6/28 - Diseases of Immune System Flashcards
immune reactant for Type II HS
IgG and some cases IgM
antigen for Type II HS
cellular or extracellular matrix antigens
what causes type II HS? what does it result in?
cause: destruction of cells
result: inflammation or interference w/ normal cell function (dysfunction)
mechanisms of type II HS
- opsonization and phagocytosis (destruction)
- inflammation (destruction)
- cellular dysfunction
describe opsonization and phagocytosis in type II HS
antibody coats cell and and is marked for phagocytosis
what causes tissue damage in type II HS
cellular lysis induced by direct binding of antibody to cell surface antigens
what do antibodies attack in inflammation of type II HS
attack leukocytes or RBCs (mobile cells) or bind to fixed cells (part of solid tissues)
what do antibodies involved in inflammation activate? what does this result in
activate complement generating by-products , including chemotactic agents (mainly C5a)
this directs migration of neutrophils and monocytes and anaphylaxtonins
what are the anaphylatoxins? what does it do?
C3a, C4a, and C5a
increase vascular permeability
pathway for type II HS inflammation and tissue injury
- antigen + target cell + antibody
- complement protein (C3a and mainly C5a)
3a. complement 5b-9MAC
3b. + membrane attack complex (MAC) insert into cell
4b. results in osmotic lysis or drill holes in cell membrane
- complement protein (C3a and mainly C5a)
2 main examples of antibody-mediated cellular destruction. what type of HS?
- autoimmune hemolytic anemia
- erythroblastosis fetalis (hemolytic disease of newborn)
both type II
what is the disease where individuals produce antibodies to their own blood? HS type?
autoimmune hemolytic anemia - type II
what is the disease where there is an antigenic difference between mother and fetus and IgG antierythrocyte antibodies from the mother cross the placenta and destroy the fetal red cells? HS type?
erythroblastosis fetalis - type II
what are the two main examples of cellular dysfunction for type II HS
- myasthenia gravis (interferes w/ cellular function)
- grave’s disease (cellular hyperfunction)
what disease:
antibodies reactive with Ach receptors in motor end plates of skeletal muscles block neuromuscular transmission and cause muscle weakness? what type of HS
myasthenia gravis - type II HS
what disease:
antibody-mediated stimulation of cell function is the basis; antibodies against the TSH receptors on thyroid epithelial ells stimulate the cells, resulting in hyperthyroidism
what type of HS
Grave’s disease = type II HS
autoimmune hemolytic anemia
target antigen, mechanism of disease, clinical manifestation, HS type
TA: red cell membrane protein
MoD: opsonization and phagocytosis of RBCs
CM: hemolysis anemia
HS: type II
autoimmune thrombolytic purpura
target antigen, mechanism of disease, clinical manifestation, HS type
TA: platelet membrane protein
MoD: opsonization and phagocytosis of platelets
CM: bleeding
HS: type II
B)
pemphigus vulgaris
target antigen, mechanism of disease, clinical manifestation, HS type
TA: protein in intercellular junctions
MoD: antibody-mediated activation of proteases disruption of intercellular adhesion
CM: skin vesicles
HS: type II
vasculitis caused by antineutrophil cytoplasmic AB
target antigen, mechanism of disease, clinical manifestation
TA: neutrophil granule proteins released from activated neutrophils
MoD: neutrophil degranulation and inflammation
CM: vasculitis
HS: type II
good pasture syndrome
target antigen, mechanism of disease, clinical manifestation, HS type
TA: non collagenous protein in BM of kidneys
MoD: complement and Fc receptor mediated inflammation
CM: nephritis, lung hemorrhage
HS: type II
acute rheumatic fever
target antigen, mechanism of disease, clinical manifestation, HS
TA: streptococcal cell wall antigen, antibody-cross react w/ myocardial antigens
MoD: inflammation, macrophage activation
CM: myocarditis, arthritis
HS: type II
myasthenia gravis
target antigen, mechanism of disease, clinical manifestation, HS type
TA: Ach receptors
MoD: antibody inhibits acetylcholine binding, down modulates receptors
CM: muscle weakness, paralysis
HS: type II
insulin-resistant diabetes
target antigen, mechanism of disease, clinical manifestation, HS type
TA: insulin receptor
MoD: antibody inhibits binding to insulin
CM: hyperglycemia, ketoacidosis
HS: type II
graves disease
target antigen, mechanism of disease, clinical manifestation, HS type
TA: TSH receptors
MoD: antibody mediated stimulation of TSH receptors
CM: hyperthyroidism
HS: type II
pernicious anemia
target antigen, mechanism of disease, clinical manifestation, HS type
TA: intrinsic factor of gastric parietal cells
MoD: neutralizatin of intrinsic factor, decreased absorption of Vit B
CM: abnormal erythropoiesis anemia
HS: type II
immune reactant for type III HS
IgG or IgM
antigen for type III HS
solubule antigen
type III HS rxn is mediated by formation of what
antigen-antibody aggregates called immune complexes
how are type III HS rxns frequently initiated
when antigens combine with antibodies in circulation (creating immune complexes)
how are type III HS rxns less frequently initiated
when immune complexes are formed at sites where antigen has been “planted” previously
type III HS immune complexes can precipitate in various tissues (such as skin, joints, vessels, or glomeruli) resulting in what?
tissue damage and inflammation at the site of deposition thru triggering of classical complement pathway