4. You have millions of Helper T-cells, each one making a slightly different T-cell receptor (analogous to B-cells each making a different antibody receptor).

A helper T-Cell (the same ones that HIV infects), with a matching T-cell receptor to the displayed antigen will bind to the antigen/MHC-II receptor of the APC. (MHC-II)(MHC-II)


B. Specific immunity (The Immune System)vi. Cell-mediated immunityFig. 24.13c. STORY5. The APC will secrete interleukin-1, a cytokine (a protein that acts as a signal to instruct cells what to do), which will bind to interleukin receptors on the Helper T-Cell.Interleukin-1 (IL-1)Interleukin-2 (IL-2)Interleukin:Inter between; leukos - whiteA signal between white blood cells. 5The combination of IL-1 and the MHC-II complex activates the Helper T-Cell, and the specific immune system has been notified!Time to find out what the Helper T-Cell does


B. Specific immunity (The Immune System)vi. Cell-mediated immunityFig. 24.13c. STORY6. The helper T-cell will secrete interleukin-2, also a cytokine, which will bind to receptors on the T-cell itself, cytotoxic (toxic to cells) T-cells, and B-cells, both of which that have been partially activated by the SAME antigen (remember earlier that I said a B-cell would not fully activate with a helper-T cell)Interleukin-1 (IL-1)Interleukin-2 (IL-2)65IL-2 stimulates the same Helper T-cell that secreted it to undergo mitosis IL-2 will activate the B and cytotoxic T cells, which have been partially activated already by the SAME antigen antigen binds to antibodies on B-cell surface or MHC-II on Cyto T-cell surface.Cytotoxic T-Cell is also called a Killer T-Cell


B. Specific immunity (The Immune System)vi. Cell-mediated immunityFig. 24.13Interleukin-1 (IL-1)Interleukin-2 (IL-2)


B. Specific immunity (The Immune System)vi. Cell-mediated immunityFig. 24.13c. STORY**All of these lymphatic cells (B and T cells) need two signals to be active:Interleukin-1 (IL-1)Interleukin-2 (IL-2)651. The antigenAn APC displays the antigen bounds to MHC-II (the antigen/MHC-II complex), which will bind to the T-celI receptor of a Helper T-cell Binds directly to T-cell receptor of a Cytotoxic T-cell that recognizes that antigen. - Binds directly to an antibody on the surface of a B-cell.


B. Specific immunity (The Immune System)vi. Cell-mediated immunityFig. 24.13c. STORY**All of these lymphatic cells (B and T cells) need two signals to be active:Interleukin-1 (IL-1)Interleukin-2 (IL-2)651. The antigenWhat if the T-cell or B-cell does not have an T-cell receptor or antibody, respectively, that can bind to the antigen?Nothing, that cell will not be selected.


B. Specific immunity (The Immune System)vi. Cell-mediated immunityFig. 24.13c. STORY**All of these lymphatic cells (B and T cells) need two signals to be active:Interleukin-1 (IL-1)Interleukin-2 (IL-2)652. InterleukinsIL-1 from the APC will activate the partially activated Helper T-cell.IL-2 from the Helper T-cell will activate the already partially activated Cytotoxic T-cells and B-cells as well as itselfNow what will the activated Cytotoxic T-cells do?


B. Specific immunity (The Immune System)vi. Cell-mediated immunityFig. 24.13c. STORYThe cytotoxic T-cells will now bind to infected cells displaying the SAME antigen on MHC-I (MHC-ONE) receptors. APCs display antigen using MHC-II, while infected cells use MHC-I. Cytotoxic T-cells secrete the protein perforin onto any cell with the proper MHC-I/antigen complex. Perforin puts holes in the cell membrane causing the cell to lyse...


B. Specific immunity (The Immune System) - OVERVIEWMemory T-cells are also made from T-cells activated by Helper T-cells. For a future encounter with the same antigen carrying pathogen.


B. Specific immunity (The Immune System) - OVERVIEWRecap: It all begins when a microbe is phagocytosed by a macrophage or an antigen from the microbe binds to the antibody receptor of a B-cell. The macrophage becomes an APC when it displays pieces of the microbe attached to MHC-II on its surface. The Helper T-cell with a T-cell receptor that matches the antigen binds and it activated by interleukin-1 released by the APC. The Helper T will in turn secrete IL-2 and activate itself to undergo mitosis as well as cytotoxic T-cells that have also been partially activated by antigen binding to their T-cell receptors and B-cells that have already been partially activated by antigen binding to their antibody receptors. The cyto T-cells will undergo mitosis to make memory T-cells and other cyto T-cells that will bind to the same antigen displayed on MHC-I receptors of infected cells and lyse those cells using the protein perforin, which puts holes in the membrane. B-cells will undergo mitosis to make plasma cells and memory B-cells. The plasma cells will secrete antibodies, which will bind to antigen and mark objects with this antigen for death (phagocytosis by macrophages). Memory B and T cells hang in the lymph nodes and spleen awaiting the return of the antigen


B. Specific immunity (The Immune System)vii. Memory cellsFig. 24.8a. Memory B and T-cells are reservists for next time that specific antigen shows up:Primary immune responseSecondary immune responseThe first time the lymphocytes see the antigen. Antibodies are made, but relatively slowly due to the small number of B-cells activated and only a relatively small number of antibodies are made compared to the second time the lymphocytes see the antigen for the same reason.The secondary response results upon re-exposure to the antigen. You have millions of memory B-cells. Most of them will be activated and antibodies are made quickly and in large number thanks to the large number of cells. You do not get sick. It must be the same antigen. Any mutation that changes the structure of the antigen will not elicit the secondary response.


B. Specific immunity (The Immune System)viii. Active vs. passive immunitya. Active1. Body produces own antibodies (plasma cells)2. Permanent for the most part (memory cells)b. Passive1. Fetus gets antibodies from mom (doesnt produce its own).- conveys immunity2. Antibody shots3. Not permanent. Explain.Protein are not highly stable like DNA and will only last a short amount of time before they lose their structure (denature) and must be recycled. You are only protected for as long as the antibodies (immunoglobulins) last. There is no way to replace themResearchers are currently attempting to generate antibodies that will stick to cancer cells. How would this help us?


B. Specific immunity (The Immune System)viii. Active vs. passive immunitya. ActiveHow can we use active immunity to our advantage?Vaccinestrain the immune system to recognize antigens in a safe waythis can be done by injecting bacterial/viral antigens into us


B. Specific immunity (The Immune System)Smallpox - infectious disease unique to humans, - caused by either two virus variants: Variola major and Variola minor - Localizes in small blood vessels of skin, mouth and throat. - V. major - mortality rate of 3035%. - Long-term complications of V. major infection - characteristic scars on face: occurred in 65-85% of survivors- Blindness resulting from corneal ulceration and scarring: 2-5%

- Emerged about 10,000 BC- killed ~400,000 Europeans each year during the 18th century - responsible for a third of all blindness- Between 20 and 60% of all those infectedand over 82% of infected childrendied from the disease

-20th century, - 300500 million deaths- 1967, the World Health Organization (WHO) estimated that 15 million people contracted the disease and that two million died in that year.- 1979 - small pox is gone


B. Specific immunity (The Immune System)ix. Vaccinesa. First vaccine - small pox - 17971. Edward Jenner3. Took pus from cowpox pustule and inserted it into an incision on a boy4. Boy could not get small pox (he was immune)2. Two related diseases: cow pox and small pox


B. Specific immunity (The Immune System)ix. Vaccinesb. Inject a harmless variant of disease causing microbe1. Body responds to antigens2. Memory cells produced3. Immune system primed for the real thing 4. Thats easyso where is the HIV vaccine?HIV is a retrovirus. Viral particles that use reverse transcriptase and prone to making more errors in their DNA that a virus using DNA polymerase. This results in a quickly changing virusthe antigens change quicker than out immune systems can keep up with. It is like a criminal that can shape-shift (change what they look likebecome anyone).


C. OverviewNon-specificSpecific


D. Autoimmune diseasesi. Immune system turns against the body1. systemic lupus erythromatosus (lupus or SLE)- Chronic autoimmune disease lymphocytes attack connective tissue- Causes inflammation- Nine times more likely in women than men- Unpredictable with periods of illness alternating with remission- There is no cure, symptoms are treated- Can be fatal, but fatalities are now rare with medical technologyButterfly rash- Precise cause is not known genetic with environmental triggers like UV light


D. Autoimmune diseasesi. Immune system turns against the body2. Rheumatoid Arthritis- Chronic systemic inflammatory disorder that mainly affects the joints- 1% of worlds population affected by this, women 3X more likely than men- Onset typically between 40 and 50 years of age- Problems in addition to joints can occur like inflammation of lung tissue and tissue surrounding the heart- Precise cause is unknown- Treated of symptoms with physical therapy and anti-inflammatory drugs- No cure, lifespan reduced 5 to 10 years (estimated)


D. Autoimmune diseasesi. Immune system turns against the body- Immune system attacks (beta)-cells of the pancreas, which secrete insulin- No insulin = no blood sugar regulation:3. Insulin dependent (Type 1 early onset) diabetes 1. You eat a candy bar2. Absorb monosaccharides into blood at jejunum3. Blood sugar increases sensed by proteins on the surface of beta cells in the pancreas4. Beta cells secrete the hormone insulin (a protein) into the blood5. Insulin circulates in the blood and binds to insulin receptors on the surface of muscle and liver cells.6. Muscle and liver cells respond by sending glucose transporters to the cell surface causing the uptake of glucose in the blood, which will be stored as glycogen in the liver and muscle cells.- Treatment is insulin injections


D. Autoimmune diseasesi. Immune system turns against the body- Immune system attacks schwann cells4. Multiple sclerosis (MS)- Schwann cells are nervous system cells that wrap around and insulate neurons forming what is called the myelin sheath because the cells are filled with myelin a mixture of 80% lipid and 20% protein.- Without these cells, electrical signals will leak and the signal will not make it to where it needs to go- 5 to 10 years lifespan reduction, but suicide is a major concern


E. Immunodeficiency diseasesi. Lack one or more components of immune system1. Severe combined immunodeficiency (SCID)- Aka Boy in the bubble syndrome- Disorder in which both B and T cells are crippled due to defects in several possible genes- The defective genes typically code for interleukin receptors.- Most common treatment is bone marrow transplant- Bubble is a sterile (microbe-free) chamber


E. Immunodeficiency diseasesi. Lack one or more components of immune system2. HIV human immunodeficiency virus- Reminder infects and destroys CD4+ Helper T-cells- No Helper T-cells, no activation of Cytotoxic T-cells and B-cells- AIDS does not kill patient, a secondary infection or cancer typically does due to a compromised immune system.- Treatment: Drug cocktails that inhibit multiple enzymes at once to get the many variants and avoid artificial selection due to rapid mutation of the virus.


F. Allergiesi. Overreaction to environmental antigens (allergens)1. Allergen = surface protein of pollen, salivary proteins of dogs/cats, hair of animals, etc2. Histamine binds cellular histamine receptors resulting in allergy symptoms3. How do you think antihistamines work?Histamine


F. Allergiesii. Anaphylactic shock- hypersensitivity to an allergen (ex. Bee sting)- sudden release of histamine by mast cells- rapid dilation of blood vessels (swelling) / constriction of bronchioles- rapid drop of blood pressure (shock)- Emergency treatment = epinephrine (adrenaline)- hormone that counters anaphylactic shock- counters airway constriction (dilates airway) - increases cardiac output to counter drop in BPEpi-pen = epinephrine pen


******Interferons as antiviral drug??*Interferons as antiviral drug??Liver make complement proteins??*Interferons as antiviral drug??*Interferons as antiviral drug??A histamine antagonist, commonly referred to as antihistamine, is a pharmaceutical drug that inhibits action of histamine by blocking it from attaching to histamine receptors. H1 antihistamines are used to treat symptoms of allergy, such as runny nose and watery eyes. Allergies are caused by a body's excessive type I hypersensitivity response to allergens, such as pollen. An allergic reaction, which if severe can lead to anaphylaxis, results in excessive release of histamines and other mediators by the body. Other uses of H1 antihistamines alleviate symptoms of local inflammation that result from various conditions, such as insect stings, even if there is no allergic reaction. Other common antihistamines include the H2 antagonists (cimetidine), which are widely used for the treatment of acid reflux and stomach ulcers, because they decrease gastric acid production.*Interferons as antiviral drug??*Septic shock is caused by cytokines (substances made by the immune system to fight an infection (see Biology of the Immune System: Cytokines) and by the toxins produced by some bacteria. These substances cause the blood vessels to widen (dilate), which results in a drop in blood pressure. Consequently, blood flow to vital organsparticularly the kidneys and brainis reduced. This reduction in blood flow occurs despite the body's attempts to compensate by increasing both the heart rate and the volume of blood pumped. Eventually, the toxins and the increased work of pumping weaken the heart, resulting in a decreased output of blood and even poorer blood flow to vital organs. The walls of the blood vessels may leak, allowing fluid to escape from the bloodstream into tissues and causing swelling. Leakage and swelling can develop in the lungs, causing difficulty breathing (respiratory distress).*Septic shock is caused by cytokines (substances made by the immune system to fight an infection (see Biology of the Immune System: Cytokines) and by the toxins produced by some bacteria. These substances cause the blood vessels to widen (dilate), which results in a drop in blood pressure. Consequently, blood flow to vital organsparticularly the kidneys and brainis reduced. This reduction in blood flow occurs despite the body's attempts to compensate by increasing both the heart rate and the volume of blood pumped. Eventually, the toxins and the increased work of pumping weaken the heart, resulting in a decreased output of blood and even poorer blood flow to vital organs. The walls of the blood vessels may leak, allowing fluid to escape from the bloodstream into tissues and causing swelling. Leakage and swelling can develop in the lungs, causing difficulty breathing (respiratory distress).*Interferons as antiviral drug??*Interferons as antiviral drug??*Interferons as antiviral drug??*Interferons as antiviral drug??*Interferons as antiviral drug??*Interferons as antiviral drug??*Interferons as antiviral drug??*Some believe them to be involved in helping fight off pharyngeal and upper respiratory tract infections, but there is no conclusive evidence to that effect.

*Interferons as antiviral drug??*Interferons as antiviral drug??*Interferons as antiviral drug??*Interferons as antiviral drug??*Interferons as antiviral drug??*Interferons as antiviral drug??*Interferons as antiviral drug??*Interferons as antiviral drug??*Interferons as antiviral drug??*Interferons as antiviral drug??*Interferons as antiviral drug??*Interferons as antiviral drug??*Interferons as antiviral drug??*Interferons as antiviral drug??*Interferons as antiviral drug??*Opsonization when bacterium is phagocytosed after being coated with antibodies*Interferons as antiviral drug??*Interferons as antiviral drug??*Interferons as antiviral drug??*Interferons as antiviral drug??*Interferons as antiviral drug??*Interferons as antiviral drug??*Interferons as antiviral drug??Cytokines (Greek cyto-, cell; and -kinos, movement) are any of a number of small proteins that are secreted by specific cells of the immune system and that carry signals locally between cells, and thus have an effect on other cells.[1] They are a category of signaling molecules that are used extensively in cellular communication. They are proteins, peptides, or glycoproteins. The term cytokine encompasses a large and diverse family of polypeptide regulators that are produced widely throughout the body by cells of diverse embryological origin.[2]

*Interferons as antiviral drug??Cytokines (Greek cyto-, cell; and -kinos, movement) are any of a number of small proteins that are secreted by specific cells of the immune system and that carry signals locally between cells, and thus have an effect on other cells.[1] They are a category of signaling molecules that are used extensively in cellular communication. They are proteins, peptides, or glycoproteins. The term cytokine encompasses a large and diverse family of polypeptide regulators that are produced widely throughout the body by cells of diverse embryological origin.[2]





*Interferons as antiviral drug??*Interferons as antiviral drug??*Interferons as antiviral drug??*Interferons as antiviral drug??*Interferons as antiviral drug??*Interferons as antiviral drug??*Interferons as antiviral drug??*Interferons as antiviral drug??*Interferons as antiviral drug??*Interferons as antiviral drug??*Skit in class to demonstrateRabies is treated by injecting antibodies *Systemic lupus erythematosus can affect nearly any part of your body. Body systems most commonly involved include the skin, joints, lungs, kidneys and blood. When people talk about lupus, they're usually referring to systemic lupus erythematosus.

Hodkins - cure rate 93%, one of most curable forms of cancer, must catch in early stagesOccurs in lymph nodes typically

HIV - infects CD4+ Helper T-cells*Systemic lupus erythematosus can affect nearly any part of your body. Body systems most commonly involved include the skin, joints, lungs, kidneys and blood. When people talk about lupus, they're usually referring to systemic lupus erythematosus.


HIV - infects CD4+ Helper T-cells*Systemic lupus erythematosus can affect nearly any part of your body. Body systems most commonly involved include the skin, joints, lungs, kidneys and blood. When people talk about lupus, they're usually referring to systemic lupus erythematosus.


HIV - infects CD4+ Helper T-cells*http://video.about.com/ms/Multiple-Sclerosis.htm


HIV - infects CD4+ Helper T-cells*Hodkins - cure rate 93%, one of most curable forms of cancer, must catch in early stagesOccurs in lymph nodes typically

HIV - infects CD4+ Helper T-cells*Hodkins - cure rate 93%, one of most curable forms of cancer, must catch in early stagesOccurs in lymph nodes typically

HIV - infects CD4+ Helper T-cells*Antihistamines coat histamine receptors, prevent binding*Antihistamines coat histamine receptors, prevent binding*Eosinophil granulocytes, usually called eosinophils or eosinophiles (or, less commonly, acidophils), are white blood cells that are one of the immune system components responsible for combating multicellular parasites and certain infections in vertebrates. Along with mast

Chapter 24: The Immune System

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Transcript of Chapter 24: The Immune System