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Antigenic response beyond what’s normal. Undesirable reaction produced by normal immune system.
–4 types, types I - IV
Failure of organism to recognize own constituents as “self” resulting in immune response against own cells and tissues.
Immune system’s ability to fight infectious disease is compromised or absent.
Hypersensitivity Type 1
•Immediate, IgE-mediated; anaphylactic
–Plasma cells secrete IgE & bind mast cells or basophils causing degranulation & release of histamine
Hypersensitivity Type 2
–Ag cause form. of IgM & IgG that bind & destroys target cell
Hypersensitivity Type 3
–Ab & Ag cause inflammation
Hypersensitivity Type 4
–Ag activate Tc that kill target cells
2 - 3 days before you develop allergies
t cells involved
4 Types of Hypersensitivities
- Type 1 Immediate, IgE-mediated; anaphylactic
- Type 2 Cytotoxic
- Type 3 Immune complex
- Type 4 Cell mediated
Type I – Immediate, IgE-mediated
•Affects ~25% of the US population
•Examples? PCN, asthma, hives
•How does it develop? Reexposure to a specific type of antigen.
Type I – Immediate, IgE-mediated 2
•Symptoms? Breathing difficulty, shock, fever, asthma
•Treatments? Epinephrine, antihistamines, corticosteroids
Sensitization/IgE production (part 1)
- 1. allergen particles enter mucous membrane
- 2. they get carried to lymph nodes
- 3. B cell recognizes allergen with help of T cell
- 4. B cell proliferates into plasma cell
- 5. Synthesize IgE
Sensitization/IgE production (part 2)
- 6. igE binds to mast cell surface receptors
- 7. allergen attaches to igE on mast cells and triggers degranulation and release of allergic mediators
- 8. distribution of mediators in bloodstream
- 9. symptoms in various organs
- - runny nose, hives, etc
Type I Hypersensitivity
•Mast cells – found in tissues
•Basophils – found in blood
- Release granules that contain:
Dilates blood vessels and makes vessel walls abnormally permeable
- Hormone that causes symptoms of hay fever
- and asthma
–Functions in contraction & relaxation of smooth muscles, dilation & constriction of blood vessels, control of BP, & modulation of inflammation
associated with ingested Ag (food/pollen)
•Examples: fish or plant pollen, dust mite feces.
•Symptoms: Hives, systemic anaphylaxis or itchy eyes, sneezing.
Individual sensitized to Ag exposed to it again
•Examples: PCN sensitivity, peanuts, insect (bee sting)
Symptoms: More sever, difficulty breathing, shock
Treatment for Type I Hypersensitivies Allergy Shots
What is injected?
Increasing dosages of antigen
Treatment for Type I Hypersensitivies Allergy Shots
1. What is the goal of this therapy?
2. Why don’t you want the antigen to bind to ige?
1. To produce igg instead of ige.
Why? Because if you are exposed to the antigen the igg will intercept. It will come in place and bind to the antigen before the antigen binds to ige.
- 2. It will cause degranulization and
- therefore a hypersensitivity reaction.
How does it develop
Type II – Cytotoxic
Ab bind to Ag’s on patients own cell surfaces. Cells are recognized by APC causing B cell response where Ab’s are produced against foreign Ag.
- Examples: Transfusion reactions, hemolytic dz
- of newborn
Type II – Cytotoxic
1. lysis of RBC’s, severe anemia
- 2. Passive immunization: RhoGAM,
- transfusion. Anti-inflammatory & immunosuppressive
When a mother and her unborn baby carry different Rh protein factors. It is specifically caused when a mother is Rh-negative and her baby is Rh-positive. If a woman is Rh-negative and her baby is Rh-positive, then her body will determine the Rh-positive protein to be foreign. if blood cells from the baby cross into the mother’s bloodstream, the mothers immune system will make antibodies against the baby’s red blood cells. Once an Rh-negative mother’s body has made these antibodies her body will send these antibodies across the placenta to attack the baby’s red blood cells
Type III - Immune Complex
How does it develop: Ag-Ab complexes deposited in organs. Cause inflammatory damage
Examples: Glomerulonephritis, inflammatory damage to kidney glomeruli (site of blood filtration). Serum sickness. Lupus.
Type III – Immune Complex
Symptoms: Chronic inflammation.
Treatments: Steroids, prednisolone.
Type IV - Cell Mediated, Delayed Hypersensitivity
How does it develop: caused by T cells
Examples: transplant rejection mediated by CTLs. TB test
Type IV – Cell Mediated, Delayed Hypersensitivity
•Symptoms: hypersensitivity of skin
- •Treatments: immunosuppressive agents,
Type IV hypersensitivity
- HLA = human leukocyte antigen
- It’s a histocompatibility antigen the major histocompatibility antigen = MHC
- human version of MHC
- proteins classified as antigen
body recognizes self or nonself
HLA Reactions 2
- •T cells recognize Ag + MHC
- –1-10% of T cells will recognize a foreign MHC molecule
•Important for transplant rejection
Tissue moved to different location within same individual
Transplant between two identical individuals.
Transplant from one person to another. Account for many human transplants: from cadavers, living related & unrelated donors.
Surgical graft of tissue from one species to an unlike species.
ie. Graft from baboon to human.
Immune response that regards graft as foreign.
How is graft rejection prevented?
Cyclosporin, Tacrolimus – block T cell activation
Sirolimus, mycophenolate mofetil – block proliferation of T & B cells
Basiliximab & daclizumab – Abs that block IL-2
•Affects 5% of the developed world
•Disproportionately affects women
•Loss of self tolerance
- •Patients can have auto reactive T cells
- and Abs
Autoimmune reactions can be mediated by
–Cell mediated hypersensitivities
Type II (Cytotoxic) Hypersensitivity
–Ab attach to thyroid stimulating to overproduced thyroid hormones. results in enlarged thyroid (goiter), bulging eyes.
Ab coat acetylcholine receptors at nerve impulse/muscle junction. results in muscle weakness, respiratory arrest, death
Type III (Immune Complex-Mediated) Hypersensitivity
Systemic lupus erythematosus
–How does it develop: Present at time of birth. Result of genetic defect.
–Example: Di George’s syndrome
Congenital immunodeficiencies 2
–Symptoms: respiratory infections, chronic sinusitis, chronic bronchitis.
–Treatment: depends on subtype
- 1.Congenital immunodeficiencies (primary)
- 2.Acquired immunodeficiencies (secondary)
- How does it develop: virus selectively
- infects helper T cells.
Acquired immunodeficiencies 2
–Symptoms: body vulnerable to life threatening infections & cancer. (Kaposi’s sarcoma).
–Treatment: anti-viral or drugs to strengthen immune system.
•Acquired Immunodeficiency Syndrome
•Causative agent: HIV (human immunodeficiency virus)
AIDS category A
–asymptomatic or persistent lymphadenopathy
AIDS category b
–persistent infections with Candida albicans, may also have shingles, persistent diarrhea & fever
AIDS category c
–(clinical AIDS) Candida albicans infection of esophagus, bronchi & lungs; cytomegalovirus eye infection; TB; pneumocystis pneumonia; toxoplasmosis of the brain; Kaposi’s sarcoma
•Less than 200 CD4+ T cells/ mm3
•normal numbers are 800-1000 CD4+ T cells / mm3
virus infects CD4+ T cells and macrophages. results in immunodeficiency
–Secondary lymphoid tissue in the gut mucosa is destroyed 1st, early on in infection
•some virions remain in vacuoles inside the cell = latent virus
•Provirus, viral DNA integrated into host chromosome and new viruses are released by budding
AIDS lifecycle 2
–Rapid immunogenic change allows it to evade the immune system; due to mutation rate of RT
intact virion remains in a vacuole inside the cell
•viral DNA is integrated into the host’s DNA
number of people worldwide infected with HIV
35.9 - 44.3 million people worldwide are infected with HIV
transmission via direct contact with bodily fluids (especially blood) – sexual contact, IV drug use, & perinatal contact
< 1 virion/ml
HIV can survive only
~6hrs. outside of a cell
(no cures) anti-HIV drugs prolong life
–HAART: highly active antiretroviral therapy = 3+ drugs
condom use, discouraging promiscuity, not sharing needles, screening of blood and organ donors
AIDS - Obstacles to vaccine development
–Virus clades differ greatly from 1 geographic area to another
–Neutralizing Abs are exceedingly difficult to stimulate
AIDS - Obstacles to vaccine development 2
–Cells infected by HIV are often not recognized by the immune system and therefore not susceptible to CTL lysis
–Provirus & latent viruses are immunologically invisible