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22 Cards in this Set

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how do you control mature lymphoid cells from reacting to self antigens
tolerance- state of unresponsiveness which is specific for a particular antigen, and is induced by prior exposure to that antigen. The most important form of tolerance is self-tolerance to prevent autoimmune responses.
Tolerance Maintenance
Clonal Deletion- like in the thymus if the cells show too much affinity to self, but it's not completely efficient.

Clonal anergy- cell is turned off

Suppression- via regulatory T cells
Central Tolerance is where? Peripheral Tolerance is where?
Central- thymus and bone marrow; where deletion happens

Peripheral-elsewhere where mature T and B cells are; where anergy, deletion and suppression happens
General predisposition of autoimmune diseases has this genetic component
MHC genes are ass'd with autoimmune diseases
Systemic Lupus Erythematosus
autoimmune disease that involves chronic, systemic inflammation.

-anti-nuclear antibodies (ANA)
-antibody against ds DNA
-increased serum complement levels
-immune complex deposition
-mad autoantibodies
-malar rash
Rheumatoid Arthritis
chronic, recurrent, systemic inflammatory disease of joints.

-rheumatoid factor (abnormal Ab against Fc region of IgG)
-immune complexes
-joint inflammation
-symmetrical joint problems
-morning stiffness
Insulin-dependent diabetes mellitus (IDDM)
autoantibodies and autoreactive T cells are produced against the beta cells of the pancreatic islets of langerhans, resulting in diminished insulin production and chronic hyperglycemia.
Hashimoto's Thyroiditis
-excessive thirst, polyuria, weight loss, lethargy
-inflamm disorder of thyoid
-cellular infiltration of thyroid
-high titer auto-Abs
-enlarged thyroid (goiter) and abnormal thyroid function
Addison's Disease
-abdo discomfort, malaise, weight loss, hyperpigmentation, low cortisol levels and Abs to the adrenal cortex
-adrenal insufficiency
-autoAbs against adrenal cells
-hypotension, anorexia, malaise, hyperpigmentation
Polyglandular Autoimmune Syndromes
-circulating autoantibody against multiple endocrine glands
-type I, II, and III
-may have multiple endocrine diseases
Grave's Disease
Auto-Ab develop that stimulate thyroid function
-hyperthyroidism
-Auto-Ab against TSH receptor
-Proptosis (bug-eyes)
Goodpasture's Syndrome
-affects young males,
Triad: pulmonary hemorrhage, glomerulonephritis, circulating antibody to basement membranes
-lungs and kidneys
-Ig and complement deposits
-
Bloddy diarrhea, tenesmus, fever, weakness, doesnt skip large intestine. disease of mucosa
Ulcerative colitis
abdominal pain, diarrhea, malabsorption, from mouth to anus
Crohn's Disease
Immune Hemolytic Anemias
immunologic reactions against rbs proteins, usually mediate by antibody, complement, or phagocytes. may be from drugs that bind to rbc membranes , inducing Ab responses, and cause immune-mediated destruction of the rbc.

-fatigue, from complement (intravascular) or phagocytic cells (extravascular)
Which is warm-antibody types? Which is cold-antibody types?
Warm- IgG (70% of hemolytic anemias)
Cold- IgM (16%)
Direct Coomb's Test
add Ag to in vivo antibody-coated RBCs, see agglutination
Indirect Coomb's Test
uncoated RBCs added with serum with Ab to RBC, then you get coated RBC, then you add that with anti-Ig, then wait for agglutination
Myasthenia Gravis
Type II hypersensitivity
Autoreactive Abs against the ACh receptors in the NMJ. complement is activated, and the post-synaptic membrane is dunzo. you then present with muscle weakness.
Name 3 inflammatory vasculitides
1. giant cell arteritis
2. wegener's granulomatosis
3. henoch-schonlein purpura

*all have inflammation of the blood vessels
Pemphigus Vulgaris
an immunobulloud disease
-blistering diease of skin and mucous membranes
-auto-Ab against keratinocyte antigens
Multiple Sclerosis
-inflammatory demyelination of the CNS, progressive motor weakness, parethesias, visual impairment, ataxia
-oligoclonal Ig bands in CSF
-HLA Ag associations
-altered immunoregulatory T cell populations