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what's the different between type 2 and 3 HS?
both are antibody-mediated but Type 3 is against soluble antigen in the blood vs antigen bind to basement membrane or non-blood area
mechanism of AB-mediated injury in type 2
opsonization (complement dependent)
- Fc-mediated on the leukocyte --> initiate inflammation (fix tissue, basement membrane)
- Inc production of C3a-C5a --> inc vasodilation and recruitment of PMN and immune cells
AB-mediated by binding to the receptor --> can both activate and inactivate the receptor (Myasthenia gravis and Grave disease)
steps involve in type II HS
1.Deposition of Immune Complexes
- Antigen-antibody complexes produce tissue
- damage by eliciting inflammation at site of deposition
- Antigens: exogenous (foreign protein)
- endogenous (self-component)
- -get circulating immune complexes
- that can be deposited in many organs or localized to one.
3 phases of systemic type III HS
- 1.Introduction of antigen triggers an immune response that produces antibodies. (Takes about a week)
- Antibodies are secreted into blood where
- they react with antigen still present in circulation, forming an antibody-antigen complex.
2.Next phase: Deposition of immune complex
Circulating Ab-Ag complexes are deposited in various tissue.
- What determines whether complex formation will lead to tissue deposition and
1.Complexes that are medium size
2.Formed in slight antigen excess
- 3.Tissue Injury caused by immune
- complex: Once in tissue, complexes
- initiate acute inflammatory response.
clinical features of Type III
Type III: Immune complex found in
Small blood vessels
Distinguishing characteristics Type III Hypersensitivity
•Intense neutrophilic infiltration
- •Necrotic tissue will have deposits of
- immune complexes (called fibrinoid necrosis)
•Acute necrotizing vascularitis (necrosis of the vessel wall)
Examples of Type III hypersensitivity
- I.Single large exposure to antigen
- Usually resolves
- •acute serum sickness
- •Streptococcal glomerulonephritis
- II. Chronic exposure to antigen
- •Systemic lupus erythematosus
- •Streptococcal glomerulonephritis
- III. Local immune complex disease (Arthus
- •Usually in skin
- •Reproduced by injecting antigen in
- an immunized animal
take time to form complex --> deposit lead to fever vasculitis arthritis and nephritis
delayed in response of inflammation
•Most common in children 6-10 years old after a streptococcal infection
•Antibody to streptococcal ag form compounds that deposit in glomeruli.
vasculitis and intense neutrophil reponse
repeat and prolong exposure --> lupus
local immune complex disease
Localize area of tissue necrosis resulting from acute immune complex vasculitis
take 1-2 hours
Type IV Hypersensitivity - 3 effector mechanism
- 1.Macrophage activation by TH1 cells, which
- results in an inflammatory response.
- 2.Damage is caused by activation of TH2
- cells. Inflammatory response is predominated by eosinophils
- 3.Damage is caused directly by cytotoxic T
- cells (CTL).
whicchc type IV HS is predominated by eosinophil
Type IV Hypersensitivity Responses
•Reactions are mediated by T cells
•All take some time to develop (delayed
- •3 syndromes, grouped according to
- the route by which antigen passes into body.
- Injected into the skin
- abosorbed into skin
- Aborbed by gut
Type IV hypersensitivity - 3 stages
Take 24-72 hours
- 1st phase: uptake, processing and presentation of the antigen by local antigen
- presenting cells
- 2nd phase: TH1 cells that were primed by a previous exposure to the antigen migrate
- into the site of injection and become activated. Because these specific cells are rare, and
- because there is little inflammation to attract cells into the site, it can
- take several hours for a T cell of the correct specificity to arrive.
- 3. These cells release mediators that activate local endothelial cells, recruiting an inflammatory cell infiltrate dominated
- by macrophages and causing the accumulation of fluid and protein. At this point, the lesion is apparent.
Elicitation of Type IV (delayed) hypersensitivity
- 1.A contact sensitizing agent is a small
- highly reactive molecule that can easily penetrate intact skin. It binds to a variety of endogenous proteins, which are taken up and processed by Langerhan cells (major antigen presenting cell of the skin)
- 2.These APCs present the peptides to
- effector (and previously primed) TH1 cells
3.Activated TH1 cells secrete IFN-g that then activate kerintocytes to secrete more cytokines and chemokines.
- 4.These products recruit and activate
- macrophages resulting in an inflammatory lesion.
Mechanism of T cell mediated HS
- Delayed type HS and immune inflammation:
- Th1 (macrophage) and Th17 (neutrophil)
- --> depend mostly on cytokine secreted. TH17 at the lesser extense
- Tcell-mediate: CLT --> kill
Delayed Hypersensitivity (DTH) rxn (what test?_
1.Injection of tuberculin in sensitized individual
2.Local T cell inflammatory reaction
3.Peaks at 24-72 hrs
- Perivasular cuffing
- Driven by T-cell secreted cytokines:IFNg, IL-12, IL-2, TNFa & lymphotoxin
special form of DTH
- lymphocyte on theh outside
- epitheliod cell on the inside w/ giant cell
rxn of CD*+ Tcells
cell-mediated cytotoicity --> graft rejection and
2 mechanism for rejection of allograft
direct and indirect recognition
T-cell Mediated Graft Rejection - direct allorecognition
Host T cells (transplant recipient) are activated by APC within the transplanted tissue (graft).
Host T cell activated by Graft APC
T-cell Mediated Graft Rejection - -Indirect
APC from the host present graft antigens to host T lymphocytes --> chronic rejection to graft
- mediated by CD4 Tcell --> macrophage
- and AB mediated
between direct and indirect pathwya for graft rejection
3 type of graft rejection
graft vs host disease
when immunologically competent cells are transplanted into immunologically criplled recipient