Term
| How do DC insert a dendrite through tight junctions without disrupting integrity of epithelial barrier? |
|
Definition
| new tight junction like structures are formed between the DC and the epithelial cell. When a DC process binds an antigen this somehow causes downregulation of tight junction protein on the DC, dendrite is removed an tight junction between epithelial cells is restored |
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Term
| After epithelial cells have bound an antigen via basolateral TLR or NOD proteins, they secrete chemokines taht attract which cells? |
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Definition
from blood-neutrophils and monocytes
from local tissue- macrophages, DC, and natural killer cells |
|
|
Term
| What do you call T cells that are a part of the epithelium? |
|
Definition
| intraepithelial T lymphocytes (often these are T gamma delta cells) |
|
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Term
| Why are gamma delta T cells called "innate-like"? |
|
Definition
| because they are less restricted than alpha beta T cells |
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|
Term
| Why are NKT cells "adaptive-like"? |
|
Definition
| they have a TCR (killing is not completely MHC unrestricted) |
|
|
Term
| What antibodies bridge the gap between adaptive and innate immunity? |
|
Definition
|
|
Term
| Which cells are innate effectors with FcReceptors? |
|
Definition
| macrophages, NK cells, neutrophils, monocytes, DC |
|
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Term
|
Definition
| adaptive dependent cellular cytotoxicity. This is when NK cell binds many Fc's from many antibodies covering an antigen causing crosslinking of Fc receptors which signals NK cell to kill the target cell via apoptosis |
|
|
Term
| ADCC is important for eliminating what type of pathogens? |
|
Definition
|
|
Term
| T/F gamma delta T cells are neither CD4+ nor CD8+. |
|
Definition
| FALSE! they can be CD4+ or CD8+ |
|
|
Term
| What percentage of T cells are gamma delta? |
|
Definition
|
|
Term
| T/F gamma delta T cells undergo gene rearrangement. |
|
Definition
| True, but they have limited diversity in V regions when compared to alphabeta t cells |
|
|
Term
| What is the primary "V" type of gamma delta T cells? |
|
Definition
|
|
Term
| T/F Gamma delta t cells recognize peptides in MHC like alpha beta T cells. |
|
Definition
|
|
Term
| Once they have recognized an antigen, which mounts a faster immune response: alpha beta or gamma delta t cells? |
|
Definition
| gamma deltas are faster because many gamma deltas can be activated by a single antigen |
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Term
| Vgamma9:Vdelta2 T cells are all activated by what? |
|
Definition
| three different phosphoantigens that contain a shared pyrophosphate group (these are intermediates in the production of isoprenoid) |
|
|
Term
| What are the protective functions of gamma delta T cells? |
|
Definition
| kill infected cells (like NK cells or CD8+CTL), secrete granulysin (anti-microbial peptide), and secrete inflammatory IFN-gamma and TNF-alpha |
|
|
Term
| Which TCR and receptors do many gamma delta T cells in the mucosa express? What do these receptors recognize? |
|
Definition
| Vgamma:Vdelta1 TCR and NKG2D; both of these bind to stress-induced MIC proteins which activates the gamma delta T cell |
|
|
Term
| T/F viral infections can induce MIC proteins. |
|
Definition
|
|
Term
| T/F MIC proteins are sometimes expressed by healthy cells. |
|
Definition
|
|
Term
| What happens when a gamma delta T cell binds to an infected cell expressing MIC? |
|
Definition
| gamma delta t cell induces apoptosis of infected cell and then helps repair the wound |
|
|
Term
| What markers do NK cells express? |
|
Definition
|
|
Term
| T/F NK cells mediate MHC-unrestricted killing of virus infected cells (like CD8+ CTL). |
|
Definition
|
|
Term
| How do NK cells discriminate between healthy and virus infected cells? |
|
Definition
| inhibitory receptors make NK tolerant to self and recognize MHC Class 1 molecules on cell surface (either all MHC class 1 or only class 1 with specific sequences). They also have activatory receptors (NKG2D) that bind to MIC proteins of infected cells |
|
|
Term
| What is the effect of viral infections on surface receptors of cells? |
|
Definition
| decrease MHC class 1 and increase surface MIC-A or MIC-B (MHC class I-like molecules) |
|
|
Term
| An NK cell that binds to a healthy cell binds to ... |
|
Definition
| MHC class I via the inhibitory receptor |
|
|
Term
| An NK cell that binds to a virus infected cell binds to... |
|
Definition
| MIC via NKG2D which is the activatory receptor. (MHCI expression is downregulated due to virus and so there is no inhibitory signal) |
|
|
Term
| What happens if a NK cell binds both an MHC class I and an activating molecule? |
|
Definition
| the inhibitory signal overrides the activatory signal |
|
|
Term
| What receptors do NKT cells characteristically express? |
|
Definition
| NK receptors and an invariant alpha beta TCR (restricted repertoire of Valpha24-J18) |
|
|
Term
| Which MHC molecule are NKT cells restricted to? |
|
Definition
| MHC classI-like CD1d molecule which presents lipid antigens from a wide range of pathogens |
|
|
Term
| NKT cells respond rapidly to infection by secreting _______ and upregulating the expression of _______ on their cell membrane. |
|
Definition
|
|
Term
| NKT cells upregulate CD40L when they encounter infection in order to... |
|
Definition
| stimulate IL-12 secretion by DC |
|
|
Term
| What happens when DC cells secrete IL-12? |
|
Definition
| this initiates the inflammatory response which attracts NK cells, neutrophils, and monocytes to the site |
|
|
Term
| T/F NKT cells generate memory cell responses. |
|
Definition
|
|
Term
| T/F NK cells ability to kill other, virus infected cells is not completely "MHC unrestricted". |
|
Definition
|
|
Term
| How long do antibodies produced during the primary response prevent reinfection for? |
|
Definition
|
|
Term
| What's another name for strain? |
|
Definition
| serotype (because strains are distinguished in serological tests by using a panel of antisera which each contain antibodies against one of the strains |
|
|
Term
| An individual can get bacterial pneumonia multiple times by the "same" pathogen due to the existence of ______. |
|
Definition
| multiple strains of the same pathogen |
|
|
Term
| How does the body overcome antigenic shift in a pathogen when it is a minor change like a point mutation? |
|
Definition
| a point mutation can result in minor disease because T cells and antibody that recognize unaltered epitopes eventually control infection. Causes mild and limited epidemics (local outbreaks) ex. influenza A |
|
|
Term
| In the case of influenza virus, what proteins on the surface of the virus bind the neutralizing antibody? |
|
Definition
| hemagglutinin or neuraminidase |
|
|
Term
| How does the body respond to a pathogen that has undergone an antigenic shift by combining with a nonhuman virus? |
|
Definition
| the human/nonhuman hybrid virus (like avian flu, which is a strain of influenza A) cause major changes in hemagglutinin or neuraminidase proteins resulting in severe disease and mortality because the new protein is not recognized by pre-existing antibody, or memory B or T cells. This causes global pandemics |
|
|
Term
| How does insect-borne African Trypanosome exhibit programmed gene rearrangements? |
|
Definition
| the gene for the major outer surface antigen (varient-specific glycoprotein or VSG) is continously switched during infection via gene conversion. |
|
|
Term
| What do you call it when a pathogen varies its outer surface proteins during infection to evade neutralizing antibodies? |
|
Definition
| programmed gene rearrangements |
|
|
Term
|
Definition
| used during programmed gene rearrangments; it is exicision of gene from expression site and replacement by a copy of a homologous gene |
|
|
Term
| What does the clinical course of trypanosome infection look like? |
|
Definition
| chronic cycles of antigen clearance lead to immune complex damage, inflammation, and eventually neurological damage which results in coma (trypanosomiasis or "sleeping sickness") |
|
|
Term
| Name three examples of organisms that exhibit gene conversion (programmed gene rearrangement)? |
|
Definition
| trypanosome, salmonella typhimurium (food poisoning- alters 2 versions of surface flagellin protein), and neisseria gonorrhoeae (gonorrhea- alternates versions of surface pilin protein) |
|
|
Term
| T/F Latent viruses have absolutely NO viral replication during the latent period. |
|
Definition
| False, they can have extremely low levels of replication |
|
|
Term
| How does Herpes Simplex Virus type 1 (HSV-1) evade elimination from its host? |
|
Definition
| latency- it infects epithelial cells in the oral cavity then spread to nearby sensory neurons (trigeminal ganglion). Primary immune response clears it from epithelial cells but not from neurons. Stress causes reactivation of HSV-1 which can travel down the neuron and reinfect epithelial cells. CD8 cells kill infected epithelial cells creating the sore and HSV-1 goes dormant again |
|
|
Term
| What are the symptoms of primary exposure to epsteinn-barr virus? |
|
Definition
| cold-like for children, mononucleosis in adolescents and adults |
|
|
Term
| How does EBV infect a cell? |
|
Definition
| via CR2 component of the BCR |
|
|
Term
| How are B cells infected with EBV elimanted? |
|
Definition
|
|
Term
| What one protein is still produced in EBV latent phase? |
|
Definition
|
|
Term
| Why aren't B cells infected by latent EBV recognized by CTL? |
|
Definition
| although the virus is producing foreign protein during the latent phase (EBNA-1), this protein can not be degraded by proteasomes in the B cell cytoplasm. Because of this, foreign antigens are never presented by MHC class I and so the B cell appears uninfected to the CTL |
|
|
Term
| What viruses suppress the immune response by a virally encoded Fc receptor? |
|
Definition
|
|
Term
| What viruses suppress the immune response by a virally encoded complement receptor? |
|
Definition
|
|
Term
| What viruses suppress the immune response by a virally encoded complement control protein? |
|
Definition
|
|
Term
| What viruses suppress the immune response by a virally encoded chemokine receptor homonlog? |
|
Definition
|
|
Term
| What viruses suppress the immune response by a virally encoded soluble cytokine receptor? |
|
Definition
| vaccinia, and rabbit myxoma virus |
|
|
Term
| What viruses suppress the immune response by viral inhibition of adhesion molecule expression? |
|
Definition
|
|
Term
| What viruses suppress the immune response by protection from NFKB activation by short sequences that mmic TLRs? |
|
Definition
|
|
Term
| What viruses suppress the immune response by inhibition of MHC class I upregulation by IFN-gamma? |
|
Definition
|
|
Term
| What viruses suppress the immune response by inhibition of peptide transport by TAP? |
|
Definition
|
|
Term
| What viruses suppress the immune response by a virally encoded cytokine homolog of IL-10? |
|
Definition
|
|
Term
| How does the toxoplasma gondii parasite subvert the immune system? |
|
Definition
| infects cell and creates a membrane-enclosed vesicle that does not fuse with other cellular vesicles. This prevents incorporation of T gondii-derived peptides into MHC and hence detection by T cells |
|
|
Term
| How does treponema pallidum spirochete (syphilis) subvert the immune system? |
|
Definition
| evades antibody by coating itself with human proteins |
|
|
Term
| What is a bacterial superantigen stimulation of a massive but ineffective T cell response? |
|
Definition
|
|
Term
| How does an antigen "sabotage" the immune system? |
|
Definition
| by binding to a MHC class I molecule on an antigen presenting cell and simultaneously binding certain Vbeta chains on CD4 T cell (naive or memory). THis activates multiple polyclonal T cells because most T cells have the Vbeta binding site so 2-20% of CD4 cells have Vbeta binding site. |
|
|
Term
| Bacterial sabotage of the immune system results in.. |
|
Definition
| massive production and release of cytokines (IL-1, IL-2, TNF-alpha, and LT by T cells; IL-1 TNF-alpha, IL-6, IL-12 by APC monocytes and DC) causing systemic toxicity and suppression of the adaptive responses |
|
|
Term
| How many binding sites for MHC do most superAgs have? |
|
Definition
|
|
Term
| S. aureus causes the disease ______ by ___________. |
|
Definition
| toxic shock syndrome Toxin-1, acting as a superantigen |
|
|
Term
| What is the differences between antigenic drift and antigenic shift? |
|
Definition
| drift is a minor mutation during infection. shift is a amajor change involving recombination between viruses in order to evade both humoral and cellular immunity |
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