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66 Cards in this Set
- Front
- Back
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what happens in the first 30 mins of T cell activation
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new genes are expressed that are required for proliferation of active T cells
*c-myc *transcription factors produced required in order to transcribe IL-2 gene |
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what is IL-2 required for
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proliferation of T cells
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where is IL-2 produced
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it is produced by T cells and acts on the same T cells that produced it (autocrine)
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what do activated T cells produce within hours
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cytokines
cytokine receptors |
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what is the difference between lymphocyte activation and lymphocte proliferation/maturation
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activation involves cell to cell contact (naive T cells make contact with APC and then become active)
proliferation/maturation requires soluble cytokines |
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what are intercellular messengers
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cytokines
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what is pleiotropy
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when a single cytokine has more than one distinct biological activity
IL4 can cause proliferation of B cells, Thymocytes, and mast cells |
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what is redundancy
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when the same activity can be caused my more than one cytokine
IL2/IL4/IL5 all induce B cell proliferation |
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what are the network interactions
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cascade
receptor transmodulation synergism |
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what is a cascade
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TNF alpha acts on macrophages and causes them to make IL1 and TNF alpha
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what is Receptor transmodulation
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receptor upregulation
-IL4 and IL5 act on T cell causing more IL2 receptors receptor down regulation -TGFbeta acts on T cells and decreases the number of IL2 receptors |
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how does TGF beta has a immunoreppressive effect on inflammation
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because it downregulates the number of IL2 receptors
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what is synergism
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TNF and IFN gamma seperately induce certain amount of MHC2 but if you have both of them together the amount of MHC2 produced increases
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what do T lymphocytes come out of the thymus as
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they come out in an uncommited stage (TH0)
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how does TH0 go to TH1 or TH2
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it depends on the situtation they encounter
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what kind of immunity does TH1 mediate
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cell mediated immunity
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what kind of immunity is TH2 associated with
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antibody mediated immunity (humoral)
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what is associated w/ allergic responses
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TH2
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what are asthma therapies designed to reduce
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TH2 responses
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how are TH1 and TH2 distinguished
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by the cytokines they make
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what cytokines does TH1 make
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IL 2
IFN gamma |
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what cytokines does TH2 make
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IL 4
IL 5 IL 6 IL 10 IL 13 |
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how do TH1 and TH2 cells regulate each other
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IFN gamma (TH1) regulates activity and proliferation of TH2 cells
IL 10 and IL 4 inhibit TH1 cells |
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what causes TH0 cells to become TH1 cells
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antigen presenting cells
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how do TH0 to go to TH1
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antigen presenting cells drive this process
conventional dendritic cells produce IL 12 and IFN gamma IFN gamma causes TH0 to make more IFN gamma IL12 and IFN gamma act on the TH0 cells making them TH1 autocrine effect cascade effect |
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how are TH0 cells turned into TH2 cells
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allergen/virus makes contact w/ tissue (epithelial cells) and acts on immature dendritic cells in the tissue
dendritic cell picks up the virus/allergen in the tissue and goes to the lymph node under the influence of TSLP dendritic cells make surface protein OX40L OX40L makes contact with receptro on naive cell (OX40) OX40 - OX40L interaction induces naive t cell to become TH2 THIS WILL ONLY HAPPEN IF IL12 IS NOT THERE the newly formed TH2 will release IL4 which acts on the TH2 cell and amplifies the response |
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what do Thymic stromal lymphopoeitin do to dendritic cells
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causes them to make the surface protein OX40L
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what cytokines do convetional dendritic cells produce
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IL 12
IFN gamma |
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what does TH2 response lead to
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asthma
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what happens in mycobacteria infection
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TH1 cells secrete IFN gamma which activates the macrophage helping it to kill the mycobacteria
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what are the forms of leishmania
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localized cutaneous
chronic mucocutaneous |
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what is observed in localized cutaneous leichmania
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lesion is filled with IL2 and IFN gamma
this indicates that TH1 cells are active and limiting the infection from spreading same thing is done in TB infections |
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what is observed in chronic mucocutaneous leishmania
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lessions filled with IL4
this suggests that TH2 dominate and the absence of TH1 means the disease has spread |
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what increases the number of IL2 receptors
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IL4 and IL5
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what causes a decrease in the number of IL2 receptors
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TGF-Beta
or when an antigen is cleared/infection is fought off this is done to reduce activity of T cells |
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what does chronic activation of IL2 receptors lead to
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apoptosis of T cells
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what occurs during/after tissue infection/inflammation
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endothelial cells express adhesion molecules
adhesion molecules attract neutrophils and eventually lymphocytes (T memory cells) T memory cells bind to endothelial cells via adhesion molecules/homing receptors T memory cells activated by APC present in the tissue after T memory cells are activated they release cytokines that amplify response/attract additional leukocytes |
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what is chemotaxis
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occurs when cells release chemokines to attract other cells
cells with receptors for the chemokines will follow the concentration gradient of those chemokines back to their sources |
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what is an important chemokine receptor
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CCR4 and CXCR5
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how are macrophages activated
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IFN gamma
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how are viruses combated
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Type 1 IFN (alpha or beta) inhibit replication of vireses in infected cells
TNF alpha kills virus infected cells |
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what does TNF alpha do
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causes macrophages to produce more TNF alpha and IL1
kills virus infected cells |
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what is needed for the activation of CTLs
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dendritic cells and the licensing of dendritic cells
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what is the licensing of Dendritic cells
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CD40L (TH1) binds to CD40 (dendritic cell)
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how are CTL generated
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dendritic cell can be infected with a virus and if a virus infection causes it to present antigens to TH1 cells
CD40L (TH1) binds to CD40(DC) CTL precurssor binds to MHC1 on DC (signal 1) and CD28 of CTL binds B7 of DC the CTL is now activated the TH1 will produce IL2 to help with CTL proliferation |
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how is inflammation regulated
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IL 10 (made by TH2)
reduces antigen presentation by APC supresses production of IL1, IL2, and TNF alpha can tilt immune response in direction of TH2 |
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how is there a reduce in antigen presentation by APC
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down regulation of genes that encoude MHC
reduce expression of costimulator and adheasion molecules this is done by IL 10 |
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what are the inhibitors involved in Inflammation regulation
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soluble TNF-R and IL1-R
-these receptors will bind TNF alpha and IL-1 in the serum and not let them bind to receptors on cell surface IL-1 Antagonist this competes with IL1 for the binding to IL1 receptor and prevents activation of IL1 receptor |
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what mediates the proliferation/maturation of B cells
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cytokines
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what is required for B cell proliferation and what does it do
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IFN gamma
this is needed in order for B cells to produce plasma cells that make IgG |
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what does IFN gamma do to B cells
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switches from IgM to IgG
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what does TGF beta do to B cells
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switch from IgM to IgA
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what does IL4 do to B cells
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switch from IgM to IgE
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what occurs in the germinal centers
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B cell effector produced
B cells undergo proliferation B cells undergo somatic hypermutation selection of higher affinity surface Ig TH to B cell interaction isotype switching plasma cells form memory B cells form |
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where do B cells undergo somatic hypermutation
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germinal centers
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where is FDC located
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germinal centers
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what controls immunoglobulin class switching
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CD40
Cytokines |
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what is the primary response
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IgM
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what is the secondary response
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IgA
IgG IgE |
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what type of memory cells produces the best antibodies
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memory B cells
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how are B cells kept in a semi active state
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FDC present antigen which stimulates the B cells keeping it in a semiactive state so it can quickly respond to new antigen
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why do memory B cells have a high affinity Ig on the surface
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they have already undergone somatic hypermutation
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why do memory t cells have increased affinity to APC
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they have increased the number of adhesion molecules on the surface and can therefore bind APC w/ higher affinity resulting in a stronger signal
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what activates naive T lymphocytes
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ONLY CONVENTIONAL DENDRITIC CELLS
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what activates memory T cells
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a wide range of APC (b cells/macrophages)
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where do FDC present antigen
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in lymph nodes
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