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Hypersensitivity Antigenic response beyond normal Hypersensitivities are: inappropriate immune responses Allergies are on familiar type of: hypersensitivity Allergen a substance (antigen) that induces an allergic response Type I (Anaphylactic) Reactions Immune reaction involving IgE antibodies, mast cells and basophils Anaphylaxis name literally means "opposite of protected" Type 1 Reactions occur: Very quickly (within 2 to 30 minutes of exposure to allergen) Type 1 reactions are caused by: chemical mediators found in mast cells and basophils Histamine causes redness, swelling, mucus secretion and smooth muscle contraction Leukotrienes cause: prolonged contraction of smooth muscle, esp bronchial tubes Prostaglandins increase mucus secretion and affect smooth muscle tissue
- On first exposure to an allergen:
APCs process and present allergen epitopes with MHC II to T helper cells
- Th2 cell then release: Il-r and Il-12 which activates the B cell.
- B cells proliferate and: differentiate into plasma cells that synthesize and secrete IgE antibody.
- IgE binds to: mast cells by Fc region, sensitizing the mast cells
- Upon subsequent exposure to allergen, mast cells with IgE bind to: antigen and release inflammatory molecules, resulting in allergy symptoms. What is Systemic Anaphylaxis? an immediate whole-body reaction Symptoms of Systemic Anaphylaxis Blood vessels dilate, blood pressure drops resulting in shock Epinephrine combats anaphylaxis by: constricting blood vessels and raising blood pressure Localized Anaphylaxis Usually associated with ingested or inhaled antigens Symptoms depend on the route of entry inhaled allergens cause: itchy/watery eyes, congestion, coughing, sneezing asthma is an: allergic reaction affecting lower respiratory system.
Type II hypersensitivity hemolytic transfusion reaction: Leads to hemolytic anemia Steps in Type II hypersensitivity blood transfusion:
- Donated type A blood with type A antigens enters bloodstream of type B recipient
- Anti-A antibodies in plasma of type B recipient bind to donated type A RBCs
- Bound anti-A antibodies activate complement cascade, resulting in hemolysis and the release of hemoglobulin, which destroys the donor RBCs Drug-induced cytotoxic reactions Hapten (drugs that are too small to be antigenic on their own) bind to blood platelets and an be seen by antibodies and are destroyed by complement What is Thrombocytopenic purpura loss of platelets causes many tiny hemorrhages throughout the body Rh factor is another: antigen that can be expressed on RBCs (85% of population is Rh+) Antibodies that react with Rh factor do NOT: occur naturally in Rh- individuals Rh- individuals will make antibodies to Rh if: their blood is exposed to it. Blood transfusion reactions can develop if: Rh- person receives Rh+ blood Heymolytic Disease of Newborn If an Rh- woman carries an Rh+ fetus, mixing of the blood can prime her immune system. The next time she carries an Rh+ fetus, her antibodies can cross the placenta and attack the fetus' RBCs
Hemolytic disease of the Newborn, results in: severe jaundice and anemia. Hemolytic Disease of the newborn can be severe enough to: require blood transfusion immediately upon birth Rh+ Newborn is treated with: RhoGAM RhoGAM an immune serum that prevents a mother's blood from becoming sensitized to foreign antibodies from her fetus. Usually given during 28th week of pregnancy RhoGAM binds up: any Rh antigens before the immune system can make antibodies. When an Rh- mother has a Rh+ fetus: fetal erythrocytes are introduced into the mother's circulatory system before or during birth, leading to production of anti-Rh IgG antibodies. Immune complexes (Type III Sensitivities) clumps of antigen/antibodies that escape phagocytosis How do immune complexes escape phagocytosis? They circulate in the blood and pass between endothelial cells of blood vessels, then becoming trapped in the basement membrane beneath cells Trapped immune complexes attract: neutrophils, causing inflammatory reactions Glomerulonephritis inflammatory damage inflicted on kidney glomeruli due to the presence of immune complexes following certain infections Serum Sickness systemic inflammatory response elicited against horse antibodies used in toxin neutralization treatments
Memory helper T cells become reactivated, producing inflammatory cytokines that stimulate macrophages and cytotoxic T cells to induce a inflammatory lesion at exposed site. This lesion will persist until the allergen is removed, can inflict significant tissue damage if it continues long enough. Autoimmune Disease immune reaction to self antigens that damages one's own organs autoimmune disease occurs: when there is a loss of self-tolerance, the ability to distinguish self from non-self. Production of antibodies or sensitized T cells to self antigens: follow the same groupings as hypersensitivity reactions Cytotoxic Autoimmune Reactions antibodies react with cell-surface antigens; affected cells are not killed but respond to activation through receptors Grave's Disease thyroid gland is stimulated to produce too much TSH Symptoms of Grave's Disease tachycardia, trembling, sweating, goiter, bulging eyes Myasthenia gravis Antibodies bind acetylcholine receptors where nerve endings meet muscle cells (Muscles cannot respond to nerve signals and can cause respiratory arrest/death of respiratory muscles are affected) In myasthenia gravis, autoantibodies block receptors for: Acetylcholine on muscle cells, resulting in paralysis systemic lupus erythematosus (SLE) a more severe form of lupus involving the skin, joints, and often vital organs. Symptoms include: butterfly rash, join pain, anemia, endocarditis, glomerulonephritis, neurological disorders, depression SLE affects: primarily women and antibodies are produced to DNA and other nuclear antigens. Rheumatoid Arthritis
IgM antibodies are made against the Fc region of IgG resulting in immune complexes depositing into the joints.. Chronic inflammation leads to cartilage and bone damage Diseases determined by which type of cells are destroyed Multiple Schlerosis Insulin-Dependent Diabetes Mellitus Psoriasis Multiple Sclerosis T cells and macrophages attack the myelin sheath of nerves. Symptoms of MS Fatigue, muscle weakness, paralysis, even death. Possibly linked to a reaction to an infectious agent Insulin-Dependent Diabetes Mellitus T cell destruction of insulin-secreting cells; Uptake of glucose by all cells is halted when insulin is not produced Symptoms of Insulin-Dependent Diabetes mellitus increased thirst, excessive urination, fatigue, weight loss, ketoacidosis Psoriasis chronic skin condition producing red lesions covered with silvery scales (thickened skin) immune surveillance theory the theory that cells of the immune system play a monitoring function in searching for and destroying abnormal cells such as those that form tumors Cancer cells arise frequently when: cell-cycle control genes are mutates. One of the primary jobs of cell-mediated immunity is to protect against cancer. Tc cells recognize tumor-associated antigens and: kill cells bearing them. cancer only arises when: Tc cells don't recognize or destroy cancer cells Immunotherapy for cancer
David Vetter "Bubble Boy" born with SCID, lived most of his life isolated inside a plastic bubble. AIDS caused by HIV With aids, Glycoprotein spike: attaches to CD4 receptor, mostly found on Th cells. Coreceptors CCR5 or CXCR4 must also be bound to spike protein. In HIV capsid enters cell and reverse transcriptase makes a DNA copy of RNA genome. DNA integrates into the host genome and directs production of new virions. 3 stages of HIV infection asymptomatic, symptomatic, AIDS Phase 1 HIV- Initial Infection Viral RNA molecules reach 10 million+ in the first few weeks. Billions of CD4+ T cells are infected during this time. Asymptomatic or lymphadenopathy, but immune system appears to rebound. Phase 2 HIV (CD4+ T Cell Decline) HIV replication continues slowly thanks to CD8+ Tc Cells, but steady decrease. Not many T cells are releasing new virus, but many contain viral DNA in their genome. Some vague indications of declining immunity: shingles, persistent thrush and diarrhea Phase 3 HIV- Clinical AIDS CD4+ T cell counts fall below 200 cells (normal 800-1000) Patient becomes sensitive to opportunistic pathogens leading to death. HIV Opportunistic pathogens Pneumocystis Candida Mycobacterium Toxoplasma Cytomegalovirus
Kaposi's Sarcoma Diagnostic Methods for HIV Standard is the ELISA ELISA test Enzyme-Linked immunosorbent assay, diagnose HIV, positive test is confirmed with a Western Blot HIV Transmission Requires transfer of infected body fluids Blood contains: 1000-100,000 viruses/ML Semen contains: 10 to 50 viruses/mL Routes of HIV transmission sex, anal receptive, vaginal, oral blood transfusions, needles, transplacental infection of fetus and breastmilk HIV and Chemotherapy Anti-HIV medications have changed HIV into a chronic disease rather than certainly-fatal, but they are not a cure. Fusion/cell entry inhibitors Nucleoside reverse transcriptase inhibitors cause termination of viral DNA by competitive inhibition Non-nucleoside inhibitors inhibit RT by changing its 3D structure highly active antiretroviral therapy (HAART) potent combination of NRTIs and NNRTIs commonly used Integrase Inhibitors- prevent integration of cDNA into host Protease Inhibitors
