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;
36 Cards in this Set
- Front
- Back
4 main categories
CHIT |
Chemokines
Interferons Hematopoeitins Tumor Necrosis Factors |
|
2 Main Cytokine producers
|
Macrophages/Th cells
|
|
What are 3 major effects of Cytokine production?
|
-Hematopoeisis
-inflammation -Innate immune response -Addaptive immune response |
|
5 attributes
|
pleiotropy
redundancy synergy antagonism cascade induction |
|
3 ways of acting
|
Autocrine
Endocrine Paracrine |
|
Best-understood Cytokine Receptor:
|
IL-2Receptor
expressed on Tcells after initial Ag activation; must bind IL-2 for proliferation/differentiation |
|
What is required for signal transduction and high-affinity binding by IL-2R?
|
For signal transduction: only B/y chains
BUT for high affinity: must have alpha too. |
|
What are 3 ways of achieving specificity with Cytokine signalling?
|
1. Lable - short half life of cytokine.
2. High-affinity receptors are only expressed on activated cells. 3. Paracrine signalling - Cytokines induce effect after close contact and release. |
|
what is the main role of Th cells?
|
to secrete cytokines, which activate other things.
|
|
What are the two types of Th cells?
|
Th1
th2 |
|
What cytokines are secreted by Th1 cells?
What do they induce? |
Antiviral, DTH-stimulating, Tc Cell-mediated response.
Il2, IFN Y, TNF-B |
|
What cytokines are secreted by Th2 cells?
What does this induce? |
Il-4, all the IL's except IL-2.
Promote a Bcell and humoral response. |
|
What is the purpose of IL-4?
|
Promotes class switching to IgE. Determines amt of DNA looping for class switching.
Enhances mast cell proliferation. |
|
What is the purpose of IFN-y?
|
Increases antigen presentation
Increases MHC1 and 2 expression. |
|
What is the role of chemokines?
|
Leukocyte trafficking
|
|
What is the role of Hematopoietic cytokines, what are 3?
|
Control the leukocyte population.
-Il-2 is secreted by activated Tcells; promotes Bcell Ig class switching. -IL-4 promotes class swithcing to IgE -CSF |
|
What is the role of Interferons; what are 3?
|
Induce an antiviral state, upregulate MHC1 and MHC2
IFN a/G/beta |
|
What are two roles of Tumor Necrosis Factor (TNF)?
|
-Cytotoxic
-Vasodilation Systemic effect |
|
3 Cytokine receptors to know:
|
CTLA-4
Fas CD40-L |
|
function of CTLA-4:
|
Competes with CD28 to bind B7, the co-stim signal for activating Th cells.
|
|
What is the effect of dysfunctional CTLA-4?
|
You'll have TOO much activation of Th cells; enlarged lymph nodes and spleen.
|
|
What is the function of Fas and Fasl?
|
Induce apoptosis of activated T cells.
|
|
What is the effect of dysfunctional Fas and Fasl?
|
not enough death of activated T cells; too many activated ones, lymphadinopathy.
|
|
What is the role of CD40/CD40L?
|
Signal 2 in bcell activation/differentiation.
Causes CYtokine receptors to be expressed on the Bcell. This allows Cytokines to signal #3 and tell the bcell how to class switch. |
|
What is the effect of dysfunctional CD40/CD40L?
|
No class switching
overabundance of IgM |
|
2 main components of a cytokine receptor:
|
-Ligand bind unit (alpha)
-Signal transducing unit (Beta) |
|
What determines whether Leprosy will be lepramotous or tuberculoid?
|
The Th1/Th2 balance.. if
more th1 = cell-mediated response more th2 = humoral response |
|
Differences betwn Lepramotous and Tuberculoid Leprosy?
|
Tuberculoid: mainly cell-mediated response, DTH, clears the bacteria, can recover.
Lepramotous: Humoral response, macrophages try to clear, cartilage/neurodegeneration. LEss chance of recovery |
|
What determines whether Th1 or Th2 cells will be the responding cells to an infection?
|
The cytokine environment.
|
|
2 ways to inhibit cytokine activity:
|
-Bind cytokine receptors w/out activation.
-Bind the cytokine itself. |
|
2 Cytokine-related diseases:
|
-Bacterial Septic Shock
-Bacterial Toxic Shock |
|
What types of bacteria cause SEPTIC shock?
How? |
Gram negatives - the endotoxin stimulates macrophages to produce too much IL-1 and TNF-a cytokines, which induce a state of shock.
|
|
What causes Toxic Shock?
|
GRAM POSITIVES - Staph Aureus - Toxic Shock Syndrome.
|
|
How do Superantigens cause tss?
|
-Bind a particular Vbeta sequence of the TCR, and also bind MHC2;
This is regardless of TCR Ag specifity. |
|
What is a natural cytokine antagonist?
|
-Can be produced by enzymatic cleavage of cytokine receptors; they float around and neutralize other cytokines.
-Some are produced with the express role of binding and inhibiting cytokines. |
|
2 ways viruses inhibit cytokine action:
|
-Mimic cytokines; bind their receptors and prevent the real function.
-Mimic cytokine receptors; bind the real cytokine, and prevent intended functio. |