Week 3 Allergies & Autoimmune Diseases Flashcards
(34 cards)
Type 1 Hypersensitivity
IgE - mediated
Onset = 1 hour
Ex. anaphylaxis
Type 2 hypersensitivity
IgG or IgM Cytotoxic
onset = hours to days
ex. hemolytic anemia
Type 3 hypersensitivity
Immune Complex Mediated
onset = 1-3 weeks
ex. serum sickness SLE
type 4 hypersensitivity
T-cell mediated
onset = days to weeks
ex. Rash SJS
why type of hypersensitivity do contacted materials cause
type 4
t-cell mediated
Most Common Atopic Conditions Are?
atopic asthma, allergic eczema, hay fever = allergic disease
People with one atopic condition are more likely to develop another
Allergic March
IgE- clinical symptoms that appear early in life persist over years or decades and often remit spontaneously with age
Type 1 Hypersensitivity Reactions
Sensitization: First exposure to allergen → produce IgE antibodies.
Re-exposure: Allergen binds IgE Abs → activates mast cells.
Mast cells release histamine and cytokines, causing allergic reaction.
Normal process:
Phagocytic cell ingests allergen, presents antigen.
Cascade: B cell produces IgE.
Sensitization:
IgE binds to mast cells during first exposure.
Initial symptoms mild or negligible.
Re-exposure: Immediate memory response triggers mast cell degranulation.
Release of histamine and cytokines leads to atopic symptoms.
Anaphylaxis
Characterized by widespread edema, vascular shock, and dyspnea.
Severity:
Depends on previous sensitization.
Even small amounts of antigen can trigger.
Symptoms:
Itching, hives, skin erythema.
Bronchospasm, respiratory distress.
Complications:
Laryngeal edema, obstruction.
Shock, potential death within hours.
Treatment:
Epinephrine injection (EpiPen).
Epinephrine increases blood pressure and relaxes smooth muscles.
Desensitization Therapy
- Allergy shots
- Principle = divert immune response from IgE to IgG (less symptoms)
How does Hypersensitivity II Reactions destroy the antigen?
Opsonization and Phagocytosis:
Cells coated (opsonized) to attract phagocytes.
Antibody-Dependent Cellular Toxicity (ADCC):
IgG binds to surface antigen.
NK cell recognizes and kills antibody-coated cell.
Complement Activation:
IgG binding activates complement system.
Causes lysis by membrane attack complex or phagocytosis.
Recruitment of neutrophils and monocytes.
Release of injurious substances, leading to inflammation and tissue damage.
Hypersensitivity II reactions
- Type II antibody-mediated hypersensitivity reactions are mediated by IgG or IgM antibodies directed against target antigens on cell surfaces
- The antigens may be endogenous antigens that are present on the membranes of body cells, or exogenous antigens that are absorbed on the membrane surface
Rh Incompatibility
Rh Incompatibility:
Occurs when mother is Rh-negative and baby is Rh-positive.
Rh factor is a protein on red blood cells.
Inherited trait.
During Pregnancy:
Baby’s Rh-positive blood can cross into mother’s bloodstream.
The mother’s body reacts, creating antibodies against the baby’s blood.
Usually not problematic in first pregnancy.
Subsequent Pregnancies:
Antibodies remain in mother’s body.
Can cause problems in later pregnancies with Rh-positive babies.
Complications:
Antibodies attack baby’s red blood cells, causing hemolytic anemia.
Prevention:
Rhogam (immunoglobulin) given to Rh-negative pregnant women to prevent antibody formation against baby’s Rh-positive blood
Hypersensitivity III Reactions
Type III Hypersensitivity: Immune complex-mediated
- Formation of insoluble antigen-antibody complexes.
- Activates complement system, leading to localized inflammation.
- Immune complexes in circulation can damage vessel linings or tissues.
- Trigger inflammatory response by recruiting neutrophils.
Examples:
Vasculitis in autoimmune disorders like SLE (lupus).
Kidney damage in acute glomerulonephritis (post-strep infections).
Post Streptococcal Glomerulonephritis
Poststreptococcal Glomerulonephritis (PSGN):
- Rapid kidney function deterioration due to inflammatory response.
- Follows streptococcal infection, often group A beta-hemolytic streptococci.
- Affects glomeruli and small kidney blood vessels.
- Usually seen in children after sore throat or skin infection.
Mechanism:
- Formation of immune complexes containing streptococcal antigen and human antibody.
- Deposited in kidney glomeruli.
- Activation of alternate complement pathway.
- Leukocyte infiltration, cell proliferation, impaired capillary perfusion, and glomerular filtration rate (GFR).
Complications:
Reduction in GFR leading to renal failure, oliguria, anuria, acid-base imbalance, electrolyte abnormalities, volume overload, edema, and hypertension.
Classic Triad:
Hematuria, edema, and hypertension
Hypersensitivity IV Reactions
Type IV Hypersensitivity: Cell-Mediated
- Delayed-Type Hypersensitivity (DTH).
- Involves immune response mediated by T cells.
- Requires previous exposure to antigen for response.
Example: Contact dermatitis from poison ivy.
- Initial exposure may not cause reaction; subsequent exposures trigger immune response due to sensitization.
Type IV hypersensitivity DTH (delayed-type)
- antigen is introduced into subcut tissue
- TH1 effector cell recognizes antigen and releases cytokines which act on vascular endothelium
- recruitment of t cells, phagocytes, fluid, and protein to site of antigen injection causes visible lesion
example: TB skin test - Characterized by perivascular accumulation of CD4 T cells and macrophages.
Local secretion of cytokines increases microvascular permeability, causing redness and swelling.
Normal Immune Response:
- an invader (virus) enters the body
- lymphocytes create antibodies to fight invader
Autoimmune disease
- Autoimmune disorders represent a group of disorders that are caused by a breakdown in the ability of the immune system to differentiate between self and non-self antigens. Caused by an inappropriate B cell (antibody) and/or T cell immune responses
- Results in destruction of your own cells/organs.
Self antigen/Autoantigen
an antigen expressed on your own cells
Autoreactive cells
T or B cells that bind to a self antigen
Autoantibody
antibody that binds to a self antigen
Self-tolerance
o To function properly the immune system must be able to differentiate foreign antigens from self-antigens: this is called self tolerance
o It results from central and peripheral mechanism that delete self-reactive immune cells that cause autoimmunity or render their response ineffective in destroying self-cells and self tissue
Central tolerance
Deletion or inactivation of self-reactive T and B cells.
Occurs in thymus (T cells) and bone marrow (B cells).
Mechanisms: receptor editing, absence of costimulatory signals, immunologic ignorance.
