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24 Cards in this Set

  • Front
  • Back
What cytokines are involved in activating the Th1 response?
IL-12. INF-gamma and IL-2 sustain the Th1 response after it's committed.
What cytokines are involved with the Th2 response and Ab formation?
IL-4 (and IL-13).
What cytokines suppress the Th1 response?
IL-10, IL-4.
What cytokines suppress the Th2 response?
INF-gamma (which also activates the Th1 response).
What cytokine is always associated with neutrophils?
What cytokine is always associated with eosinophils?
What cytokine is associated with fever?
In an Arthus Reaction, what information from the biopsy can you use for a diagnosis?
Anti-C3 (complement reaction)
Anti-IgG (secondary immune response)
Describe the sequence of events in an Arthus Reaction.
1) Ag binds to Ab
2) Classical complement pathway - C3b opsonizes the Ag-Ab complex.
3) Neutrophils respond when their Fc-gamma receptors are activated.
4) IC's build up and neutrophils attack, resulting in local tissue damage.
What is one steroid that suppresses the immune response?
Cortisol (Corticosteroids)
Why are females more susceptible to autoimmune diseases?
More vigorous Ab response to certain pathogens, presumably due to the influence of estrogens.
What is a Type I Hypersensitivity Reaction?
Atopy, allergy, asthma, anaphylaxis.
What is a Type II Hypersensitivity Reaction?
Ab to cell structures.
What is a Type III Hypersensitivity Reaction?
Immune complex diseases (SLE)
What is a Type IV Hypersensitivity Reaction?
Delayed hypersensitivity (TMMI response) - sarcoidosis.
What causes fatigue?
IL1, IL6 - inflammation and fatigue.
What causes kidney disease, skin rash, and joint pain?
Circulating immune complexes build up in these areas because there are high levels of Fc-gamma-R and C3b-R which attract basophils and mast cells that attack tissue. These regions are also attractive due to the broad vasculature in these locations.
What information can be taken from a skin biopsy of a patient with SLE?
Anti-IgG, Anti-C3,C4, Anti-C1Q (IC disease indicator).
What are treatment options for SLE?
Suppression of inflammatory response by corticosteroids.
Suppression of B-Cell synthesis of Ab's to prevent IC formation by blocking IL-4 and IL-10.
Forming an autoreactive Ab to eliminate B-cell clones.
What might cause bacteria to be resistant to phagocytosis?
Encapsulation of bacteria, and those located in fibrin may be resistant as well.
What is the cause of red urine in IC disease?
Damage to the glomerulus due to accumulation of immune complexes.
What is the reasoning behind the patient's polyclonal hypergammaglobulinemia?
Persistent infections frustrate the immune response resulting in further somatic hypermutation of B-cells to produce more efficient Ab's that are specific to different antigenic epitopes.
What is the pathogenesis of Goodpasture's syndrome?
Patient produces IgG's that are specific to his/her own Type IV collagen, leading to an attack on the basement membrane of the glomerulus and alveolus, not directly on either tissue.
How is the pathogenesis of Goodpasture's syndrome different from an immune complex disease? To what class of hypersensitivity disease do each belong to?
The first three diseases were Type III hypersensitivity diseases, meaning that immune complexes were the precipitating force. Goodpasture's is Type II, which is when Ab binds to a cell structure. Here, the problem was that Ab bound to collagen, not the glomerulus.