Immunopathology II (H.R) Flashcards
(38 cards)
What are hypersensitivity rxns❓
Here, an organism responds to a renewed contact with an antigen that it already knows and to which it is hypersensitive
Describe the 4 hypersensitivity rxns and their effectors using the Gell and Coombs classification
Type I
Description: Immediate rxn
Effector: IgE antibodies
Type II
Description: Cytotoxic rxn
Effector: IgG and IgM antibodies
Type III
Description: Immune complexes
Effector: IgG and IgM antibodies
Type IV
Description: Delayed rxn (48hrs)
Effector: T cells
What do Type I, II and III hypersensitivity rxns have in common❓
What is the mediator of Type IV hypersensitivity rxn❓
- Mediated by Antibodies/Plasma cells
2-6hrs after exposure
- T-cell and macrophages
24-36hrs after exposure
List the examples of allergens that can cause type I hypersensitivity rxns
Tree, grass, weed pollens
Cat/animal dander antigens
Dust/mite/fecal/pellet antigens
Mold spores
What makes individuals susceptible to Type I hypersensitivity rxn❓
The propensity to make strong Th2 responses and make IgE antibodies against allergens
- What are the other names for type I hypersensitivity rxn❓
2. What is it characterized by❓
- Anaphylactic rxn
IgE allergy
IgE hypersensitivity rxn - IgE production
Describe the pathogenesis of Type I hypersensitivity rxn
Allergen inhalation/ingestion/injection ⬇️ Production of local chemokines *eotaxin ⬇️ Recruitment of Th2 cells ⬇️ Th2 secrete cytokines that are responsible for hypersensitivity rxn
IL-4: produces IgE
IL-5: activates eosinophils
IL-13: secretes mucus
⬇️
IgE is implanted on FcR of mast cells and basophils
⬇️
Priming of mast cell occurs
⬇️
Cross linking of IgE Fc on surface of mast cells on 2nd exposure
⬇️
Mast cell is stimulated and releases all its products (degranulates)
*eotaxin recruits eosinophils
Describe the function of:
IL-4
IL-5
IL-13
In Type I hypersensitivity rxns
IL-4: stimulates B cells to undergo heavy-class switching to IgE
IL-5: activated eosinophils
IL-13: stimulates mucus secretion
In Type 1 hypersensitivity rxn, the complement system isn’t activated
True or false❓
Which other hypersensitivity rxn mimics this❓
True
Type II (ADCC) Type IV H. R
List the cells that express FceRI (Fc portion of the E heavy chain on IgE)
Mast cells
Basophils
Eosinophils
What are the primary and secondary mediators of hypersensitivity rxns❓
What do they cause❓
1. Primary mediators: •Histamine •Serotonin •NCF, ECF •Proteases
Cause:
•Vasodilation
•Bronchoconstriction
2. Secondary mediators: •Leukotrienes •Prostaglandins •PAF •Cytokines
Cause:
•Lead to inflammation
List the consequences of the mediators of Type I hypersensitivity rxn
⬆️vascular permeability
⬆️glandular secretion
Smooth muscle contraction
Edema
Inflammatory cell attraction
List the mediators that cause:
- Chemotaxis
- Vasoactivity
- Smooth muscle spasms
In type I hypersensitivity rxn
Chemotaxis:
LTB4
ECF
NCF
Vasoactivity: Histamine PAF LTC4, D4, E4 Neutral protease PGD2
Smooth muscle spasms: Histamine LTC4, D4, E4 PG PAF
Mention some important medical conditions that fall into Type I hypersensitivity rxns and their symptoms
- Penicillin/Bee sting allergy (systemic anaphylaxis)
Symptoms: Acute asthma Laryngeal edema Diarrhea Urticaria Shock
- Food allergies/Allergic rhinitis/Hay fever (local anaphylaxis/atopy)
Symptoms:
Asthma
Hives
- What are the other names for type II hypersensitivity rxn❓
- What is it characterized by❓
Cytotoxic rxn
IgG/IgM immunoglobulins
Describe the pathogenesis of Type II hypersensitivity rxn
•Complement-dependent cytotoxicity: Ag/Ab rxn ⬇️ Complement pathway (classical pathway) is activated ⬇️ Cell lysis
eg Transfusion rxns
Autoimmune hemolytic anemia
Erythroblastosis fetalis
Goodpasture’s syndrome
•Antibody-dependent cell-mediated cytotoxicity:
Low conc of IgG/IgE (parasitic) coat target cells
⬇️
Inflammatory cells bind to FcE receptors
⬇️
Cell lysis
🚫phagocytosis
Eg Transplant rejection
Immune rxns against neoplasms/parasites
•Anti-receptor antibodies:
IgG antibody is directed against receptors in target cells
⬇️
Complement-mediated destruction of the receptors
⬇️
Functional derangement
🚫cell injury
Eg Mysthenia graves (anti ACh receptor)
Graves’ disease (anti TSH receptor/TSI)
Pernicious anemia
- What are the other names for type III hypersensitivity rxn❓
- What is it characterized by❓
- Immune complexes
2. Ag-Ab complexes
Describe the pathogenesis of Type III hypersensitivity rxn
⬆️Circulating, soluble immune complexes containing IgG/IgM antibody ⬇️ Deposition in tissues 🚫removal by mononuclear phagocytes ⬇️ Activation of complement
*C3b and C5a attracts neutrophils and are used up
Is serum complement increased or reduced in:
- Complement-dependent, Type II H.R
- Immune complex, Type III H. R
- Serum complement ⬆️ in type II complement dependent H. R
2. Serum complement ⬇️ in type III H. R
Which H. R is sometimes classified as TYPE V❓
Antireceptor antibodies, Type II H. R
What are the differences between Complement-dependent (Type II H.R) and Immune complex (Type III H. R)❓
- Serum complement ⬆️ in type II complement dependent H. R
Serum complement ⬇️ in type III H. R
- The Ag is not an intrinsic component of the target cells in Type III H. R
Mention some important medical conditions that fall into Type III hypersensitivity rxns
Systemic immune complex:
Glomerulonephritis
Serum sickness
Vasculitis
Local immune complex/Arthus rxn:
Pneumonitis/Farmers lung
SLE Polyarteritis nodosa Rheumatoid arthritis Lupus nephropathy Post-streptococcal GNs
What is Arthus rxn❓
Injection/local transplant of antigen in the presence of preformed Ab ⬇️ Ag-Ab binding ⬇️ Formation of immune complexes locally ⬇️ Precipitation in vessel walls ⬇️ Fibrinoid necrosis and thrombosis ⬇️ Ischemic injury
What is Serum Sickness❓
Systemic deposition of Ag-Ab complexes in multiple sites (esp kidneys, heart, joints)
