Unit 7 & 8 Lecture Flashcards
List 6 innate defenses that you might find in several different body systems
- Phagocytes
- Mucous membranes (barrier, 1st line of defense)
- Normal microbiota
- Interferon (immune cells)
- Complement
- Inflammation
Which 3 body systems have mucous membranes as a defense?
- Respiratory system
- Digestive system
- Reproductive system
Why is mucous and or mucous membranes an important part of the immune system? What line of defense?
- First line of defense (barrier) chemicals inhibit entities trying to enter out body
- Importance
a. protection
b. secretes chemicals
c. sloughing (shed and removes entities)
d. microbiota
has lysozymes, breaks down things
Phagocytes (macrophages, dendritic cells) line of defense?
Second
Which 4 body systems have normal microbiota as a defense?
- Skin
- Digestive
- Respiratory (nose)
- Reproductive (specifically female)
What role does the normal microbiota work in out immune system? What line of defense?
- First line of defense
- Role
a. competition against pathogens for resources (microbial antagonism)
b. stimulates second line of defense (antimicrobial substances) — trains the immune system
mutualistic relationship
What is the role of each virulence factor?
Coagulase: clotting of blood or fibrinogen, allows microorganisms to hide from phagocytes
Hemolysin: breaks down red blood cells releasing iron which bacteria uses as an iron source
Hyaluronidase & Collagenase: holds cells together in connective tissues, work together to degrade hyaluronic acid and collagen makes it easier for microorganism to invade tissues
Type III secretion systems: disrupts metabolism in eukaryotic cells and allows bacteria to attach, bacteria can then secrete infectious related proteins to promote infection and suppress the host immune response tells eukaryotic cells to increase uptake of microorganisms, decrease cells division of host cells and increase apoptosis (cell suicide) in macrophages and other cells
M protein: act as an adhesion, bind fibrinogen to prevent or inhibit phagocytosis, help with invasion into the body (S. pyogenes)
Streptokinase: digests blood clots or fibrin, allows microorganisms to invade the tissues in our body
Capsule: used to evade the immune system, and white blood cells to prevent phagocytosis
What are some ways that pathogens can avoid phagocytosis?
- Capsule
- Mycolic acid (waxy cell wall causes mycobacterium to grown inside macrophages, can hide)
- Leukocidins (pore forming toxin that destroys neutrophils, and other white blood cells (NK cells, cytotoxic T cells) degrade lysosome
- M proteins (bind to fibrinogen to act like adhesion, prevent phagocytosis and helping invasion)
If the adhesion gene in E.coli is mutated in such a way that make it ineffective, then what would be the effect?
Attachment is the first step
no attach -> no infect
Sweat glands in armpits
Armpits are moist neutral pH environment
bacteria grows best in this environment
Vulnerability to infection with impaired circulation
Circulatory problems disrupts the inflammation response, phagocytes and complement to get to area of infection
Innate immune response
First line of defense & second
Adaptive immune response
third line of defense
specificity
molecular recognition
activated by a specific pathogen
unresponsive to self
memory
Do responses work together?
Yes
Skin syndrome why is this a disease
first line) skin is barrier
breached
microorganisms can enter the body
(second line) could remove phagocytes which eat invaders
E. coli in colon/intestine vs. other parts of the body
it is no longer policed by the other members of the microbiome and will induce an immune response when it gets past the barrier
Microbiome importance
germ free vs have microbiota
benefits: mutualistic roles -> vitamin deficiency
have to provide essential nutrients
susceptible to real world environments
Toll like receptors (TLR’s)
Bind to pathogen associated molecular patterns (PAMP’s) (peptidoglycan, gram + bacteria)
(LPS of gram -, flagella
viruses- ss and ds RNA)
Are membrane proteins on phagocytes
What is the role of TLR’s?
Recognize general markers about “foreign attackers”
If TLR fails to recognize PAMP’s then what might happen?
phagocytes can’t recognize the PAMP’s
this disrupts the second line of defense which is part of the innate immune system and it fails
NOD proteins
another set or receptors for PAMP’s
located in the cytoplasm can trigger inflammation, apoptosis, and other innate responses
linked to Chrons
What is phagocytosis?
“eating by a cell”
second line of defense
non-specific response to a pathogen detected via TLR’s
a way to get rid of pathogens that have gotten past the first line of defense
List the steps in phagocytosis
chemotaxis (follow chemical trail to pathogen)
adhesion (complement protein or antibody)
ingestion (endocytosis)
maturation (phagolysosome acidic pH kills organisms)
killing
elimination (exocytosis)
Neutrophils kill by:
Phagocytosis
creating chemicals such as hypochlorite and hydrogen peroxide, nitric oxide to kill
creating NET’s (with antimicrobial peptides) from nuclear + cytoplasmic components then committing suicide releasing NETs, trapping/killing microbes
If a patients WBC count is high esp in eosinophils, then what is most likely the type of infection that the patient has?
Parasitic worm
or allergic reactions
High neutrophil counts? and total leukocytes
bacterial infection
High lymphocyte count?
viral infection
What is inflammation?
non specific response to tissue damage from various causes (burn, pathogens, etc.)
What is the purpose of inflammation ?
second line of defense
migration of phagocytes (to site of infection)
tissue repair
prevent spread of infection
increase blood flow
ex. prostaglandins
What are the 4 signs and symptoms of inflammation?
redness (rubor)
localized heat (calor)
swelling (edema)
pain (dolor)
chemicals:
histamine causes dilation in the blood vessels and causes redness and heat
prostaglandins and leukotrienes leak fluid from the blood into the tissues causing swelling or pain
Not a sign or symptom of inflammation
fever
4 main vasodilating chemical mediators
bradykinin
prostaglandins
leukotriene
histamines
What triggers inflammation besides tissue damage?
What is complement’s role in inflammation?
Triggers:
Complement: specific complement proteins involved in inducing inflammation response to some extent
C5a, C3a, and C4a
What would happen if you had a mutation that prevents production of bradykinin?
decrease in vasodilation which leads to decrease in inflammation response
decrease prostaglandins concentration
other inflammation routes:
could rely on leukotrienes released by macrophages to dilate veins
could rely on histamines released by basophils and mast cells to dilate arteries
Complement pathways leads to
1) inflammation
2) opsonization recruiting phagocytes and increasing phagocytosis
3) the formation of MAC’s which leads to cell lysis
Don’t produce C3? C5?
No C3 -> no functional complement cascade (no opsonization, inflammation, MAC formation) phagocytosis
No C5 -> no MACs; but can make C3a (inflammation) and C3b (opsonization)
C8 and C9 no synthesis
C3 and C5 inactivated
C8 and C9 no synthesis: prevent MAC formation which is effective against gram - bacteria
but complement proteins C3a C3b and C5b contributes to inflammation, opsonization, recruiting phagocytes. so this can serve to attack gram + and gram - bacteria
C3 and C5 inactivated: more susceptible to bacterial pathogens
No synthesis of C8
Can’t make MAC
but luckily she has C3a, C3b, and C5b that can induce inflammation, opsonization, and recruitment of phagocytes
Would MAC’s be effective against viruses?
MAC’s can be effective against an envelope virus
Pus from pimple from early or late infection?
dead tissue and dead leukocytes
neutrophils arrive at site of infection first, fight and then die
monocytes arrive then matures into macrophages, fight and keep fighting
lots of macrophages + few neutrophils = infection winding down
so late stages of infection
How do aspirin and ibuprofen act to reduce fever?
Should you take fever reducing drugs or let a fever run its course?
Act:
aspirin blocks COX enzymes that reduces prostaglandins production -> reduce body temperature
Drugs: low grade fever should run its course because the higher temperature may inhibit growth of pathogens
Unit 8: what comes to mind?
MHC I
MHC II
Antigens
Antibodies
Fab
Fc
BCR
TCR
CD4
CD8
Clonal selection
Clonal expansion
ADCC
Tc action
MHC I: what is happening inside
MHC II: what is happening on the outside of the cell
Antigens: immune response
Antibodies: Ig’s
Fab: binds to antigen
Fc: stem
BCR: made before encountering any antigen
TCR: MHC I and MHC II
CD4: found on T-helper cells
CD8: found on cytotoxic T cells
Clonal selection: when you make contact with the antigen or epitope
Clonal expansion: when you divide and differentiate after being selected or activated
ADCC: antibody dependent cell cytotoxicity, apoptosis
Tc action: effector cytotoxic T cells, apoptosis virus
Unit 8
MHC-I on B cells would be used to present _____
Endogenous antigens, peptides originating from within the cell
viral peptides or cancer peptides
Unit 8
T or F
Dendritic cells can be presenting more than one epitope at an given moment
True;
endogenous on MHC I and exogenous of MHC II
Unit 8
Dendritic cells present epitope to ____ cells
T- helper cells;
B cells relay their information to T helper cells because B cells can recognize foreign agents using their BCR’s and engulf them and process them into specific epitopes to present to T helper cells
Unit 8
B cells have which MHC?
MHC I: since they’re on all cells, nucleated cells, except RBC’s
and MHC II: because they have a role as an antigen presenting cell
Unit 8
B cells detect epitope with their ______
BCR
Unit 8
T or F
B cells can recognize their epitope before they ever encounter it
True;
B cells are randomly made through rearrangements of the genes that are involved in making parts of the BCR in hopes that one of the combinations will meet its “soulmate”
Unit 8
T helper cells have which 3 things on cell surface?
MHC I: because they are a nucleated cell and gives immune system an idea if any of our cells have problems
CD4: glycoproteins on a specific immune cell that helps coordinate the immune response by acting as a co-receptor on the T helper cell, immune cell marker
TCR: because this is how they recognize processed antigens or epitopes presented by MHC II on an antigen presenting cell
Unit 8
What is used by Th to present their normal epitopes?
MHC I: because MHC I are on all nucleated cell and it tells the immune system is that particular cell is functioning properly or not
Unit 8
What is used by Th to detect MHC II presenting epitope?
TCR: binds to the processed antigen or epitope presented to it by the antigen presenting cell via the antigen presenting cells MHC II
CD4: glycoproteins that acts and a co receptor, it will lock the TCR processed antigen MHC II into place
its like a second key for a safe deposit box
Unit 8
T or F
TLR can detect the same epitope as BCR
False;
the TLR only recognize general PAMP’s not specific to epitopes that the BCR does
Unit 8
Dendritic cells infected with a replicating virus present antigen on _____
MHC I: used to tell other immune cells its health status
Unit 8
If you looked on the cell surface of cells of the innate (eg. macrophages) vs. that of the adaptive (eg. B or T cells), then how could yo u tell the difference between the two?
In an innate immune response specifically like macrophages they will have Toll like receptors (TLR’s)
Adaptive immune response (B cells or T cells) will have BC’s or TCR’s depending upon which cell you’re looking at
Unit 8
B cells: Humoral immunity – B cells produce antibodies, which are a hallmark of humoral immunity.
Helper T cells: Cellular immunity – They assist other immune cells (both humoral and cellular) by releasing cytokines but are part of the cellular immune response.
Cytotoxic T cells: Cellular immunity – They directly attack and kill infected or abnormal cells, a key aspect of cellular immunity.
