Chapter 19 - Hypersensitivity Flashcards
what is characteristic of type II hypersensitivity?
Ag in tissue, solid Ag (Ab against tissue)
ex. pancreas
What is involved in type 3 hypersensitivity?
what does it lead to?
immune complex diseases, soluble Ag in circulation, complement system
vasculitis
What are some examples of type 4 hypersensitivity?
what does it result from?
infection, environmental Ag, post vaccination
cell-mediated
inflammation caused by ctyokines from Th1 and Th17 cells, or CTLs
what is atopy?
genetic tendency to develop allergic diseases
describe the sequence of events in the development of immediate hypersensitivty
activation of Th2 cells and IgE production in response to Ag
binding of IgE to FcERI receptors of mast cells
exposure to Ag, cross-linking of bound IgE by Ag and release of mediators
what happens immediately after Ag exposure (1st hour)?
what is the morphology characterized as?
vascular and smooth muscle reaction to allergen
vasodilation, congestion, and edema
when does the late phase reaction develop?
how is it characterized?
2-24 hours
inflammatory infiltrate of eosinophils, neutrophils, and T cells
what are the most important mediators produced by mast cells?
vasoactive amines, proteases, prostaglandins, leukotrienes, and cytokines
what causes dilation of small blood vessels and increases vascular permeability?
histamine
what do proteases do?
cause damage to local tissue
what do prostaglandins do?
leukotrienes?
cause vascular dilation
stimulate prolonged smooth muscle contraction
what do cytokines do?
induce local inflammation (late-phase reaction)
how is type II hypersensitivity activated?
how else?
IgG and IgM activate the classical complement system, resulting in the production of byproducts that recruit leukocytes and induce inflammation
chemoattractants (opsonization) and phagocytosis of cells
what damages adjacent tissues?
ROS and lysosomal enzymes released
what binds to neutrophils and macrophage Fc receptors and activates leukocytes, resulting in proinflammatory response?
IgG Abs
what are the 3 effector mechanisms of type II?
1) opsonization and phagocytosis
2) Complement and Fc receptor-mediated inflammation
3) Abnormal physiological responses without cell/tissue injury
what type of hypersensitivity is goodpasture’s syndrome’s, the mechanism of disease and clinical manifestation?
type II, complement and Fc receptor mediated inflammation
nephritis, lung hemorrhage
what type of hypersensitivity is Grave’s syndrome’s, the mechanism of disease and clinical manifestation?
type II, Ab-mediated stimulation of TSH receptors
hyperthyroidism
what type of hypersensitivity is Myasthenia gravis syndrome’s, the mechanism of disease and clinical manifestation?
type II, Ab inhibits Ach binding, down-regulates receptors
muscle weakness, paralysis
what type of hypersensitivity is Pemphigus vulgaris syndrome’s, the mechanism of disease and clinical manifestation?
type II, Ab-mediated activation of proteases, disruption of intracellular adhesions
skin vesicles (bullae)
what type of hypersensitivity is Pernicious anemia syndrome’s, the mechanism of disease and clinical manifestation?
type II, Neutralization of intrinsic factor, dec. absorption of Vit B12
anemia
what type of hypersensitivity is Rheumatic fever syndrome’s, the mechanism of disease and clinical manifestation?
type II, inflammation, macrophage activation
myocarditis, arthritis
Ab-Ag complexes of what Abs may be formed in the circulation and deposited in blood vessels and other sites
IgG, IgM
what type of hypersensitivity is Systemic lupus erythematosus syndrome, what are the clinical manifestations?
what auto-Abs are found and what is formed from them?
type III, rashes, arthritis, glomerulonephritis
anti-DNA Abs, immune complexes formed responsible for effects
what type of hypersensitivity is Rheumatoid Arthritis syndrome, the mechanism of disease and clinical manifestation?
mixed type II and III
Th1 and Th17 cells, activated B, plasma cells and macrophages
involves small and large joints where inflammation of the synovium and destruction of joint cartilage and bone occurs
in RA, what kind of Abs react with what in their own body?
what are these auto-Abs called?
IgG and IgM react with the Fc of their own IgG molecules
rheumatoid factors
what type of hypersensitivity is polyarteritis nodosa syndrome, the clinical manifestation and what Ab specificity does it have?
type III, vasculitis
microbial Ags ie hep B
what type of hypersensitivity is Post-streptococcal glomerulonephritis syndrome, the clinical manifestation and what Ab specificity does it have?
type III, nephritis, streptococcal cell wall Ag
what type of hypersensitivity is serum sickness syndrome, the clinical manifestation and what Ab specificity does it have?
type III, systemic vasculitis, nephritis, arthritis
protein Ag
what type of hypersensitivity is Arthus reaction syndrome, the clinical manifestation and what Ab specificity does it have?
type III, cutaneous vasculitis
protein Ag
What are the major causes of T-cell mediated hypersensitivity reactions?
autoimmunity and exaggerated/persistent responses to environmental Ags
tissue injury also may accompany T cell response to what?
microbes (M. tuberculosis)
what type of hypersensitivity is multiple sclerosis, the clinical manifestation and what specificity of pathogenic T cells does it have?
type IV, demylenation in CNS, motor and sensory dysfunction
myelin proteins
it is an autoimmune disorder
what type of hypersensitivity is Type I diabetes, the clinical manifestation and what specificity of pathogenic T cells does it have?
type IV, impaired glucose metabolism, vascular disease
pancreatic islet Ags
autoimmune disorder
what type of hypersensitivity is Crohn’s disease, the clinical manifestation and what specificity of pathogenic T cells does it have?
inflammation of bowel wall, abdominal pain, diarrhea, hemorrhage
g.i. microbes
what type of hypersensitivity is contact sensitivity, the clinical manifestation and what specificity of pathogenic T cells does it have?
type IV, DTH reaction in skin and rash
modified skin proteins
what type of hypersensitivity is chronic infections, the clinical manifestation and what specificity of pathogenic T cells does it have?
Chronic inflammation
microbial proteins
what is DTH?
when does it occur?
give an example
injurious cytokine-mediated inflammatory reaction resutling from act. of CD4 T cells
occurs 24-48 hours after Ag challenge
ex: PPD Ag to TB
how are granulomas formed?
prolonged reactions in which cytokines are involved in the generation of Th1 cells, activation of macrophages and recruitment of leukocytes
what are the immunotherapy methods?
anti-inflammatory agents (corticosteroids) INHIBITS NF-KB
depletion of cells and Abs (anti-CD20 Ab for B cells)
Anti-cytokine (anti-TNF Ab)
Inhibitory agents of cell-cell interactions and Leukocyte migration (anti-CDL)
Treg therapies
what does anti-p40 do?
blocks Th1 and Th17 responses
what does IL-2R do?
block T cell proliferation
what do inhibitors of calcineurin, Jaks and other kinases do?
inhibit signaling
Immediate type I involves what kind of responses?
what does it result from?
allergic
mediators secreted by mast cells
