Immunopathology type 2 Flashcards
Direct antibody effects
autoantibody direct against cell surface receptor and behave as an agonist/antagonist
—> feedback don’t work because the end result does not affect antibody
ex: Graves (agonist) myasthenia gravis (antagonist)
Complement mediated damage
antibody activates complement –> destruction of cells –> lysis, release of ROS, granules
ex: goodpasture’s
myasthenia gravis
antibody dependent cell mediated cytotoxicity (ADCC)
NK cells bind Fc of IgG (on self)
Activates apoptosis of self cell
no immunizing exposure require
not MHC restricted
Type II mechanism in muscle
Myasthenia gravis
antibody to Ach receptor of muscle
neutrophil damage at NMJ, no muscle contraction
Type II mechanism in kidney
Goodpasture’s
autoantibodies to basement membrane of kidney –> persistent glomerulonephritis
Type II mechanism in lung
Goodpasture’s
autoantibodies to basement membrane of lung –> pneumonitis and pulmonary hemorrhage
similarity between lung and kidney
share antigen at basement membrane
goodpasture’s
Type II mechanism in heart (1)
Rheumatic heart disease
after strep infection, antibody to strep M protein cross reacts with laminin on heart valve –> neutrophil destruction
Type II mechanism in heart (2)
dressler’s syndrome
autoantibody to heart after MI
Type II mechanism in red cells
autoimmune hemolytic anemia
viral infection/drugs –>
RBC coated with antibody –> opsonization/destruction
warm aiha = IgG
cold aiha = IgM
Type II mechanism in platelets
autoimmune thrombocytopenic purpura
platelets opsonized and destroyed by antibodies –> bleeding
Type II mechanism in thyroid (1)
hashimoto’s thyroiditis
antibodies against thryoid cells –> destroy hormone secreting cells –> hypothyroidism
Type II mechanism in thyroid (2)
grave’s disease
antibody mimics TSH binding to TSH receptor –> hyperthyroidism
type II mechanism in pancreatic islet cells
juvenile (type 1) diabetes
antibody to Beta cells in pancreas (produce insulin) –> activates complement –> destroys cell
Direct test
1) patient’s kidney (already with antibody on glomerular basement membrane)
2) add goat fluorescent anti-IgG
3) if pt has goodpasture’s, linear binding on basement membrane
indirect test
1) take a normal kidney biopsy
2) add patient serum
3) add goat fluorescent anti-IgG
4) antibody on basement membrane –> linear
antibody complex forms –> lumpy bumpy
Linear immunofluorescent pattern
antibody is binding to a specific structure–> shows clear structure antibody is coating
= TYPE 2
lumpy bumpy immunofluorescent pattern
immune complex formed, antigen and antibody clump together and precipitate
not line any particular strxr –> TYPE 3
innocent bystander
neutrophils/macrophages try to destroy foreign antigen (bacteria) using ROS, granules, inflammation
in the process, attack normal adjacent host cells
cross reaction of a foreign antigen with self
rheumatic heart disease
cross reaction between foreign antigen and self antigen
antibody coats normal self cells –> destroyed by complement
coupling self antigen with a foreign antigenic carrier
1) anti-self B-cell escapes clonal deletion, binds self antigen + foreign antigen
2) since self + foreign, present foreign antigen via MHC II
3) Th cell recog foreign antigen, activate B cell to produce antibody to SELF ANTIGEN
(B-cells don’t necessarily see or get excited about the same antigens/epitopes as T-cells )
Exposure of a sequestered antigen
normally, self antigens sequestered so immune system doesn’t see
but if immune response in the sequestered area, then immune cells attack self antigens
(blood-testis barrier)
Inadequacy of regulatory T cells
insufficient Treg, so high Th1 and Th2 mechanism
causes tissue damage by hyperactive responses to normal antigens (food)
Rheumatoid factor
IgM antibody against self IgG
agglutination of IgM and IgG
