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36 Cards in this Set

  • Front
  • Back
All self-reactive T cells were deleted at what location?
Auto-immunit means failure of what
negative- selection

If negative selection is broken, you get self-reactivity --> auto immune
body's defense mechanisms lacks reaction to foreign substances

consists of a direct induction of peripheral lymphocyte tolerance

No normal immune response against a specific antigen, usually a self-antigen.
Instead of killing of T cells, anergy
switches off T cells
Father and mother
have same gene with different sequences

POLYMORPHIC: alleles of same gene
Movement from North to Southern hemis
risk of getting AI
environmental geographic factors
Infection in early childhood involves
MIMICRY: pathogen's protein similar to own
Generate resposne to cell
% of Autoimmune disease
Organ Specific AI
direct cellular damaged
Mediated by Ab or cell-mediated immunity

Ab can also block function
Three diseases classified as organ specific AI
Goodpasture's syndrome (GS)

Diabetes (IDDM)

Myasthenia Gravis
Self antigen and immune response for GS
basement membrant and auto AB
IDDM self antigen and immune response
pancreatic B cells-

Th (DTH) (delayed type hypersensitivity)
Myasthenia Gravis self antigen and appropriate immune response
Ach receptor-

Auto antigen blocks
Goodpasture's syndrome. Details and mechanism
Glomeruli and alveoli

Basal membrane has Antibodies that bind to it
Auto Ab recognizes self-antigen
Ab binding--> complement-- Cell damage

high c3b present

Results in alveoli and glomeruli cell damage-
FATAL, no treatments.
Diabetes Detials and Mechanism
Pancreas- beta cells- Islets of Langerhans

Specific antigen moves from lymph node to different part of cell

Auto immune against beta cells
Cytokines, Cd4+ and macrophages

DTH response- tissue damage
Damage beta cells leads to
decrease insulin, increase in blood glucose
Myasthenia Gravis
Nerve release Ach used for muscle contraction

Endplace AchReceptors-
generate auto ag
block Ach binding to receptors
What are two examples of systemic AI
Multiple Sclerosis

- lipid proteins that wrap around nerve's myelin sheath
- th and tc

Rheumatoid Arthritis
- Connective tissue
Creates auto Antibody
Creates immune complex
Multiple Schlerosis
Speeds up conductivity to get saltatory conduction
Neurological dysfunctions
Rheumatoid Arthritis (RA)
Chronic inflammation on joints

Some of these react against Fc of igG
igM recognizes igG Fc protion
Generating against your own igG antibodies
Fc of igG Plus igM
Huge immune complexes
deposits on joints
trigger complement

Activation of neutrophils (first response, ROI, radicals, tissue damage)(chronic inflammation)

Type III antibody mediated immune formation

Can't resolve the immune response. keeps it going
INflammatory response on joints
EAE for Multiple Schlerosis
Model usually down on mice
Give them MBP (myelin basic protein)
Auto immune against myelin
You transfer EAE to an unaffected animal
one animal to another
Give them CD4 T cells
EAE and th1 vs. th2
th2 Can be protected
Inject th1 from EAE mouse into normal mouse
normal mouse gets EAE
Inject th2 from EAE mouse into normal mouse
stays normal, doesn't cause anything to happen
th2 plus normal then add th1 cells
Ankylosing sponginitis MHC association
Class 1- CD8 Cells
90 fold increase
Goodpasture's syndrome MHC association
Class 2
16 fold increase
Diabetes and MHC association
Class 2
100 fold
MS and MHC association
Class 2
5 fold increase
How proteins are cut up is changed during immune response

Early stages of immune response
IFN gamma causes new subunits
plug in
change specificity
Anchor residues
Release of sequestered antigen
Hidden in body
Immune system is not supposed to see
Traffick T cells because thought that Ag's were there
No deletion of auto-reactive T cells
Brain Trauma- release Ags, T cells, back to brain
Early head trauma and MS
blood vessels in early MS are elaky, damage-causing antigens leak out
Molecular mimicry
generate good immune response
at expense of similarities to self-proteins

Measles and MB protein sequence
Polyclonal B cell activation
Gram negative bacteria and viruses like EBV and CMV induce AI mechanism regardless of specificity

generate IgG autoantibodies to the cross-reactive (mimicking) epitope of host protein

Herein, we demonstrate that transgenic expression of transforming growth factor-beta (1) (TGF-beta) within the pancreatic beta cells prevented mice from developing autoimmune myocarditis after CBV infection. In contrast, transgenic expression of interleukin-4 did not inhibit virus-mediated heart disease