Alterations of the Immune system Flashcards
Immune disorders
- hypersensitivity
- autoimmune disease
- immunodeficiency
Hypersensitivity definition
-Inappropriate or excessive immune response to antigens
allergies = excessive
Autoimmune disease definition
when the immune response mistakenly targets normal body cells and tissues
-inappropriate
Immunodeficiency definition
- the immune system fails to develop normally or is blocked in some way
- not working
Hypersensitivity reactions
- an exaggerated immune response that causes inflammation (more than needed) and results in the injury of healthy tissue
- atopic person
- repeated exposure to relatively large doses of allergen is required to produce sensitization of the individual (genetic tendency)
- there are for interrelated mechanisms
Atopic person
individual who is predisposed to form specific IgE antibodies to antigens that do not affect most people (allergic person)
Hypersensitivity Types
- Type I: immediate IgE-mediated reactions (allergy) B cells
- Type II: antibody- mediated reactions (tissue specific reactions)
- Type III: immune complex-mediated reactions (autoimmune)
- Type IV: delayed hypersensitivity (cell-mediated reactions) T cells
Mechanism of Type I
- IgE-mediated reactions
- immediate hypersensitivity, usually in response to an environmental allergen
- an “allergen” is an antigen that causes allergies
- allergic individuals must first be sensitized to the allergen
- chemical mediators of inflammation (major player is Histamine)
Sensitizaiton
- 2 steps
1. contact with the allergen causes formation of a specific IgE antibody
2. IgE attaches to cell membrane of mast cells - later when the sensitized person is exposed to the same allergen, the allergen attaches to the IgE (just takes time)
- union of allergen and IgE causes the mast cell to degranulate and release chemical mediators of inflammation, especially histamine
Histamine
- contracts bronchial smooth muscles (bronchoconstriction or bronchospasm)
- vasodilation and increased vascular permeability (swelling, due to leaky blood vessels)
- increases respiratory mucus secretions
- produces itching sensation (have chemoattractants
Atopy
- atopic individuals tend to produce higher concentrations of IgE and to have more IgE receptors on their mast cells
- IL4 (interleukin 4 and chemical mediator of inflammation) causes plasma cells to switch from making IgG to making IgE
- atopic people make 10 x IL4 > normal people
- atopy is a reaction to inhaled allergens; often referred to as “hay fever” (pollen, cat dander, dust mites, etc)
Examples of Type I Hypersensitivity
- Atopy
- Bronchial asthma
- Urticaria (hives)
- Atopic dermatitis
- Anaphylaxis
- Gastrointestinal (food) allergy
- drug allergies
- different responses in different places based on HI receptors
Atopy
- allergic rhinitis, allergic conjunctivitis
- common allergens: cat dander, pollen, dust mites
Bronchial asthma
- histamine -> bronchospasm, inflammation, increased mucus secretion
- not all asthma is due to allergies
Uticaria
- hives
- -> severe itching, raised, red rash
- not all hives are due to allergy
Atopic Dermatitis
- Eczema
- refers to any itchy red rash that weeps or oozes serum and may become crusty
- not all eczema is due to allergies
Anaphylaxis
- severe, potentially life-threatening allergic reaction
- -> selling of throat and larynx, respiratory distress, decreased blood pressure, shock and death
- there can also be mild cases and localized cases
Gastrointestinal (food) allergy
- vomiting, diarrhea, abdominal pain, and/or anaphylaxis
- may be a food, product of food breakdown, additive, or preservative in the food
- some people claim to have “food allergies” are actually intolerances due to the lack of a digestive enzyme (dif. allergies have dif. runs at dif. levels)
Drug allergies
-some are true allergies, but other so called “drug allergies” are side effects and not true allergies
Treatment of Type I reactions
- antihistamines
- cromolyn drugs
- desensitization
antihistamines
- bind with histamine before it can reach its receptors
- has no effect on all other chemical mediators of inflammation
- still have inflammation
cromolyn drugs
prevent mast cell degranulation
desensitization
- allergy-shots
- causes formation of specific IgA and IgG antibodies against the allergen
- IgA and IgG combine with the allergen before it can attach to the IgE on the mast cells and trigger degranulation (“race”)
Mechanism of Type II reactions
- tissue-specific
- antibodies are formed against a specific antigen that is located in only one tissue
- these cells care then destroyed by phagocytosis
- Non-autoimmune Type II reactions:
- transfusion reactions (mismatched blood types)
- hemolytic disease of the newborn (Rh incompatibility)
- Autoimmune type II reactions:
- a person’s immune system makes antibodies against one of its own normal tissues
Type II: Ab vs. RBCs
chronic hemolytic anemia
Type II: Ab vs. platelets (thrombocytes)
thrombocytopenia purpura
Type II: Ab vs. myelin
multiple sclerosis
Type II: Ab vs. beta cells of pancreas
diabetes mellitus type 1
Type II: Ab vs. throid tissue
autoimmune throiditis
Type II: Ab vs. ACh receptors on skeletal muscle
myasthenia gravis
Mechanism of Type III
Immune Complex Mediated Injury
- antibodies are formed vs. a soluble antigen in the serum
- causes circulating antigen-antibody complexes
- the largest complexes form when there is equivalence
- these complexes can get deposited in many different places “sticks”
- location of deposition will determine the symptoms
harmful effects due to complement activation
- complement is chemotactic to neutrophils
- large amounts of lysosomal enzymes are released
- results in tissue damage where the complex gets stuck
- the phagocyte can’t completely surround the Ag/Ab complex, so their enzymes damage surrounding tissues (“innocent bystanders”)
Examples of Type III
- immune complex glomerulonephritis
- rheumatoid arthritis
- rheumatic fever: develops post Group A beta-hemolytic streptococcal infection; a small % of these patients develop rheumatic heart disease (anti-bodies bind to heart cells)
- systemic lupus erythematosus
- ulcerative colitis
Mechanism of Type IV
Delayed Hypersensitivity
- symptoms have slow onset: 24-48 hrs. after exposure
- T lymphocytes, not antibodies, are responsible for tissue injury
- reason for delay= time necessary for sensitized T cells to accumulate at site and generate an inflammatory reaction
- T cells release chemical mediators of inflammation, attack and destroy cellular targets directly
clinical examples of type IV
- contact dermatitis: -> inflammation only at point of contact (immediate reactions are usually more widespread)
- posion ivy/poison oak: a specific type of contact dermatitis
- graft rejection: grafts contain foreign antigens
- need to inhibit recipient’s immune system
