Exam 4 Flashcards
Type I Immediate Hypersensitivity (Anaphylactic)
This type of immune reaction is responsible for an allergic disease, which is dependent on antigen-mediated activation of IgE coated tissue mast cells. The mast cells release mediators that cause increased vascular permeability, vasodilation, bronchial and visceral smooth muscle contraction and local inflammation.
Type II Cytotoxic(antigens on cell)
Antibody dependent (IgM or IgG)
Complement or phagocytosis involved to destroy cells
Transfusion reactions
Type III Hypersensitivity
Occurs when antibodies associated in immune complexes are deposited into the surfaces of vascular tissues. The complexes cause the activation of complement and the attraction of phagocytes to the area and leads to tissue damage. Diseases that are associated with this include post streptococcal glomerulonephritis and systemic lupus erythematosis
Type IV Delayed hypersensitivity (CD4’s)
Ran by T cells
CD8’s T cell mediated by cytotoxicity
Contact sensitivity
In Type III hypersensitivity why is there an antigen-antibody complex causing problems?
Neutrophils and macrophages should have cleared the complexes. But they don’t, so it causes problems.
Why is skin testing widely used to test for type I hypersensitivity?
It has good sensitivity (mast cells are in the tissue), but they cause false positives
What is the immune response involved in contact hypersensitivity?
Hapten-carrier complex is recognized by T cells
What immune elements are involved in a positive skin test for tuberculosis?
T cells (CD4’s) and macrophages
Organ specific autoimmune disorder
Antibodies and lesions are confined to a specific organ. Clinical serologic overlap (thyroid, stomach, etc). The antigens are only available to lymphoid system in low concentrations and evoke organ specific antibodies. Example: Grave’s disease
Non organ systemic autoimmune disorder
Antibodies and lesions are not confined to a single organ. Antigens are at high concentrations, familial tendency to develop connective tissue disease. Example: SLE
What are immunopathogenic mechanisms of autoimmune disorders specifically caused by complement
Self cell with surface antigen, with antibody bound on the surface binds complement leading to lysis of cell and inflammation
What are immunopathogenic mechanisms of autoimmune disorders specifically caused by cytoloxic T cells
T cells have a specificity toward “self” and contribute to autoimmune responses
What are immunopathogenic mechanisms of autoimmune disorders specifically caused by NK cells
Recognize a “self” cell as foreign and attack and kill cells
Warm reactive autoantibodies
Most common—antibody IgG will bind to RBC and be destroyed in the RE system
Cold reactive autoantibodies
<20%–IgM attaches to RBC’s in colder areas of body during circulation, bind complement leading to lysis
Paroxysomal cold hemoglobinuria
Often after viral infections—transient. IgG antibody is biphasic-reacts with antigen in cold and lysis when it is warm
Drug induced
(20%) RBC’s are coated with drug and antibody complexes
Describe the different types of Systemic Lupus Erythematosus?
The individuals with this disease produce multiple autoantibodies. In the laboratory antinuclear antibodies appear, immune complex problems, decreased complement levels, tissue deposition of Ig’s and complement
What is the main cause of tissue injury in systemic lupus erythematosus?
Deposition of immune complexes
Which antibodies can be detected using FANA technique?
Different patterns will be visible indicating specific antibodies
• Anti-dsDNA—present in Crithidia luciliae kinetoplasts
• Anti-histone antibody
• Anti-DNP (deoxyribonucleoprotein)
• Anti-Sm (uridine-rich RNA)
• Anti-SS-A/Ro (RNA protein)
• Anti-SS-B/La (Processing products of RNA polymerase)
• Anti-nRNP (RNA antibody-nuclear, against 7-8 nonhistone proteins)
• Anti-nucleolar RNA
Describe Fluorescent Antinuclear Antibody testing. Discuss the different patterns and antibodies involved
Usually human epithelial cells are placed on a glass slide. Patient serum is added to the slide. If the patient has antibodies to nuclear material it will bind to the cells on the slide. A wash phase is then completed to remove any antibodies that are not attaching. Anti-human antibodies with a fluorescent tag are then overlaid on top followed by a second wash step. If the patient antibody is present the AHG with the tag will bind and not be removed during the last wash phase.
Discuss crithidia FANA testing
Crithidia is an organism used as a substrate (usually on a solid phase). The kintoplast of the Crithidia is pure native dsDNA and can be used instead of another source like HEp-2 cells and is useful in IDing anti-dsDNA
Discuss the immunopathogenic mechanisms of rheumatoid arthritis
Rheumatoid factor is an antibody that has specificity for antigen determinants of the Fc fragment of human IgG’s, IgM’s and IgA’s.
What organ and manifestations are involved in Hashimoto’s disease?
thyroid, cytotoxic autoantibody production related to HLA-DR4 and DR5, (presence of anti-microsmal antibodies of the thyroid) has diffuse lymphocytic infiltration, hypothyroidism
What organ and manifestations are involved in Graves disease?
Type II hypersensitivity. This disease is a leads to a thyroid problem. Antibodies (IgG or IgM) bind to Thyroid Stimulating Hormone (TSH) receptor and causes their stimulation. This leads to the body thinking that more thyroid hormone is being bound to the receptors, but it is the antibodies leading to hyperthyroidism
Mechanism for Diabetes mellitus type I
Type IV hypersensitivity. Occurs when individual’s T cells attach the inslet cells within the pancreas. Causes impaired glucose metabolism and vascular disease. (90% have HLA DR3 and DR4)
Mechanism for myasthenia gavis
This occurs when antibodies (IgG and IgM) bind to acetylcholine receptors. Acetylcholine is a neurotransmitter found in the junctions of neurons, including muscle junctions and cause their stimulation. If the acetylcholine can’t bind, the stimulation won’t occur leading to muscle weakness and paralysis
Mechanism for Multiple Sclerosis
demyelinating disorder of CNS, T cell dependent disorder
Describe the principle of anti-nuclear antibody testing?
- Purchased cells are on a microscope slide such as HEp-2 cells
- Patient antibody is overlayed serum
- Wash phase
- Florescent tagged AHG is overlayed
- Wash phase
- View using a fluorescent Scope
- If the patient has anti-nuclear antibodies, characteristic patterns of fluorescent will appear