Term
|
Definition
| neutrophils, macrophages, eosinophils, dendritic cells, mast cells |
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Term
| granule release cells (6) |
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Definition
| cytotoxic T cells (CD8), NK cells, neutrophils, eosinophils, basophils, mast cells |
|
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Term
| which cells can release granules? |
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Definition
| most cells, but Thelper (CD4), macrophils, and basophils are especially good at it |
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Term
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Definition
| induce cell death in cells inducing foreign antigen and also for T cell homeostasis |
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Term
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Definition
| neutrophils, eosinophils, basophils, mast cells |
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Term
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Definition
|
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Term
| what is phagocytosis triggered by? |
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Definition
| PAMPs (pathogen associated molecular proteins), or antibodies/CD3 (opsonins) |
|
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Term
| how do mast cells recognize thier targets? |
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Definition
| they hold on to IgE, which grabs the pathogen |
|
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Term
| how do antibodies induce phagocytosis through the Fc receptors? |
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Definition
| antibodies coat the pathogen, and phagocytes have Fc receptors that recognize them and therefore grab that pathogen and eat it. |
|
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Term
| what happens when antibodies bind to mast cells? |
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Definition
| they induce cytokine release through IgE receptors. Whatever is attracted by these cytokines releases histamine granules. |
|
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Term
| what are four ways antibodies can deal with extracellular bacteria/fungi? |
|
Definition
1. coat pathogen to induce phagocytosis through Fc receptors
2. can trigger classical pathway of complement (antibody bound to pathogen results in C3b coating)
- inactivation of the pathogen
- antibody-dependant cell mediated cytotoxicity (ADCC) which is when the antibody coating attracts usually an NK cell through Fc receptors and it gets destroyed directly with cytotoxic antibodies |
|
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Term
| in the case of an intracellular bacteria or fungi, what is a cell-intrinsic effector? |
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Definition
| caused by cytokines; this is when the cell itself is able to shut down or apoptose or release antibacterial effectors on itself |
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Term
| if a cell is infected with intracellular bacteria and fungi, it will start expressing Fas. What interacts with Fas and what does it do? |
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Definition
| CD4 interacts and it induces cell death. |
|
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Term
| a virus downregulates Class I MHC. Why? What happens? |
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Definition
| downregulating class I MHC keeps it from expressing a piece of the virus to T cells. The NK cells are programmed to notice this, so they kill. |
|
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Term
| what are the biggest viral killer cells? The second biggest? |
|
Definition
1. cytotoxic (CD8) t cells
2. NK cells that notice that MHCI is downregulated |
|
|
Term
| what are the most common or typical response to a virus? |
|
Definition
| mast cells releasing cytotoxic histamine granules |
|
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Term
| during heavy chain rearrangement, what is the B cell known as? |
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Definition
|
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Term
| what is the first B cell developmental checkpoint? |
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Definition
| expression of a pre-B cell receptor. Checks for heavy chain rearrangement. Pre-B cell receptor does NOT have to reach the surface of the cell |
|
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Term
| how does a pre-B cell receptor signal? |
|
Definition
| Iga and Igb (analogous to CD3 and zeta chain of T cell) |
|
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Term
| light chain rearrangement |
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Definition
| happens in bone marrow to pre-B cell. There are 4 ways to arrange light chain. |
|
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Term
| second B cell checkpoint in the bone marrow |
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Definition
| expresses B cell receptor, which does have to make it to the cell surface. Checks for functional light chain. |
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Term
| an immature B cell can have what two kinds of antibodies? |
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Definition
|
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Term
|
Definition
|
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Term
| B cell negative selection |
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Definition
| happens in the bone marrow. The B cell IgM will be grabbed repeatedly by self antigens, rearranging every time, until it isn't recognized. If it keeps being recognized, it will go into circulation but become anergic. |
|
|
Term
| B cell positive selection |
|
Definition
| happens in lymph node. B cells that have passed negative selection go to lymph node, are activated by a dendritic cell, and become mature B cells |
|
|
Term
| Describe B cell activation |
|
Definition
1. antigen recognition (primary)
- signalling involving ITAM, Iga, Igb.
- this makes cells clump, after which they become activated.
---if clumping doesn't happen, you have coreceptor binding
2. after this you get the secondary signal (TI1, TI2, or T-dependant) |
|
|
Term
| B cell activation coreceptor |
|
Definition
- binds B cells if clumping didn't happen after primary signal (antigen recognition)
- made up of CD19, CR2, CD81 |
|
|
Term
|
Definition
B cell activation coreceptor proteins
CD19: signalling molecule; used as a B cell marker
CR2: compliment receptor 2
CD81: nobody knows what this is |
|
|
Term
| TI-1, TI2, T-dependant secondary B cell activation |
|
Definition
TI-1: the antigen-activated B cell binds to a toll-like receptor
TI-2: just very strong TI-1
T-dependant: antigen activated B cell gets second signal from helper T cell using CD40-CD40L ligand and cytokines |
|
|
Term
| secondary B cell activation signals, no matter which of the 3 kinds, result in... |
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Definition
|
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Term
|
Definition
B cells in the germinal center (centroblasts) have point mutations as they rapidly divide in the hypervariable/complementarity determining regions.
This happens because of AID, which point-mutates into uracil, which gets excised |
|
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Term
|
Definition
| B cells that are rapidly dividing in the germinal center |
|
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Term
|
Definition
| after finish dividing (now centrocytes) B cells have antigen presented by follicular dendritic cells. They compete for the binding/survival signals. At this time also bind helper T cells to determine survivability. |
|
|
Term
| during clonal selection, how does a B cell decide if it becomes a memory B cell or a plasma cell? |
|
Definition
if helper T cell presents IL-10: plasma cell
IL-4: memory cell |
|
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Term
|
Definition
| helper T cells that bound during clonal selection deliver signals via CD40-CD40L. This changes the constant region on the heavy chain to make IgG, IgA, IgE antibodies |
|
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Term
| all antibodies can do two things: |
|
Definition
1. neutralize - coat pathogens and toxins to keep them from interacting
2. activate complement (except for IgE) |
|
|
Term
| only which type of antibodies can activate Fc receptor-mediated endocytosis? What else do these two antibodies do? |
|
Definition
| IgA and IgG; can also activate immune cells to make them function better |
|
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Term
|
Definition
- forms pentamers
-Has low affinity binding, but it's big and so can bind multivalent antigens very well
- is GREAT at activating complement
- too big to get from blood into tissue; gets caught in bodily fluids |
|
|
Term
|
Definition
- forms dimers
- very important for mucosal immunity, but not so great at complement activation and opsonization
- can undergo receptor-mediated endocytosis and cross into tissue
- present in breast milk |
|
|
Term
|
Definition
- monomer
- can cross the placenta
- can cross into tissues
- induces ADCC (antibody dependant cell-mediated cytotoxicity) which is when antibodies tell NK cells to kill pathogen |
|
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Term
|
Definition
| binds Fc receptors of mast cells and basophils, causing them to release granules (which induce the symptoms we call allergies) |
|
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Term
|
Definition
| Ebola blocks interferons (which are a type of cytokine) which then can't do their jobs of upregulating antiviral proteins - instead it stops them at the beginning and prevents the whole cascade. It also competitively binds the interferon receptors to get taken into the cell itself. |
|
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Term
|
Definition
| Ebola causes TNFa to be secreted, which are antibacterial cytokines, which makes immune system go haywire and causes runaway bleeding |
|
|
Term
| RNA interference treatment |
|
Definition
| 2nd treatment for Ebola; putting single stranded RNA in cells with Ebola so the body kills the cell |
|
|
Term
| how does herpes suplex infect so many cells so quickly? |
|
Definition
| It comes with its own ready-made proteins, instead of having to make them all |
|
|
Term
| herpes and viral post-shutoff |
|
Definition
| herpes virus randomly destroys all RNA in its vicinity. This includes its own, but since it has so much it's more likely to hurt the cell and keep the cell from making proteins. |
|
|
Term
| theory on why herpes goes dormant in the neurons |
|
Definition
| because it has to travel all the way down the axon to the nucleus and by the time it gets there it's lost all its replication proteins, so the DNA just circularizes and sits there. |
|
|
Term
| NGF (nerve growth factor) |
|
Definition
when nerve cells aren't stressed, makes sure they grow and signals protiens to be produced. When it is stressed, will shut down the cell for a bit (no growth).
- this shutdown allows dormant herpes virus to receive a transcription factor. |
|
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Term
|
Definition
| basophils/eosinophils will recognize just a tiny bit of parasitic antigen and release cytokines. This will cause IgE to bind to mast cell Fc receptors. The mast cells release histamine-containing granules. |
|
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Term
|
Definition
| drugs like penicillin or other chemicals modify self cells until the body attacks them. (cytotoxic response to self-cells) |
|
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Term
|
Definition
| local injection causes immune complex formation, mast cells to release granules, and local inflammation |
|
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Term
|
Definition
DTH (delayed type hypersensitivity reaction)
- something that shouldn't be toxic accidentally gets processed by an antigen processing complex, triggering an immune response against it. T cell mediated. |
|
|
Term
| four things that can trigger autoimmunity |
|
Definition
1. bad negative selection in thymus or bone marrow
2. injury causes lymphocytes to get exposed to things they don't recognize as self
3. Tregs don't work so immune activation threshhold is too low
4. pathogen expresses stuff that looks like self-proteins |
|
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Term
|
Definition
| growing a live virus in something nonhuman until it can't attack a human but DOES trigger an immune response |
|
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Term
|
Definition
| treat virus with formelyn, which keeps it from getting into cells, but it WILL trigger immune response through immune receptors (like toll-like receptors) |
|
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Term
|
Definition
| inject with just one specific protein. Include adjuvant to provide the danger signal. |
|
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Term
|
Definition
| like subunit, but specifically makes antibodies against the TOXIN of a pathogen. Needs boosters. Keeps it from killing us until can mount full immune response. |
|
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Term
|
Definition
| gets antibodies against sugars by linking the sugar with a protein and getting both taken up by B cell, which then makes antibodies against both. |
|
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Term
|
Definition
| pre-existing antibodies cause transplant to be rejected within minutes. It can be tested for before transplantation. The most dangerous is an ABO blood type mismatch. |
|
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Term
|
Definition
| T cell mediated; happens in a few days. Happens because of mismatched MHC antigens. Induces endothelial cell damage, so highly vascularized tissues get the most acute rejection. Can be managed by immunosuppressants. |
|
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Term
|
Definition
| happens over years - smaller, low-level rejections that happen over time. Results in fibrosis (scarring.) Doesn't pay attention to immuno suppressants as much as acute does. |
|
|
Term
| HSC (hemapoeitic stem cell) transplantation |
|
Definition
you kill all of the host's immune system first. Then, you take hemapoeitic stem cells from a donor to totally replace the host immune system.
- eliminates graft-vs-host disease, because there are no host immune cells to attack the donor organ
- but has no mature cells, so native cells might survive and kick out the new ones, so you wouldn't have negative selection against donor tissue |
|
|
Term
| WBM (whole bone marrow) transplantation |
|
Definition
| you still have adult cells in your transplant after irradiation. They can eliminate host cancer cells. Can attack remaining host immune cells and clear them out to replace immune system. Result in higher blood cell counts because don't have to wait for whole immune system to grow. |
|
|
Term
| which antibodies do complement fixation? |
|
Definition
|
|
Term
| which antibodies do receptor mediated endocytosis? |
|
Definition
|
|
Term
| which antibodies do fetal and neonatal immunity? |
|
Definition
|
|
Term
| which antibodies trigger phagocytosis? |
|
Definition
|
|
Term
| which antibodies trigger ADCC? |
|
Definition
|
|
Term
| which antibodies activate mast cells? |
|
Definition
|
|
Term
|
Definition
| found on surface of cells such as NK cells, follicular dendritic, and B cells. Binds antibodies that are bound to pathogen. Stimulate phagocytosis or cytotoxic cells to destroy microbes, or (to destroy infected cells), antibody-mediated phagocytosis or ADCC |
|
|
Term
|
Definition
antibody dependant cell-mediated cytoxocity
- antibodies bind an infected cell, NK cells bind the antibodies via Fc receptors, NK cell releases cytotoxic granules |
|
|
Term
| severe combined immunodeficiency |
|
Definition
| disease where you have no functional T cells. Also affects B cells because you have no T-dependant activation and therefore much less class switching |
|
|
Term
| delayed type hypersensitivity |
|
Definition
| same as type IV hypersensitivity. This is the only allergy that isn't antibody mediated, but rather is T cell mediated. This is when something makes it into MHC that isn't foreign but gets registered as foreign. |
|
|
Term
| activation-induced cell death |
|
Definition
| mediated by Fas and FasL. Kills T cells that have been out for too long. |
|
|
Term
|
Definition
| granuleocyte. Circulates (unlike mast cells.) Bind IgE. |
|
|
Term
|
Definition
| link between T and B cells activates the B cells, triggering division, isotype switching, and turning into plasma cells to secrete antibody. |
|
|
Term
|
Definition
| found in almost every cell. Presents INTRACELLULAR pathogen fragments. Presents to cytotoxic (CD8) T cells. Uses TAP (transporter associated with antigen processing) to get protein from the cytosol to the lumen of the ER |
|
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Term
|
Definition
| found ONLY on antigen presenting cells like dendritic cells and B cells. Grabs EXTRACELLULAR pathogens. Links with CD4 on helper T cells. Activated by the removal of CLIP. |
|
|
Term
|
Definition
| triggered by IgM or IgG binding to antigen via Fc receptors. Results in formation of C3b, which results in the formation of the membrane attack complex, which forms a hole in the target. |
|
|
Term
| complement control proteins |
|
Definition
| keep complement from attacking own body |
|
|
Term
|
Definition
| leukocytes escaping the blood into the tissue during inflammation |
|
|
Term
|
Definition
|
|
Term
|
Definition
| found in NK cells and cytotoxic T cells. Induce programmed cell death. Packaged with perforin to get into the cells. They can also kill intracellular pathogens. |
|
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Term
|
Definition
| makes T cells into Tregs in the thymus, which kill self-attacking T cells. Also promote development into memory T cells. |
|
|
Term
|
Definition
| antiviral cytokines. Upregulate MHC I and II and increase immunoproteasome activity. Also activate immune cells like NK cells. |
|
|
Term
|
Definition
| giant cell that makes platelets |
|
|
Term
|
Definition
| pattern recognition receptors. Recognize PAMPs and DAMPs. Toll like receptors are a kind of PRR. |
|
|
Term
|
Definition
| present in pre-B and pre-T cells. Adds N-nucleotides during VDJ recombination. |
|
|
Term
|
Definition
| cytokine that induces inflammation. |
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