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44 Cards in this Set

  • Front
  • Back
what is important for fighting early viral infection
type I interferons (think mucous)
and NK cells
major phagocytotic cells 2
neutraphils and macrophages
what enhances phagocytosis?
opsinins
viruses require a better TH1 or TH2 response?
TH1
is the NK cell MHC restricted?
no!
Cytotoxic T cells are what kind of cells?
CD8+
T cell vs. NK

mediate ADCC
NK does this
T cell vs. NK

MHC restriction?
T: yes

NK: NO
T cell vs. NK

antigen specific
T: yes

NK: no
T cell vs. NK

induce targer cell apoptosis
Both do this
what is perforin?
like C9 protein of complement

puts a hole in the target cell
CD3
on all mature functional T cells
CRP
C reactive protein

acute phase protein

made during inflammatory rxn, measurable for systemic inflammation
C3a
complement protein

inflammatory mediator
C3b
number 1 opsinin
C5a
complement protein

inflammatory mediator

chemotactic for neutraphil
CXCR4
chemokine receptor

important for getting cells to where they are needed
CTLA-4
T-cell inhibitor

prevents co-stimulatory signals (stops CD28 to B7 binding)
CD8
cytotoxic T cell killer
C1q
complement protein

initiates classical pathway of complement activation
Granuloma
Granulomas are space-occupying chronic inflammatory lesions that form due to cell- mediated immune reactions. Certain infections tend to lead to granuloma formation, e.g. tuberculosis, Leismaniasis, Schistosomiasis
what is ADCC in general
antibodies and killer cells combine to kill shiz
TH1 leads to what?
INF gamma to macrophage activation
TH2 releases what leading to?
IL4,5 for mast cell, eosinophils and IgE production
IL 10 does what?
turns off TH1
what does TGF B do? 2
turns off T cells

isotype switch to IgA***
IL 10 and TGF B do in general?
immuno suppression
what is the primary mucosal immune Ig?
IgA
does Iga cross placenta? does it activate complement via classical pathway?
NO

NOOOOO
3 most important antiviral
type 1 interferons, NK, cytotoxic T cells
what mechanism is best at fighting extracellular bacteria

objective
Antibody and complement
what mechanism is best at fighting fungi
phagocytosis (neutraphils and macrophages)
intracellular viral infections what is most important?

objective
t cell
if you have problems with phagocytosis what are you most likely to get as far as infections go?
fungal
Describe 4 - 5 ways in which antibody, either alone or in combination with other immune system elements, can help to clear or neutralize antigen (i.e., bacteria, viruses, toxins).


**objective
Ab-assisted phagocytosis
Ab + complement lysis
Ab + antigen complexes
Ab neutralization of toxins and viruses

Ab interference with virus/bacteria cell attachment
Role of IgE in anti-parasite defense
Antibody-dependent cellular cytotoxicity (ADCC)
Role of secretory IgA on mucosal surfaces
What cell types mediate antibody-dependent cellular cytotoxicity (ADCC)?


**objective
Specific antibodies are formed (with the help of T cells) to the microbial invader. The microbe is targeted for destruction by these antibodies.

2) Killer cells that have receptors for the Fc portion of the antibody (i.e. Fc receptors) destroy the target cells.

3) The antibody (usually IgG isotype) basically acts as a bridge to connect the killer cell and the target cell.

4) ADCC killer cells include: NK cells and macrophages
What types of infections would you expect to see in a person with a total deficiency in antibody production?


**objective
extracellular bacterial infections are most common
What intracellular killing mechanisms are present within activated macrophages?


**objective
produce oxygen free radicals for intracellular killing
Describe the role(s) of T-helper cells and cytotoxic T-cells in a virus infection.


**objective
Cytotoxic T-cells (CTL), which are usually CD8+, are known to kill virus-infected cells and tumor cells. This killing is 1) antigen specific 2) MHC Class I restricted, i.e. target cell must have MHC class I with antigenic peptide in the binding groove; and may cause cell lysis by 3) inducing "programmed cell death" (apoptosis), or 4) release of pore-forming proteins like perforin.
What is a granuloma? What is the potential significance of granuloma formation?


**objective
cannot kill the cell after it is phagocytized due to lack of reactive O2 species in macrophage

a granuloma is the walled off problem that is not killed

this is seen in chronic granulatomous disease
What is the basic difference between TH1 and TH2 type T-lymphocytes?


**objective
TH1 cells release IL-2 and IFN-gamma (enhance cell-mediated responses; some IgG)

TH2 cells release IL-4, IL-5, IL- 6, and IL-10 (enhance humoral responses; IgE)
What is the primary role of Natural Killer Cells (NK cells) in the immune response?


**objective
NK cells are "large granular lymphocytes" with no discernible antigen receptor. However, antibody can provide the specificity and activate NK cells via ADCC. NK Cells major role may be to destroy infected cells
What are perforin and Nitric oxide? What are their roles in host defenses?


**objective
Nitric oxide is a gas produced in phagocytic cells and is toxic to many organisms

, which when released can polymerize and cause transmembrane pores to form. Perforin is structurally similar to the C9 component of complement. CTL granules also contain proteolytic enzymes and TNF-α, all of which can damage target cells.
What is the immunologic advantage of using an oral or nasal influenza vaccine in place of or in addition to the traditional parenteral vaccine?


**objective
advantage of oral:

absorbed in intestines, returned to heart via thoracic duct, then pumps all over your body