Term
|
Definition
|
|
Term
| Which thyemus cells have high metabolism: cortical or medullary epithelial cells |
|
Definition
|
|
Term
| Which thyemus cells have high protein production: cortical or medullary epithelial cells |
|
Definition
|
|
Term
| Cell progression in the thymus (6) |
|
Definition
| DN1 → DN2 → DN3 → DN4 → CD4+CD8+ → CD4+CD- or CD4-CD+ |
|
|
Term
| In T cell development, what does "double-negative" mean |
|
Definition
|
|
Term
| In T cell development, what does "double-positive" mean |
|
Definition
|
|
Term
| What signal differentiates a lymphoid progenitor to a T cell |
|
Definition
|
|
Term
|
Definition
| Production of T cells in bone marrow |
|
|
Term
|
Definition
| Production of B cells in thymus |
|
|
Term
| TCR is a dimer of what subunits (2) |
|
Definition
|
|
Term
| Which is rearrange first: TCR α or β |
|
Definition
|
|
Term
| TCR α is analogous to which BCR subunit |
|
Definition
|
|
Term
| TCR β is analogous to which BCR subunit |
|
Definition
|
|
Term
| Theoretical # of combinations of TCR's |
|
Definition
|
|
Term
| Expected # of combinations of TCR's |
|
Definition
|
|
Term
| This flash card is here to remind you to go through B cell rearrangement since this deck does not include them |
|
Definition
| This flash card is here to remind you to go through B cell rearrangement since this deck does not include them |
|
|
Term
| Majority of TCR diversity is due to |
|
Definition
|
|
Term
| When does a T cell become "double positive" |
|
Definition
| After successful TCR β rearrangement |
|
|
Term
| When does a T cell become "single positive" |
|
Definition
| After successful TCR α rearrangement |
|
|
Term
| After β rearrangement, how is the TCR "tested" without a rearranged TCR α |
|
Definition
| It uses pre-TCR α much like how the B cell used λ5 |
|
|
Term
| A double positive T cell has no reaction to MHC I & II, what is its fate (2) |
|
Definition
| 1) Continued α rearrangement, 2) death by neglect |
|
|
Term
| A double positive T cell has a strong reaction to MHC I & II, what is its fate |
|
Definition
| Negative selection (i.e., death) |
|
|
Term
| A double positive T cell has a mild reaction to only MHC I, what is its fate (2) |
|
Definition
|
|
Term
| A double positive T cell has a mild reaction to only MHC II, what is its fate (2) |
|
Definition
|
|
Term
| __% of double positive T cells are likely self-reacting |
|
Definition
|
|
Term
| Double positive T cells favor which fate: CD4 or CD8 |
|
Definition
|
|
Term
| Defects in TCR rearrangement often leads to |
|
Definition
|
|
Term
| Reasons why T cell cancers occur (2) |
|
Definition
| 1) DNA rearrangement, 2) hypermutation |
|
|
Term
| T cells leave blood circulation in secondary lymph tissues via |
|
Definition
|
|
Term
| How many genes are found in the MHC locus |
|
Definition
|
|
Term
| MHC I or II: which binds shorter peptides |
|
Definition
|
|
Term
| MHC I or II: which binds longer peptides |
|
Definition
|
|
Term
| Which MHC I subunit(s) bind to the antigen |
|
Definition
|
|
Term
| Which MHC II subunit(s) bind to the antigen |
|
Definition
|
|
Term
| How long of a peptide binds to the MHC I |
|
Definition
|
|
Term
| How long of a peptide binds to the MHC II |
|
Definition
|
|
Term
| MHC I or II: cytosolic pathogens |
|
Definition
|
|
Term
| MHC I or II: cross-presentation of exogenous antigens |
|
Definition
|
|
Term
| MHC I or II: intravesicular pathogens |
|
Definition
|
|
Term
| MHC I or II: extracellular pathogens and toxins |
|
Definition
|
|
Term
| MHC I or II: binds to antigen in ER |
|
Definition
|
|
Term
| MHC I or II: binds to antigen in vesicle |
|
Definition
|
|
Term
| MHC I or II: erythrocytes |
|
Definition
|
|
Term
|
Definition
|
|
Term
| MHC I or II: hematopoietic cells |
|
Definition
| MHC I on all but RBC's, and MHC II on B cells & dendritic cells and some MHC II on macrophages |
|
|
Term
| MHC I or II: non-hematopoietic cells |
|
Definition
|
|
Term
| MHC I or II: thymic epithelium |
|
Definition
| MHC I and a lot of MHC II |
|
|
Term
| Which needs more TCR/MHC interactions: naïve or primed T cells |
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| Which do CD4 & CD8 interact with on MHC: variant or invariant regions |
|
Definition
|
|
Term
|
Definition
|
|
Term
| CD4 & CD8 are associate with which tyrosine kinase |
|
Definition
|
|
Term
| What phosphorylates the TCR |
|
Definition
|
|
Term
| MHC I or II: kills the infected host cell |
|
Definition
|
|
Term
| MHC I or II: used to recruit/activate immune cells |
|
Definition
|
|
Term
| Why use antibodies instead of TCR's to treat Emma Whitehead |
|
Definition
| TCR's require costimulation, antibodies do not, to recognize antigen |
|
|
Term
| Biggest target of pharmaceuticals |
|
Definition
| Proteins involved in signaling |
|
|
Term
| Mechanisms of signal transduction (2) |
|
Definition
| 1) Modifications, 2) complex formation |
|
|
Term
| Modification signaling transduction |
|
Definition
| Covalent changes to chemical makeup of a molecule |
|
|
Term
| Complex formation signaling transduction |
|
Definition
| Non-covalent interaction between two molecules |
|
|
Term
| Which signal transduction mechanism is the most common pharmaceutical target |
|
Definition
|
|
Term
| Examples of amino acid modifications (8) |
|
Definition
| 1) Phosphorylation, 2) methylation, 3) acetylation, 4) glycosylation, 5) lipidation, 6) isomerization, 7) ubiquitination, 8) SUMOylation |
|
|
Term
| Major functions of adaptor proteins (3) |
|
Definition
| 1) Connect receptors to downstream pathways, 2) localize enzymatic proteins, 3) activate enzymatic signaling molecules |
|
|
Term
| Are adaptor proteins modules: yes or no |
|
Definition
|
|
Term
| Important adaptor proteins (3) [based on how much he talked about them, IMHO] |
|
Definition
|
|
Term
| Is inactive TCR found in a lipid raft: yes or no |
|
Definition
|
|
Term
| Is active TCR found in a lipid raft: yes or no |
|
Definition
|
|
Term
| Is Lck found in a lipid raft: yes or no |
|
Definition
|
|
Term
| How are CD4/Lck and TCR separated |
|
Definition
|
|
Term
| Sites on TCR that get phosphorylated |
|
Definition
|
|
Term
| Lck phosphorylates what on TCR |
|
Definition
|
|
Term
|
Definition
| Immunotyrosine based activation motif [kind of explains what it does, oddly enough] |
|
|
Term
| What protein binds to phosphorylated TCR |
|
Definition
|
|
Term
| What adaptor protein exists on ZAP-70 |
|
Definition
|
|
Term
|
Definition
|
|
Term
| Phosphorylation steps that amplify TCR signal (3) |
|
Definition
|
|
Term
| Results of TCR activation and signal transduction (2) |
|
Definition
| 1) Actin polymerization, 2) gene transcription activation |
|
|
Term
| Why actin polymerization in TCR signaling |
|
Definition
| Wraps T cell around presenter to increase TCR contact |
|
|
Term
| ARP2/3 activated by ___ that ___ actin |
|
Definition
| ARP2/3 activated by LAT [though a bit downstream through WASP, Rac, CDC42] that cross-links actin |
|
|
Term
| What cleaves phosphatidyl inositol into IP3 |
|
Definition
|
|
Term
| DAG activates what protein kinase |
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
| PLC-γ binds to LAT and is phosphorylated by ItK on the LAT/SLP-76/ItK complex |
|
|
Term
| What phosphorylates PI to PIP3 |
|
Definition
|
|
Term
| What dephosphorylates PIP3 to PI |
|
Definition
|
|
Term
| What leads to Akt activation |
|
Definition
|
|
Term
| Effects of Akt activation |
|
Definition
| A lot of things related to cell survival [I don't think he cares that we know the half-dozen things listed] |
|
|
Term
| Is Akt "pro-cancer" or "anti-cancer" when it is activated |
|
Definition
|
|
Term
| Why is PTEN mutation common in cancer |
|
Definition
|
|
Term
| Ways TCR activation induces gene transcription (3) |
|
Definition
| 1) Phosphorylation, 2) dephosphorylation, 3) inhibitor elimination |
|
|
Term
| TCR gene transcription: phosphorylation mechanism steps (5) |
|
Definition
| GEF → G protein → MAPKKK (Raf) → MAPKK (Mek) → MAPK (Erk) → Erk enters nucleus → Erk+TF → gene transcription |
|
|
Term
| TCR gene transcription: dephosphorylation mechanism |
|
Definition
| Ca2+ influx → calmodulin activation → calcineurin activation → NFAT dephosphorylation → gene transcription by NFAT |
|
|
Term
| Cyclosporins target what for immunosuppression |
|
Definition
|
|
Term
| Calcineurin targeted by what immunosuppressants |
|
Definition
|
|
Term
| TCR gene transcription: inhibitor elimination involves what proteins (3) |
|
Definition
| 1) IKK, 2) I-κB, 3) NF-κB |
|
|
Term
| IKK activation leads to ___ of I-κB |
|
Definition
|
|
Term
| What TCR bit is found on the intracellular side of Emma Whitehead's CAR |
|
Definition
|
|
Term
| Examples given at the start of lecture of autoimmunity (4) |
|
Definition
| 1) Psoriasis, 2) vitiligo, 3) lupus, 4) rheumatoid arthritis |
|
|
Term
| __% of new T cells are believed to be self-reactive |
|
Definition
|
|
Term
|
Definition
| Elimination of self-reactive T cells |
|
|
Term
| Removal of self-reactive T cells in thymus: central or peripheral tolerance |
|
Definition
|
|
Term
| Removal of self-reactive T cells not in thymus: central or peripheral tolerance |
|
Definition
|
|
Term
| Which expresses a huge variety of proteins in the thymus: cortical or medullary epithelial cells |
|
Definition
| Medullary epithelial cells |
|
|
Term
| What controls the expression of restricted proteins |
|
Definition
|
|
Term
| Autoimmune polyendocrine syndrome type I |
|
Definition
|
|
Term
| Thymic medullary epithelial cells increase in what special protein |
|
Definition
|
|
Term
| Reduction in AIRE might led to a(n) __ [increase or decrease] in autoimmunity |
|
Definition
|
|
Term
| How are we not reactive to food & gut flora |
|
Definition
| Thymic dendritic cells find them and bring them to the thymus for central tolerance |
|
|
Term
| Food allergies may be a dysfunction of what mechanism |
|
Definition
| Presentation of food antigens in thymus by dendritic cells |
|
|
Term
| Result of T cells with no reaction to MHC I & II |
|
Definition
|
|
Term
| Result of T cells with strong reaction to MHC I & II |
|
Definition
|
|
Term
| Result of T cells with mild reaction to only MHC I |
|
Definition
| Positive selection → CD8 T cell |
|
|
Term
| Result of T cells with mild reaction to only MHC II |
|
Definition
| Positive selection → CD4 T cell |
|
|
Term
| Purpose of signal 1 in T cell activation |
|
Definition
|
|
Term
| Purpose of signal 2 in T cell activation |
|
Definition
|
|
Term
| Purpose of signal 3 in T cell activation |
|
Definition
|
|
Term
| Ideal goal of stopping rejection of transplanted organs |
|
Definition
| Put reactive T cells into anergy by blocking signal 2 for just the transplanted organ |
|
|
Term
| What is the primary costimulatory molecule for naive T cells |
|
Definition
|
|
Term
|
Definition
|
|
Term
| What binds to B7-1 and B7-2 |
|
Definition
|
|
Term
| Activation of TCR & CD28 leads to upregulation of CD__ |
|
Definition
|
|
Term
| Activation of CD40 leads to upregulation of __ (2) |
|
Definition
| 1) B7-1/2, 2) different ligants depending on type of antigen |
|
|
Term
| B7-1 and B7-2 are upregulated by CD__ |
|
Definition
|
|
Term
| CD40L is upregulated by CD__ activation |
|
Definition
|
|
Term
| Which cells upregulate TNF receptors |
|
Definition
| Activated CD4 & CD8 T cells |
|
|
Term
| Which cells upregulate TNF receptor ligands (2) |
|
Definition
| 1) Activated antigen presenting cells, 2) activated T cells |
|
|
Term
|
Definition
| Inducibly expressed on T cells |
|
|
Term
|
Definition
| Adhesive & costimulatory function needed for T cell activity |
|
|
Term
|
Definition
|
|
Term
| CTLA-4 has action opposite to |
|
Definition
|
|
Term
| CD28 & CTLA-4: "antagonists" or "synergists" [my words] |
|
Definition
|
|
Term
| Mutations in CTLA-4 are linked to |
|
Definition
|
|
Term
| CTLA-4 is expressed on what cells |
|
Definition
|
|
Term
| PD-1 is expressed on what cells |
|
Definition
| Dendritic cells [and other cells too] |
|
|
Term
| PD-1 function (long explanation) |
|
Definition
| Activates tyrosine phosphatases that then inhibit intracellular signals activated by TCR & costimulatory receptors |
|
|
Term
| PD-1 function (short explanation) |
|
Definition
| Inhibits TCR & costimulatory signaling |
|
|
Term
| Mutations in PD-1 are linked to |
|
Definition
|
|
Term
| Emma Whitehead's CAR has what on the proximal tail |
|
Definition
| Costimulatory receptor [e.g., CD28, 4-1BB, OX40, CD27] |
|
|
Term
| Emma Whitehead's CAR has what on the distal tail |
|
Definition
|
|
Term
| Descriptors of cellular immunity (3) |
|
Definition
| HAM: 1) hostile, 2) agile, 3) mobile |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| What amino acid residue is the focus of chemokine classification |
|
Definition
|
|
Term
|
Definition
|
|
Term
| Chemokine receptors are ___ transmembrane ___ receptors |
|
Definition
| 7 transmembrane G-protein-coupled receptors |
|
|
Term
| Are chemokines & receptors one-to-one |
|
Definition
| No, multiple ligands to multiple receptors |
|
|
Term
| Dendritic cells enter lymph nodes via |
|
Definition
|
|
Term
| Lymphocytes enter lymph nodes via |
|
Definition
|
|
Term
|
Definition
|
|
Term
| Steps of extravasation (4) |
|
Definition
| Rolling → activation → adhesion → diapedesis |
|
|
Term
| Extravasation: rolling is mediated by |
|
Definition
|
|
Term
| Extravasation: activation is mediated by |
|
Definition
|
|
Term
| Extravasation: adhesion is mediated by |
|
Definition
|
|
Term
| Extravasation: diapedesis is mediated by |
|
Definition
|
|
Term
| Movement of lymphocytes throughout the body is controlled by what substances (3; broad families) |
|
Definition
| 1) Selectins, 2) integrins, 3) chemokines |
|
|
Term
| E-selectin expression induced by |
|
Definition
|
|
Term
| P-selectin expression induced by |
|
Definition
|
|
Term
| Selectins recognize what type of molecule |
|
Definition
| Carbohydrates on protein scaffolds |
|
|
Term
|
Definition
| Heterodimeric of α and β chains |
|
|
Term
| LFA-1 is what kind of molecule |
|
Definition
|
|
Term
| VLA-1 is what kind of molecule |
|
Definition
|
|
Term
| In the context of T cells, what can induce integrins into a high-affinity state |
|
Definition
|
|
Term
| Binding partner for GlyCAM-1 |
|
Definition
|
|
Term
| Binding partner for L-selectin |
|
Definition
|
|
Term
| Binding partner for CCL21 |
|
Definition
|
|
Term
|
Definition
|
|
Term
| Binding partner for LFA-1 |
|
Definition
|
|
Term
| Binding partner for ICAM-1 |
|
Definition
|
|
Term
| How do T cells "know" to leave at HEV's |
|
Definition
| Endothelium produces CCL21 |
|
|
Term
|
Definition
|
|
Term
| S1P exists really on where (2) |
|
Definition
|
|
Term
| What draws naive T cells out of lymph nodes |
|
Definition
|
|
Term
|
Definition
| Pretty much all tissues except in blood & lymph |
|
|
Term
| What downregulates S1P receptor on naive T cells |
|
Definition
| High concentration of S1P |
|
|
Term
| What draws dendritic cells to lymph nodes |
|
Definition
| CCR7 and the CCL19/21 gradient |
|
|
Term
| How many CD8 cells exist for a given TCR |
|
Definition
| 80-1200 [per mouse] i.e., "a very low number" |
|
|
Term
| How many CD4 cells exist for a given TCR |
|
Definition
| 15-200 [per mouse] i.e., "a very low number" |
|
|
Term
| Post activation, T cells undergo division every ___ hours and ___ divisions |
|
Definition
| Every 6-8 hours and 5-8 divisions [upwards of 10,000 clones] |
|
|
Term
| What changes with IL-2 on T cells when activated |
|
Definition
| Switch from moderate- to high-affinity IL-2 receptor [IL-2Rβγ → IL2Rαβγ] |
|
|
Term
| What induces activated T cells to proliferate |
|
Definition
| High-affinity IL-2 receptor and autocrine release of IL-2 |
|
|
Term
|
Definition
|
|
Term
| Newly activated T cells upregulate ___ and ___ |
|
Definition
|
|
Term
| CD69 promotes degradation of |
|
Definition
|
|
Term
| Why should a newly activated T cell stay in the lymph node |
|
Definition
| Time to differentiate & proliferate |
|
|
Term
| How are T cells guided to different tissues |
|
Definition
| Expression of different molcules on endothelium and matching molecules on T cells |
|
|
Term
| Leukocyte adhesion deficiency |
|
Definition
| Lack of function/expression of LFA-1; repeated bacterial infections |
|
|
Term
| Leukocyte adhesion deficiency: depressed or elevated WBC's in blood |
|
Definition
|
|
Term
| Leukocyte adhesion deficiency: treatment |
|
Definition
|
|
Term
| T cell effector cell subset for anti-viral immunity |
|
Definition
|
|
Term
| T cell effector cell subset for allergens |
|
Definition
|
|
Term
| T cell effector cell subset for helminths |
|
Definition
|
|
Term
| T cell effector cell subset at mucocutaneous sites |
|
Definition
|
|
Term
| T cell effector cell subset for immune regulation & tolerance |
|
Definition
|
|
Term
| T cell effector cell subset for B cell response |
|
Definition
|
|
Term
| Canonical cytokine of Th1 |
|
Definition
|
|
Term
| Canonical cytokine of Th2 |
|
Definition
|
|
Term
| Canonical cytokine of Th9 |
|
Definition
|
|
Term
| Canonical cytokine of Th17 |
|
Definition
|
|
Term
| Canonical cytokine of Tfh |
|
Definition
|
|
Term
| Th1, Th2, Th9, etc. are from which: CD4 or CD8 T cells |
|
Definition
|
|
Term
| Signal 3 by APC to convert T cell to Th1 |
|
Definition
|
|
Term
| Signal 3 by APC to convert T cell to Th2 |
|
Definition
|
|
Term
| Signal 3 by APC to convert T cell to Th17 |
|
Definition
|
|
Term
| Signal 3 by APC to convert T cell to Tfh |
|
Definition
|
|
Term
| Signal 3 by APC to convert T cell to Treg |
|
Definition
|
|
Term
| IL-12 & IFN-γ induce T cells to become what |
|
Definition
|
|
Term
| IL-4 induces T cells to become what |
|
Definition
|
|
Term
| TGF-β & IL-6 induce T cells to become what |
|
Definition
|
|
Term
| IL-6 induces T cells to become what |
|
Definition
|
|
Term
| TGF-β induces T cells to become what |
|
Definition
|
|
Term
| How does the APC know which signal 3 to provide T cells |
|
Definition
| Based upon which TCR & lectin receptors triggered its activation |
|
|
Term
| NFAT + STAT1 induce: T-bet or GATA-3 |
|
Definition
|
|
Term
| NFAT + STAT6 induce: T-bet or GATA-3 |
|
Definition
|
|
Term
| IFN-γR ___ [inhibits or activates] transcription of IL-4 |
|
Definition
|
|
Term
| IL-4R ___ [inhibits or activates] transcription of T-bet |
|
Definition
|
|
Term
| IFN-γR induces expression of what (4) |
|
Definition
| 1) T-bet, 2) IFN-γ, 3) Hlx, 4) IL-12Rβ2 |
|
|
Term
| IL-4R induces expression of what (2) |
|
Definition
|
|
Term
| IFN-γR and IL-4R have what in common in terms of gene transcription induction |
|
Definition
| They induce transcription of their own ligands |
|
|
Term
| How does Th1 differentiation inhibit the Th2 differentiation path |
|
Definition
| Inhibits IL-4 & IL-4R transcription |
|
|
Term
| How does TH2 differentiation inhibit the Th1 differentiation path |
|
Definition
| Magically inhibits T-bet & IFN-γ somehow |
|
|
Term
| IFN-γ effects on NK cells |
|
Definition
| Increase NADPH oxidase & NOS: increased cytotoxicity |
|
|
Term
| IFN-γ effects on macrophages (2) |
|
Definition
| 1) Increased phagocytosis, 2) increased peptide-MHC display |
|
|
Term
|
Definition
| Increased antibody production |
|
|
Term
| IFN-γ effects on CD8 T cells |
|
Definition
|
|
Term
| IL-4 & IL-13 effects on mucosal epithelium (2) |
|
Definition
| 1) Increased proliferation, 2) increased mucin production |
|
|
Term
| IL-4 & IL-13 effects on smooth muscle |
|
Definition
|
|
Term
| Which activates macrophages for tissue remodeling & repair: Th1 or Th2 |
|
Definition
|
|
Term
| TH2 activation of B cells does what |
|
Definition
| Differentiation into IgE secretion |
|
|
Term
| When IgE binds to parasites, how do mast cells & basophils react |
|
Definition
|
|
Term
| What causes CD4 T cells to migrate toward B cells in the germinal centers |
|
Definition
| IL-12 by dendritic cells that induces CXCR5 upregulation |
|
|
Term
| Macrophages secrete ___ that maintains Th17 cells |
|
Definition
|
|
Term
| What inhibits macrophages from secreted IL-23 |
|
Definition
| Phagocytosis of dead neutrophils |
|
|
Term
| What ultimately ends a Th17 response |
|
Definition
|
|
Term
| Balancing persistent infection with immunopathology is the result of balancing ___ and ___ |
|
Definition
| T regulator cells and T effector cells |
|
|
Term
| IPEX syndrome has defect in ___ that leads to ___ and treated by |
|
Definition
| FoxP3 that leads to autoimmunity and treated by bone marrow transplant |
|
|
Term
| How can CD8 T cells respond so quickly |
|
Definition
| Granules are pre-made and just have to be released |
|
|
Term
| Steps to CD8 killing of a cell (4) |
|
Definition
| Non-specific adhesion (LFA-1, ICAM) → antigen recognition → T cell cytoskeletal/cytoplasmic rearrangement → granule release |
|
|
Term
|
Definition
|
|
Term
| What protects CD8 T cells from its own cytotoxicity (perforin specifically) |
|
Definition
|
|
Term
|
Definition
|
|
Term
| IFN-γ effects on virally-infected cells (2) |
|
Definition
| 1) Inhibit viral replication, 2) increases MHC I expression |
|
|
Term
|
Definition
| IFN-α, β [there are others but he didn't list them] |
|
|
Term
|
Definition
|
|
Term
| From the perspective of adaptive immunity, the role of innate immunity is to |
|
Definition
| Delay pathogen proliferation until adaptive immunity can ramp up to kill it |
|
|
Term
| Why is pathogen vs. host balance necessary for both |
|
Definition
| If host always wins, pathogen is eradicated (e.g., polio); if pathogen wins, then pathogen has no more hosts to infect |
|
|
Term
| Does the immune system ever limit it's response |
|
Definition
| Yes, to avoid too much damage to self |
|
|
Term
| What does the first curve (green; peaks at 2 days) represent |
|
Definition
| Production of IFN-α, IFN-β, TNF-α, & IL-12 |
|
|
Term
| What does the second curve (blue; peaks at 3 days) represent |
|
Definition
| NK-cell-mediated killing of infected cells |
|
|
Term
| What does the third curve (red; peaks at 8 days) represent |
|
Definition
| T-cell-mediated killing of infected cells |
|
|
Term
| A cell gets infected with a virus, what does it secrete |
|
Definition
|
|
Term
| How does a host cell detect it is infected with a virus |
|
Definition
| TLR's (3, 7, 8, 9) and others (RIG-I, MDA5) |
|
|
Term
| Do viruses interfere with type 1 interferon production |
|
Definition
| You betcha! [Influenza, HCV, HHV, VACV] |
|
|
Term
| Stages of T cell response following infection (4) |
|
Definition
| Activation → expansion → contraction → memory |
|
|
Term
| T cell response: what is activation |
|
Definition
| Dendritic cell maturation |
|
|
Term
| T cell response: what is expansion |
|
Definition
| Proliferation of T cells against the specific virus |
|
|
Term
| T cell response: what is contraction |
|
Definition
| Reduction/elimination of T cells |
|
|
Term
| T cell response: what is memory |
|
Definition
| Comprised of central and effector memory that recognize the viral antigen |
|
|
Term
| Which has greater proliferation: CD4 or CD8 T cells |
|
Definition
|
|
Term
| Naive → effector T cells: change in CD62 (homing) expression |
|
Definition
|
|
Term
| Naive → effector T cells: change in CCR7 (chemokine) expression |
|
Definition
|
|
Term
| Naive → effector T cells: change in LFA-1 (adhesion) expression |
|
Definition
|
|
Term
| Naive → effector T cells: change in IL-7R (cytokine) expression |
|
Definition
|
|
Term
| Naive → effector T cells: change in IFN-γ (effector) expression |
|
Definition
|
|
Term
| Naive → effector T cells: what increases in expression |
|
Definition
| Adhesion receptors & effector molecules |
|
|
Term
| Naive → effector T cells: what decreases in expression |
|
Definition
| Homing, chemokine, and cytokine receptors |
|
|
Term
| Top or bottom graph represents out-bred animals |
|
Definition
| Bottom [peak and maximum at peak are different] |
|
|
Term
| Top or bottom graph represents in-bred animals |
|
Definition
| Top [peak and expression nearly the same] |
|
|
Term
| Humans are: in-bred or out-bred animals |
|
Definition
|
|
Term
| What does out-bred status of a population of animals indicate regarding symptoms |
|
Definition
| Symptons and extend of symptoms vary with an individual's kinetic response |
|
|
Term
| If contraction follows the clearance of an infection, what does that [incorrectly] imply |
|
Definition
| That the infection is sensed by the immune system, but it does not |
|
|
Term
| What is the alternative to contraction being induced by sensing clearance of an infection |
|
Definition
| Contraction is programmed |
|
|
Term
| Which is involved in contraction: CD95, IL-7R, Bim |
|
Definition
| Bim and other pro-apoptotic molecules [CD95 is activation-induced cell death; IL-7R is pro-survival] |
|
|
Term
| Why would central memory cells have higher IL-7Rα |
|
Definition
| IL-7 is pro-survival, which is what you want memory cells to do |
|
|
Term
| Why would memory cells have higher IL-15Rβ |
|
Definition
| IL-15 indicates viral infection, which you want memory cells to mobilize in response to |
|
|
Term
| Why would memory cells have higher CD44 |
|
Definition
| CD44 is involved in homing |
|
|
Term
| Persistent infection leads to T cell ___ |
|
Definition
|
|
Term
| First things that effector CD8 T cells lose during exhaustion (2) |
|
Definition
|
|
Term
| How does loss of IL-2 potentiate effector T cell exhaustion |
|
Definition
| IL-2 indicates proliferation, so loss of IL-2 is loss of proliferation signal [my interpretation of his lecture] |
|
|
Term
| Why is effector T cell exhaustion a desirable function of adaptive immunity |
|
Definition
| Without it, effector T cells may kill self through excessive cytotoxicity |
|
|
Term
| Why is mucosal immunity important |
|
Definition
| A lot of respiratory and GI diseases/infections (ARI, diarrheal, HIV, tuberculosis, measles, pertussis, hep B, parasites) |
|
|
Term
| Systemic immunity → sterile environment |
|
Definition
| PLACE HOLDER FOR WHATEVER THIS IS AFTER HE LECTURES ON IT |
|
|
Term
| How are the mucosal lymphoid tissues organized |
|
Definition
| Discrete compartments scattered throughout the mucosal membrane |
|
|
Term
| Mucosal immunity secretes which immunoglobin |
|
Definition
| IgA [remember? that was only like 3 weeks ago] |
|
|
Term
| Does mucosal immunity have many memory cells |
|
Definition
| Yes, a lot of them even in absence of infection |
|
|
Term
| Nonspecific protection at mucosal membranes (3) |
|
Definition
| 1) Mucus, 2) tight junctions, 3) membranes (cellular & basement) |
|
|
Term
|
Definition
|
|
Term
| Which defensin does epithelia express |
|
Definition
|
|
Term
| Which defensin do neutrophils and NK cells express |
|
Definition
|
|
Term
| Are defensins secreted constitutively |
|
Definition
| No, only upon exposure to microbial agents |
|
|
Term
| Antimicrobials produced by epithelia (3) |
|
Definition
| 1) Defensin, 2) cathelicidins, 3) histatins |
|
|
Term
| Where would you find histatins |
|
Definition
|
|
Term
| What bacteria are cathelicidins active against |
|
Definition
| Both gram + and - bacteria |
|
|
Term
| Where do you find defensin production in epithelia |
|
Definition
|
|
Term
|
Definition
| Pass microbes over to APC's in the Peyer's patches |
|
|
Term
| MALT, GALT, BALT, NALT are found in ___, ___, ___, ___ |
|
Definition
| M=mucus, G=gut, B=bronchus, N=nasopharynx |
|
|
Term
| Suppose you eat a pathogenic bacteria, what's the first step in the path to active adaptive immunity's response |
|
Definition
| Passage of bacteria across GI epithelial layer by M cells |
|
|
Term
| Ways mucosal immunity reduces immune response to enormous antigen load in the GI lumen (3) |
|
Definition
| 1) Dampening of cytotoxic T cells, 2) Treg cells, 3) suprressive cytokines (e.g., IL-10) |
|
|
Term
| Binding of IEL's to epithelium (2) |
|
Definition
| 1) CD1d—TCR, 2) gp180—CD8 |
|
|
Term
|
Definition
| Non-classical MHC on epithelia |
|
|
Term
|
Definition
| Interspersed between epithelial cells |
|
|
Term
| Mucosal Tregs: ___ [source or sink] of IL-10 |
|
Definition
|
|
Term
| Mucosal Tregs: ___ [source or sink] of IL-2 |
|
Definition
|
|
Term
| Lymph drainage of GI tract goes to which lymph nodes |
|
Definition
|
|
Term
| Mucosal homing does not use L-selectin but rather |
|
Definition
| α4β7 integrins on B cell to MadCAM-1 on epithelia |
|
|
Term
| IgA vs. IgG: which is highest in serum |
|
Definition
|
|
Term
| IgA vs. IgG: which is highest in the body overall |
|
Definition
|
|
Term
| Where do mucosal B cells get primed |
|
Definition
|
|
Term
| IgA crosses epithelium through what |
|
Definition
|
|
Term
| Which IgA form crosses the epithelial layer: monomer or dimer |
|
Definition
|
|
Term
| What binds Ig monomers into polymers |
|
Definition
|
|
Term
| pIgR is found where: basal or apical membrane |
|
Definition
|
|
Term
| How does IgA cross the basal membrane |
|
Definition
|
|
Term
| How does IgA cross the apical membrane |
|
Definition
| Exocytosis of a vesicle containing IgA |
|
|
Term
| Two sites involved in the whole process of antigen detection and IgA secretion |
|
Definition
| 1) Inductive site, 2) effector site |
|
|
Term
| Is genetic IgA deficiency common |
|
Definition
|
|
Term
| Is IgA deficiency treatable |
|
Definition
|
|
Term
| Examples of food allergies resulting from uncontrolled T cell activation (3) |
|
Definition
| 1) Gluten sensitivity, 2) wheat allergy, 3) Celiac disease |
|
|
Term
|
Definition
| Inappropriate inflammatory reactions to commensal microbilas in the gut |
|
|
Term
| Why IgA at mucosal sites and not another Ig |
|
Definition
| IgA crosses epithelium quite well, the others do not |
|
|
Term
| Reasons why B cell cancers occur (3) |
|
Definition
| 1) Hyperproliferative cells, 2) DNA rearrangement, 3) hypermutation |
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|
