Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
28 Cards in this Set
- Front
- Back
|
TNF
Where does it come from? What does it do? |
From Macrophages, Th1, stressed tissue
Causes cachexia, promotes apoptosis Pyrogen and stops cells when danger is gone |
|
|
IL-6
Where does it come from? What does it do? |
Pyrogen
Increases production of neutrophils/basophils/macrophages, inhibits TNF & IL-1; promotes IL-10; increase metabolism; sickness behavior, fever |
|
|
IL-1
Where does it come from? What does it do? |
pyrogen
From Macrophages, Th2 injured tissue. hematopoeisis, tissue repair, increases immune stimulation, fever, hyperalgesia, sickness behavior |
|
|
Cancer phase 1
|
Tumor stress signal
NK cells are activated, produce IFN-gamma |
|
|
Cancer phase 2
|
Macrophage activation by danger signals and IFN-gamma
IL-12, Inflammation, suppression of blood supply leads to necrosis |
|
|
Cancer Phase 3
|
Macrophage activation of NK cells via IL-12
Induction of apoptosis by NK cells |
|
|
Cancer Phase 4
|
Antigen presentation in lymph nodes
clonal expansion of Th1 and killer T-cells provide specificity to anti-tumor response |
|
|
What 3 things promote immune tolerance?
|
Consistant exposure
exposure though intestines lack of danger signals |
|
|
What 3 things promote immune reactivity?
|
Episodic exposure
Exposure though skin Concurrent danger signals |
|
|
What is the genetic cause of Ankylosing spondylitis?
|
most people with AS have HLA-B27 MHC-1
These combine with CD-8 t cells, in AS, cannot combine correctly, autoreactivity in CD8 cells |
|
|
What is the genetic basis of Insulin resistant diabetes?
|
HLA-DR3 and HLA-DR4
CD4 t helper cells |
|
|
IgG antibody
|
can cross placenta
2nd to develop immunity IgG1 and IgG3 activate complement Causes neutralization Long lasting Test it to see if vaccine has worked |
|
|
IgM antibody
|
first to be formed
rises in acute stage of disease can cross epithelium, but does not do so often activates complement |
|
|
IgA antibody
|
dimer
enters gut, crosses epithelium neutralization |
|
|
IgE antibody
|
sensitization of mast cells. Seen in allegy and helminth infections
|
|
|
Transplant Rejection
Hyperacute |
begins within hours
pre-formed antibodies injury via complement |
|
|
Transplant rejection
acute |
after 1 week or more
CD4/CD8 cell mediated |
|
|
Transplant rejection
chronic |
fibrosis
|
|
|
Graves disease
|
antibodies are made against thyroid cells and it leads to hyperthyroidism
|
|
|
Insulin resistant diabetes
|
Ab (fab) bindts to insuline receptor, making it so insulin cannot bind. can lead to hyperglycemia and ketoacidosis
|
|
|
TGF-beta
Where does it come from? What does it do? |
From Stressed tissue, Tregs (ntreg, itreg, th3)
Promotes apoptosis The DANGER IS GONE!!! |
|
|
IL-10
Where does it come from? What does it do? |
From Th2, monocytes, mast cells, Tregs
Inhibits IFN-gamma, MHC, IL-2, IL-3, TNF, GM-CSF, NK killing, promotes B cells |
|
|
Mast cell newly formed mediators
|
Eiconsanoids::
Prostaglandin D2-- eosinophils, basophils and Th2 Leukotriene C4:vasopermeability and brochoconstriction Cytokines:: IL-4 and TNF |
|
|
Mast cell pre formed mediators
|
serotonin, HISTAMINE<, proteolytic enzymes proteoglycans(heparin)
|
|
|
How does the immune system respond to:
Intracellular pathogens |
Th1 cells: IL-2, IFN-gamma
macrophages, killer T-cells, NK, NKT |
|
|
How does the immune system respond to:
Extracellular pathogens? |
Th17 cells
Il-17, IL-21, IL-22 Neutrophils |
|
|
How does the immune system respond to multicellular pathogens?
|
Th2 cells:
IL-4, IL5, IL-6, IL-10, IL-13 basophils, eosinophils, IgE/mast cells |
|
|
What is a monoclonal antibody?
|
"onoclonal antibodies (mAb or moAb) are monospecific antibodies that are the same because they are made by identical immune cells that are all clones of a unique parent cell." (wikipedia)
|
