Immune Lecture 24 Study Notes
1. What is an autoimmune disease?
-broadly classified as “systemic” or “organ-specific”
-possible to have more than one disease: depends on the immune mechanism
-arthritis, scleroderma and lupus are systemic autoimmune diseases
-MS/diabetes are organ specific
2. Which hypersensitivities classify as autoimmune diseases?
-2,3 and 4
3. What hypersensitivity does arthritis deal with?
-type 3: rheumatoid factor (is an antibody that binds IgG) becomes an immune
4. Discuss the diseases an the types of autoantigens they have.
-lupis many antibodies to antigens (DNA/RNA/histone/proteins)
-arthritis RF to IgG
-when the cells get killed: messy cell death; these are available to the body – bind all
over the body = huge systemic response
5. What is systemic lupus erythematasos (SLE)?
-type 3 hypersensitivity
-immune complex-mediated disease that deposit on small blood vessel walls
-c’ and FcR mediated tissue destruction
-affects the kidneys, skin, muscles, joints, lungs, heart and brain
-butterfly rash is common
6. Discuss the tissue-specific hypersensitivity.
-type 2 hypersensitivity
-IgG against cell surface antigen
-cell destruction through compliment or FcR
-alters signaling or functioning
-receptor blockade or activation
-ex/ autoimmune hemolytic anemia
7. What is autoimmune hemolytic anemia?
-red blood cells are attached to anti-RBC autoantibodies
-FcR cells cause phagocytosis
-complement activation and intravascular hemolysis -this results in a short half life = anemia
8. What is autoimmune thrombocytopenic purpura?
-type 2 hypersensitivity
-platelets are depleted which means you don’t clot well and bruise easily
-this also alters signaling through receptors
9. What is Graves’ disease?
-type 2 hypersensivity
-normally, the pituitary gland will secrete thyroid sitmulating hormone (TSH) which
acts on the thyroid to induce the release of thyroid hormones; these will act on the
pituitary to shut down production of TSH which suppresses further thyroid
hormone synthesis (feedback suppression)
-in graves disease: autoimmune B cells make antibodies against TSH receptor that
also stimulate thyroid hormone production; thyroid hormones will shut down TSH
production but have no effect on the autoantibody production which continues to
cause excessive thyroid hormone production
-this is an agonist activity
10.What results from hyperthyroidism?
-heat, increased appeptite, weight loss, other hormone-related symptoms
11.What is insulin-dependent diabetes mellitus?
-type 1 diabetes and is a type 4 hypersensitivity
-CD8 T cell-mediated specific destruction of insulin-producing beta islet cells
(glucagon and somatostatin are still produced)
12.What is MS?
-type 4 hypersensitivity
-immune response initiated in second lymphoid tissue
-get activated T cells able to access the CNS which induce local inflammation and
destruction of myelin
13.What is the mechanism?
-there is an unknown trigger that sets up the initial focus of inflammation in the
brain and blood brain barrier – becomes locally permeable to leukocytes and blood
-T cells specific for CNS antigen and activated peripheral lymphoid tissues
reencounter AP of myelin peptides on microglia in the brain
-inflammatory reaction in brain due to mast-cell activation, complement activation,
antibodies and cytokines -this causes demyelination of neurons
TH1 or TH17?
14.What are some common animal models of autoimmune disorders?
-NOD (non obese diabetic) mutation spontaneously occurs – human disease is
type 1 diabetes
-MRL/lpr occurs spontaneously; is FAS deficient = autoreactive cells (lupus)
-experimental autoimmune encephalitis in SJL (EAE) causes MS – induced with
-collagen induced arthritis in DBA/1 causes rheumatoid arthritis – uses collagen as a
peptide to induce it
-transgenic: bcl-2 transgene causes lupis (its an important regulator of apoptosis – if
bcl-2 is protected from apoptosis hen