Test 4 Flashcards
Steps in phagocytosis
- WBC find target by taxis
- Pseudopods surround particle and form a phagosome (the pouch formed when the particle is brought in)
- Fusion of phagosome + lysosome = phagolysosome
Phagolysosome
Fusion of the phagosome and the lysosome
-Where digestion of ingested materials occurs.
What happens after phagocytosis
Unique and recognizable parts (antigen) are processed and placed on the phagocytic cell surface. The WBC’s then show the level 3 defenses the antigen and they know who they need to look for.
*level 3 cells only recognize antigen when placed on a WBC surface
MHC-2
Major Histocompatibility Complex, which is the holder of the antigen.
Once a phagocytic WBC has an antigen on it what is it called
Antigen Presenting Cell (APC)
-cell has officially changed roles and will travel to lymph nodes and present antigen to level 3 cells.
APC is the ____ of all level 3 responses
Activator
Examples of bacterial antigens
- Cell wall/membrane
- Exoenzymes and exotoxins (proteins)
- Flagella, pili, or fimbrae
- Capsule or glycocalyx
Viral antigens
- Capsomeres
- If enveloped virus: peplomers
- Tegument
- Enzymes
Fungi/worms/protozoa antigens
- Cell surface protein
- Enzymes
Antigens
- Usually parts of proteins (complex)
exceptions: glycoproteins - Proteins on surfaces of abnormal “self” cells are also antigenic
Inflammation
Non specific process triggered by any damage to tissues (basophils and mast cells are the cells that respond)
Inflammation response
Release: Histamine, prostaglandins, leukotrienes, stored inside cells to have a local effect on capillaries.
What do the chemicals released due to inflammation cause?
-Increase arteriole dilation and increased capillary permeability
What is the leaving of blood from blood vessels called
Diapedesis
Result of inflammation
Number of level 2 cells increases in the tissue
Resulting signs of inflammation - latin and english
Rubor - Redness
Calor - Heat
Tumor - Swelling (accumulation of fluid and cells)
Dolor - Pain, due to increased pressure on nerve endings
Acute inflammation
Damage to tissues with good response of delivering white blood cells where they are needed
Chronic inflammation
Can cause actual damage to own tissues
Natural Killer Cells
- Come from T cell line
- Wandering WBC’s
- Use perforin to make pores
- Also use granzyme to trigger apoptosis to kill abnormal eukaryotic cells
- non-specific and destroy anything exhibiting abnormal behavior such as cancerous cells, infected self cells, protozoa/yeast
*protozoa/yeast = too large to phagocytize so once apoptosis happens, leftover pieces can be phagocytize and then APC’s can be made
Granzyme
An enzyme that causes spontaneous apoptosis to kill abnormal EUKARYOTIC cells
Interferons
- Released by infected cells to tell neighboring cells to be careful
- neighboring cells produce anti-viral proteins ahead of time (thanks to the warning from the interferons)
- Neighboring cells are thus protected from viral attack which slows down the viral passage
Complement proteins
- Created by liver and secreted into the blood
- Triggered to bind sequentially to form enzymes
- Level 2 trigger: pathogen molecule (esp. LPS in Gr- or capsule in Gr- and Gr+)
- -non specific (any Gr- or Gr+ or Gr+ with capsule)
Once complement proteins are triggered what are the results?
- Phagocytosis
- Inflammation
- Membrane attack
What do complement proteins enhance?
- Phagocytosis (opsonization) - helps get rid of small yeasts and bacteria..gives the WBC’s something to grab on to.
- Inflammation - complement proteins stik on tissues causing inflammation w/o tissue damage
- allows more phagocytes/killer T cells - Membrane attack complex - proteins form a channel in abnormal cells
- cell contents leak out causing lysis and cell death
Level 3 defenses
Command center: lymphoid organs
-Monitor body fluids
Lymphatic system
Series of vessel which drain body tissues
-punctuated by lymph nodes, which catch what is drained by the tissues
Cells involved in the level 3 defenses
T and B lymphocytes
-Both produced in the bone barrow, but mature in different locations
Where do T cells mature
The thymus
Where do B cells mature
In the bone marrow
-This is to destroy cells that would respond to antigens on our own cell surfaces so that the only ones left find antigens on foreign cells and then attack. Once mature dumped into circulation then jump into lymphatic organs (nodes, spleen, etc.)
Lymphoid organs
- Lymph nodes
- Spleen - filters blood, important in septicemia infections
- Mucosal associated lymphatic tissues (MALT) - tonsils, adenoids, peyers patches, appendix (catch pathogens at mucus membranes)
What happens if the pathogen gets into lymph organs without being processed
Phagocytosis won’t occur in lymphoid organs, so the pathogen is basically home free to reproduce
What are the 2 types of MHC holders? what do they do?
Class I MHC - all nucleated cells (except RBC’s)
-display for: recognition and ID of abnormal cells. (T&B cells don’t respond to an antigen held in MHC 1)
Class II MHC - Antigen presenting cells
-macrophages, dendritic cells, B-lymphocytes.
-Are on cells that carry antigen to lymph nodes.
Once a Th0 cell is converted to a Th1 what do the secreted cytokines do?
- Cause APC cells to kill better/faster
- Activate T cytotoxic (Tc0) to rapidly clone info about antigen which results in a huge number of T cytotoxic cells
Majority: Tc Clones are active currently and go to the bloodstream and tissues using chemotaxis to find Antigen bearing cells.
Minority (small amount): Stay dormant, don’t work during first exposure, but work later on in another exposure to the pathogen, wander around
How do T cytotoxic cells find specific infected or abnormal self cells?
Chemotaxis - antigen in MHC -1
-Use perforin and granzyme to destroy specific abnormal eukaryotic cells which includes: infected self cells, cancerous self, yeast, protozoa, worms
When the pathogenic threat is over what happens to cloned Tc Cells and Th1 cells? and memory cells
Die - they are short lived
Memory cells live forever however some research has shown that as someone ages, Tm cells decline.
What happens in a second exposure to the same pathogen?
All primary responses at normal time
- Tm cells = no need for APC
- -touch antigen to activate and become active T cytotoxic cells within minutes (the pathogen won’t have much time to reproduce/create enzymes, toxins etc - ends up saving a lot of time - host may never even feel symptoms)
Humoral immunity steps
Activation of B cells
-MHC-2 or B cell receptors in membrane
T dependent activation (most common)
-APC enters lymph nodes
–Stimulates Th0 to create Th2
—Th2 activates virgin B-cells to clone (bind to MHC-2 on B cell surface)
Cloned B-cells differentiate into:
-Majority: plasma cells which secrete antibodies which travel into plasma
-Minority: become B-memory cells - dormant plasma cells, don’t respond during first exposure.
Humoral immunity activates ____ cell while cell mediated initiates
B;T
When threat is over humoral immunity/second exposure
Antibodies last about 1-7 weeks, broken down and recycled
- plasma cells die within several days
- Bm cells remain in lymph node for potentially ever in preparation for second exposure to pathogen
Second exposure:
- Primary response plus:
- -Bm respond to antigen quicker w/o APC
- -form plasma cells which secrete antibodies in 1-2 days
Antibody structure
Globulin group of proteins (Y shaped) known as gamma globulins or immunoglobulins (Ig)
- All antibodies have Y shape/combinations of monomers
- Each has 2 long amino acid chains, and 2 short amino acid chains
Tips of Y on antibody
Fab
- Fraction which is Antigen Binding
- Variable (specific to antigen, so can change)
Base of Y on antibody
Fc
- Fraction which is crystallizable or constant
- does not change
Antibody Types
IgG IgA IgM IgE IgD
IgG Antibody
- highest percentage in circulation in blood at any time
- monomers
- found in blood and tissues, works against local, focal, septicemia
- can cross placenta to protect fetus, anything mother is exposed to the baby will also get IgG….maternal antibodies can persist for up to 6 months after birth
IgA
- 10-15% of circulating antibodies (in an active form)
- Present as monomers, get combined in glandular secretions where they turn into a dimer and then become active
- Any surface that is covered in mucus there is IgA
- Found in blood, tissues
- Transported through glands for release in secretions (found in saliva, nose, vagina, resp. lining)
- Absorbed directly w/o being broken down (babies) - helps protect them from focal/local infections because baby can absorb them in dimer form
What type of infections would IgG protect from
local, focal, septicemia
What antibody can cross the placenta?
IgG
IgM
- 5-10% of circulating antibodies
- pentomer
- primarily found in circulation (blood stream)
- works well against septicemia, but not focal or local
IgE
- less than 1% of circulating antibodies
- monomer
- found in blood and tissues
- involved in allergies
- found and bind to inflammatory cells (mast, basophils, eosinophils)
- allergies are not inherited, some of us have more B cells that then create IgE to cause allergic reaction
- a lot of things can affect production of IgE
Which antibody is involved in allergies and allergic responses
IgE
IgD
-.5% of circulating antibodies
-monomer
-Found on B cell surfaces (B-cell receptor)
-First vs. Second exposure
First:
-Virgin B cells: lag then IgM first followed by IgG
Subsequent exposure:
-lots of B memory cells releasing: IgG in large amounts and IgM (both secreted much earlier)
A few: virgin B cells lag then IgM 1st and later IgG
In the first exposure to a pathogen what do virgin B cells do to produce antibodies
B cells lag then IgM made first followed by IgG
Subsequent exposure to a pathogen virgin B cells do to produce antibodies
Lots of B memory cells releasing: IgG in large amounts and IgM (both secreted much earlier)
A few: virgin B cells lag then IgM 1st and later IgG
Antibody action: Agglutination
-Clumping
-Fab binds to different antigen, bearing, causes. causing clumping of cells (does not kill)
-Helps fight:
flagellar antigens because agglutination prevents bacteria from swimming away and/or dispersing
-bacteria and larger viruses can clump which makes them bigger and then easier to phagocytize
Antibody action: Opsonization
“enhanced phagocytosis”
-Fc end of antibody binds to cell surface of phagocyte
-Fab end binds to invaders antigen
-Antibodies deliver phagocytizable pathogens
helps fight:
-bacteria, or large clumped virus
Antibody action: Natural killer activation
- Fab binds to invaders antigen
- Fc binds to NK cell surface
- Antibody binds onto lymphocyte making it specific for antigen
- directs abnormal cell killing process
- works best against eukaryotic abnormal cells
Antibody action: complement activation
-Fab on cell surface antigen
-Fc end binds to loose complement
-stimulates chain reaction of bindings
Causes:
-opsonization (comp. proteins sticking to bac. to make them easier to phagocytize)
-inflammation (deliver more NK/phagocytic cells) -> helps get rid of eukaryotic cells and bacteria
-Membrane attack complex - works against: bacteria, yeasts, worms, fungi, infected self cells
Antibody activation: Neutralization
Make antigen no longer a threat -Fab grabs antigens and prevents binding to host cell tissues --ex: enterotoxins can't bind to intestinal lining to causes symptoms Used to fight: -toxins: only exotoxins -enzymes -viruses -bacterial ligands/adhesions
Antibody activation: oxidation
Fab binds to invaders antigens -H2O2 or O3 made in local area -before cell can make catalase disulfidismultase causes so the cell bursts and dies Used to fight: -bacteria
Allergen
Allergy producing antigen
Sensitization
Process of becoming allergic by continually adding and loading IgE onto basophils, and eosinophils
-allergens trigger production IgE antibodies
-IgE binds by Fc to: mast cells, basophils, eosinophils
Once mast, basophils, eosinophils have a certain amount of IgE on them they burst and release histamine, leukotrienes, bradykinin, serotonin which causes large allergic reaction (degranulation)
After being phagocytized what is the name of the vesicle that the pathogen is first found in?
Phagosome
What is the name of the vesicle that the pathogen is digested in?
Phagolysosome
In order for an organism to survive a phagolysosome what would it have to be resistant to?
Lysozyme, digestive enzymes, superoxide, and acids
If pathogen got into the lungs what phagocytic cell type(s) would be actively working?
Macrophages, maybe leutrophils
If a pathogen made it to the alveolar macrophages what nonspecific defense mechanisms was it able to avoid?
Nasal turbines, hairs, sneeze/cough reflex, ciliary escalator, and mucus with lysozyme
Nonspecific mechanical defenses of the eye include:
Blinking reflex, flushing action of tears, lashes
Nonspecific chemical defenses of the eye:
salt, and lysozyme in tears
Chemical and structural defenses of the skin
Sloughing, cornification, thickness of skin, normal flora, sebum and salt, dryness
How would inflammation help protect against an infection?
By delivering WBC’s such as neutrophils and monocytes which will phagocytize pathogen. NK cells would also be delivered which would kill infected self cells
What defenses in the stomach could destroy a pathogen before it gets into intestines?
Acids, and flushing via peristalsis
What WBC will seek out infect self cells?
Natural killer
What chemical do infected cells release to help neighboring cells resist infection?
Interferon
What molecules are made by cells that receive interferon?
Antiviral proteins
Chemicals that are inert when separate but physiologically active when combined in the body are:
Complement proteins (activated by LPS molecule or capsules on Gr- or Gr+)
Two important functions of phagocytosis?
- Find (through taxis), ingest, digest, and destroy foreign bodies smaller than the phagocytic cell itself including bacteria, fragments of dead cells and small yeasts.
- Alert the T and B lymphocytes of level 3 defenses as to the specific kind of pathogen that the response should target.
Name of the phagocytic cell when it is performing the function that links level 2 and 3 together?
Antigen presenting cell
Examples of pathogen molecule (antigen) that could presented in the MHC 11
Bacterial cell or membrane proteins, exoenzymes or exotoxins, fimbrae, flagella, pili; viral capsomeres, peplomers, enzymes; yeasts/protozoa/worms cell surface molecules or enzymes
cell mediated immunity first exposure
- APC goes to lymph node
- APC activates Th0
- Th0 actives Th1, Th1 secretes cytokines
4 Th1 activates Tc0 - Tc0 activates Tcc and Tm
- Tcc leave lymph nodes and brings to abnormal eukaryotic cells by an antigen in the MHC 1
humoral immunity 1st exposure
- APC goes to lymph node
- APC activates Th0
- Th0 activates Th2 and Th2 releases cytokines
- Th2 activates B cells
- B cells proliferate into plasma cells and Bm
- Plasma cells secrete antibodies which travel to tissues
Cell mediated immunity 2nd exposure to same pathogen
all responses that happen during the first exposure
-Tmemory cells touch antigen and become Tcc cells which use granzyme and perforin to drill a pore and lyse abnormal cells
Humoral immunity 2nd exposure
all responses that happen during the first exposure plus
- Bm respond to antigen quicker and without APC
- form plasma cells which secrete antibodies
Why is phagocytosis necessary?
Phagocytic cells process invading pathogens and place antigens on their surface. The antigen bearing cells travel to the lymphatic tissues and present antigens to the T and B lymphocytes. Without this processing the T and B lymphocytes would not respond to antigenic material
Phagocytic cells include ____ in the tissues ____ in the blood, and _____ in the blood and tissues
macrophages; monocytes; neutrophiles
How are NK cells and cytotoxic T cells alike/different
Both - recognize abnormal eukaryotic cells and destroy them using perforin and granzyme
-NK cells roam and destroy ANY abnormal cell while cytotoxic T cells respond to a specific antigen within the cells MHC-1 and seek cells bearing that specific antigen ONLY. Cytotoxic T cells also secrete cytokines while at the site of infection
Best defense against a pathogen that can hide within the cytoplasm of other cells
Cytotoxic T cells which recognize abnormal self cells harboring the pathogen by their MHC-1 antigen complex and destroy them with perforin and granzyme, which exposes the pathogens to other mechanisms of killing.
What antibody type is highest in breast milk
IgA (as a dimer)
What antibody is highest in the blood stream
IgG, IgM, IgA (monomer) IgE, IgD
What antibody is highest in tissue fluid
IgG, IgA(monomer), IgE, IgD
What antibody is highest in fetal tissues
IgG
What antibody is highest in tissues during an allergy attack
IgE
How would antibodies destroy a viral capsid
Neutralizaiton
How would antibodies destroy a cell wall antigen of Gr- bacillus
opsonization, complement activation (all 3), aggltination
How would antibodies destroy a flagellar antigen
Opsonization, agglutination, complement activation (all 3)
How would antibodies destroy a exotoxin
Neutralization
How would antibodies destroy a cell surface antigen of protozoa
Complement activation (MAC and inflammation), NK activation
Which antibodies are monomers
IgG, IgE, IgD
Antibodies that are dimers
IgA
Antibodies that are polymers
none
Antibodies that are pentomers
IgM
name for such a unique, recognizable protein which triggers allergic reactions.
Allergen
Which antibody type is involved in the allergic response? is it a monomer, dimer or pentamer?
IgE; monomer
To which end (hint: letters) of the antibody does the antigen bind to
Fab
Ashley is said to have become ??? because her cells are fully loaded with antibodies. (not “allergic”)
Sensitized
Name chemical found in the granules released basophils, eosinophils, mast cells
Histamine, bradykinin, leukotrienes, serotonin
Live attenuated vaccine
Live but weakened
- multiple antigens = multiple types of memory cells
- can reproduce in body to amplify response -> highest number of memory cells
- most effective type of vaccine
- slight danger of infection
Killed vaccine
Slightly less effective than alive attenuated
- no reproduction but still multiple antigens
- no danger of infection
- lots of memory cell types but not very many copies
Soluble antigen subunits
Only inject specific, single antigens
- response to antigens may be lower
- immune response is also relatively low - would need to get boosters
- needs adjuvants
- no danger of infection or reaction unless it is to the adjuvants
Adjuvants
Help boost immune response by irritating the immune system or clumping antigens (make it so fewer shots are needed)
Recombinant vaccine process
Safer, remove virulence gene and insert antigen into harmless cell
Whole cell recombinant
Harmless cell reproduces in body with antigens
soluble subunit recombinant
Harmless cell secretes soluble antigens
-not more effective than whole cell, but safer cheaper and easier to produce
natural killer cells use ___ and ___
granzyme and perforin
viral-infected cells secrete ___ to warn other cells
Interferon
T-helper 1 and 2 cells secrete
Cytokines
basophiles secrete
histamine, leukotrienes, and brandykinins
neutrophiles secrete
lysozyme, acids, superoxide, digestive enzymes
are a type of phagocytic cell so inside them they have a lysosome with these chemicals inside
Complement proteins do all of the following except:
a. create pores in cell surfaces b. help phagocytes grab onto bacterial cells better
c. cause inflammation without tissue damage
d. trigger chemical release from natural killer cells
D
Which of the following would NOT be occurring during the phagocytic process?
a. Use of lysozyme, superoxide, acids, and digestive enzymes to destroy bacteria
b. Phagocytic cells locating bacteria based on chemicals they release
c. Digestion of the bacteria within the phagosome
d. Presence of lysosomes in the cytoplasm of the phagocytic cell
C
Which of the following level 2 defenses would NOT be useful to get rid of bacteria in his kidneys?
a. Inflammation
b. Complement activation
c. Membrane attack complex
d. Natural killer cells
D
When humoral immunity begins, cell-mediated immunity:
a. Slows down
b. Stops
c. Continues at the same time, but in different lymph nodes
d. Continues at the same time, in the same lymph nodes
D
Both B memory cells and T memory cells prevent a later infection of the same pathogen by:
a. Responding more quickly to the pathogen than virgin cells.
b. Becoming much more deadly to the pathogen than the cells were during the first exposure. c. Roaming the body releasing their secretions continuously, every day, so that the secretions are in the tissues waiting for the pathogen when it enters.
d. Directly becoming cytotoxic cells when the pathogen enters a second time.
A
During the body’s response to viruses, which of the following cells will act the same way in the body?
a. T-cytotoxic cells and neutrophils
b. Natural killer cells and T cytotoxic cells
c. Natural killer cells and helper T cells
d. Helper T cells and complement proteins
B
Which cells would be found in a lymph node at all times (not just when a pathogen is present)?
a. Naïve T helper cells (Th0)
b. T helper type 1 (Th1)
c. T helper type 2 (Th2)
d. Antigen presenting cells
A
Which TWO antibody types may be given by mothers to their babies?
IgG before birth, IgA after birth
Which molecule below is produced through humoral immunity, yet is considered one of your surface defenses (in terms of location
IgA
