Acute phase includes…
Mast cell activation + de novo secretion of secondaries
Late phase is mediated by…
other activated inflammatory cells (eosinophils, neutrophils, monocytes) recruited by the mast cell mediators
Lipoxygenase activity in the acute phase leads to production of…
LTB4
LTC/D/E
Prostaglandin E
PAF
Primary mediators released from Mast cells
Histamine
ECF-A
Acid hydrolases-Heparin/tryptase complex
Effects of Histamine, SRS-As?
Edema, Mucous Secretion
Bronchoconstriction
Effects of LTs, PAF, TNFa?
Continued edema, cell infiltrates
Continued presence of the eosinophils (characteristic of Type I rxn) relies upon
IL3,4,5, GMCSF
Systemic reactions seen in anaphylaxis
Tissue Swelling, Bronchoconstriction, Peripheral Vasodilation, Dizziness and Syncope, GI symptoms
Treatment for anaphylactic reaction?
Epinephrine
What is atopy?
The tendency to form IgE in response to specific antigens and the resulting allergic responses
Three main mechanisms of type II rxns
- Ab dependent – cell mediated destruction via Fc
- Ab mediated – complement fixation cell lysis
- Ab mediated – cellular dysfunction
Antibody type associated with Type II
IgM, IgG
Two examples of antibody mediated cellular dysfxn
myasthenia gravis
Grave’s disease
Three clinical features of type II rxns
Antibody-mediated blood cell destruction
Antibodies to receptor antigens
antibodis to tissue antigens.
Examples of Type II diseases against tissue antigens
Goodpasture’s disease
Hyperacute transplant rejection
Pemphigus vulgaris
How do you diagnose a type II disease?
Coomb’s test, Ab in serum, immunoflouresence studies
Point of a direct and indirect Coombs
Direct – Look for AB on cells
Indirect – look for AB in serum
Three phases of a Type III hypersensitivity response?
- Formation of Ab-antigen complexes
- Deposition of complexes in specific tissues
- Local tissue destruction medicated by complement
Preferred sites of deposition in type III hypersensitivity responses
Renal glomeruli Joint synovium Skin Heart Small BVs
Effect of Type III tissue damage on host tissues
Cell proliferation causing tissue thickening.
Epithelial proliferation in glomeruli causes proliferative nephropathy.
Hallmarks of Type III disease
Complement Consumption
Acute Inflammation with infiltration of Leukocytes
Deposition of Immune Complexes (seen by imm.fluor)
Three classic examples of Type III
Serum sickness
Post-infectious glomerulonephritis
Arthus rxn
What is the arthus rxn?
A localized area of reaction following injection of an antigen in an immunocompetent host
Differences between an Arthus test and a TB test?
Arthus – AB mediated, occurs in hours
TB test – Cell mediated, Required 1-2 days
Time course for a Type I, II, and IV rxn
I – 10-20 minutes
II – 4-12 hours
IV – 48-72 hours
Tissue response in a Type I rxn
Wheal/Flare Rxn
No necrosis, no vesicle
Tissue response in Type III rxn
Acute inflamm w/ edema + pain
May become necrosis (w/ischemia)
NO vesicles
Tissue responses in type IV rxn
Skin induration and erythema
Vesicle formation in severe cases (due to cell mediated split of the epidermis)
Treatment for Type IV hypersens.
Minimal help from anti-histamine
Usually requires a steroid application
Classic examples of a Type IV rxn
Poison Ivy (Urshiol)
PPD test for TB
Chronic – TB granuloma
Pannus formation in RA
a RIST skin test measures…
Serum amount of IgE
a RAST skin test measures…
serum amount of ANTIGEN SPECIFIC IgE
Which Ab is best at opsinization?
Best at complement activation?
Ops. – IgG
Compl – IgM
Granulomas propagate because macrophages give out _____ and lymphocytes give out ____
Macs give Il1 and 12
Lymp. give gamma interferon
T or F. Autoimmune diseases are associated with WBC count changes.
F