1
Q
what are the main functions of the circulatory system
A
- transportation
- all substances essential for cellular metabolism including RBCs, digestive and waste products - regulation
- hormonal and thermo - protection
- from injury (clotting) and pathogens (immune)
2
Q
What are the constituents of blood
A
- plasma
- formed elements (includes RBCs and Buffy coat)
- RBCs are the most abundant blood cells
- buffy coat consists of WBCs and platelets
3
Q
what are the types of WBCs
A
- neutrophils
- eosinophils
- basophils
- lymphocytes
- monocytes
4
Q
what is hematopoiesis
A
the formation of blood cells from HSCs
- liver = major hematopoietic organ of the fetus
- bone marrow = major hematopoietic organ after birth
5
Q
differentiation of progenitor HSC
A
- progenitor HSC either becomes a common myeloid progenitor or common lymphoid progenitor
- common lymphoid progenitor will further divide into lymphocytes
- common myeloid progenitor will further divide into all other blood cells
6
Q
what is Erythropoiesis
A
- the production of RBCs in red bone marrow
- consists of stepwise differentiation of a progenitor cell - the erythroblast
- stimulated by the hormone erythropoietin
- during early stages the nucleus is expelled
7
Q
pathway of erythropoiesis
A
erythroblast - normoblast - reticulocyte - erythrocyte
8
Q
what is the significance of the nucleus being removed from erythrocytes
A
- RBCs rely on anaerobic glycolysis for ATP production
- they carry oxygen but we don’t want them to use it for energy since O2 has to reach other places
9
Q
structure of hemeglobin
A
- 4 globulin proteins each with a heme group containing a Fe atom
- 2 alpha and 2 beta chains
- the Fe atom combines with oxygen in the lungs and releases oxygen in the tissues
10
Q
Iron in hemegloblin
A
- each hemoglobin contains 4 iron atoms therefore can carry 4 O2
- the Fe atom in heme gets recycled from senescent RBCs by phagocytosis in the spleen and liver (hemolysis)
- this Fe travels in the blood to bone marrow attached to transferrin
- Fe can enter RBCs via receptor-mediated endocytosis
11
Q
what is transferrin
A
- a protein carrier that transports molecules such as iron through the blood
12
Q
what is leukopoiesis
A
- the formation of blood cells other than RBCs (so WBCs and platelets - leukocytes)
- uncommitted stem cells in the bone marrow give rise to these cells
13
Q
how lymphocytes generated
A
- lymphoid progenitor cells (different that progenitor cells of other blood cells)
14
Q
what do CDCs measure
A
- hematocrit: % total vol packed RBCs
- hemoglobin: O2 capacity of RBCs
- RBC count
- WBC count
15
Q
what does blood plasma contain
A
- water ( ~92%)
- dissolved solutes
- trace elements
- gasses
- organic molecules (~7%)
16
Q
what are the organic molecules found in blood plasma
A
Majority: plasma proteins (fibrinogen, globulins and albumins)
Minority: AAs, glucose, lipids, hormones, enzymes, etc.
17
Q
what are albumins
A
- plasma protein (55-60%)
- provide the osmotic pressure needed to draw water from the interstitial fluid into capillaries
- help to transport hormones
18
Q
What are globulins
A
- plasma protein
- alpha and beta transport lipids and fat-soluble vitamins
- gamma globulins are antibodies
19
Q
what is fibrinogin
A
- plasma protein (least abundant)
- important for clot formation
20
Q
which is the only plasma protein not produced in the liver and why
A
Gamma globulins
- since they are antibodies, they would respond to antigens in the liver (bad)
21
Q
What is the compliment pathway
A
- a defence system of serum proteins to kill a pathogenic cell
22
Q
what are the ways which pathogens can be attacked
A
- could be attacked by by innate immune cells (macrophages, neutrophils - OPSONIZATION)
- can be attacked by complement - a defence system of serum proteins
23
Q
Basis of the complement pathway
A
- there are 9 complement proteins (C1-9) that are inactive in plasma
- they become activated by the attachment of antibodies to antigens (bacteria)
- specific to the invader
24
Q
complement proteins can be subdivided into 3 categories…
A
- Recognition (C1)
- Activation (C4, 2 and 3)
- Attack (C5-9: complement fixation)
25
what is the common terminal reaction of all complement pathways
- generates the macromolecular membrane attack complex (MAC)
26
steps in the classical/lectin complement pathways
1.a) CLASSICAL is initiated by an antibody-antigen binding in the invading cells PM - activates C1
1.b) LECTIN is initiated when MBL binds mannose residues on the pathogen surface - activates C1-like
2. The C1(like) complex cleaves (activates) C4 and C2
3. active C4 and C2 bind to form C3 convertase
4. C3 convertase cleaves (activates) C3
5. active C3 binds to C3 convertase to form C5 convertase
6. C5 convertase cleaves (activates) C5
7. active C5 complexes with C6-9 to form the MAC
27
steps in the alternative compliment pathway
1. spontaneous hydrolysis (cleavage) of C3 will allow C3b to bind to microbial surfaces
2. Factor B will bind to the membrane-bound C3b
3. Factor D will cleave (activate) Factor B, which leads to the formation of C3 convertase
4. C3 convertase binds to active C3 to form C5 convertase
- the rest of the steps are the same as the classical path
28
what is the membrane attack complex (MAC)
- forms a pore inside the membrane of the pathogenic cell which allows fluid (water and Na+) to flow into it
- the cell will swell and lyse
29
how is the complement pathway innate (non-specific)
- it is ready to go and in the blood
30
how is the complement pathway adaptive (specific)
- specialized to pathogen (in the classical pathway antigen-antibody binding)
31
what happens to the complement fragments that don't become fixed into the membrane?
1. Chemotaxis: attract phagocytic cells (neutrophils, macrophages) to the site of complement activation
2. Opsonization: form bridges between the phagocyte and victim cell to facilitate phagocytosis
3. Stimulation of histamine release: C3a and C5a (cleaved off parts) can stimulate the release of histamine from mast cells and basophils, leading to vasodilation and more phagocytes to site of action
32
what is the function of the immune system
protects against pathogens, bacteria, etc.
- recognizes self from non-self
33
what is the microbiome
- the overall collection of microbes that resides inside humans or on our skin surface
- plays critical roles in the training and development of the immune system
34
commensal vs symbiotic bacteria
commensal: we provide them nutrients but they don't help us
symbiotic: we provide them nutrients and they help us with something in return
35
why are babies considered "microbe magnets"
for 2-3 years their microbiomes grow while their immune system develops
- have to learn how not to attack friendly bacteria
36
how can bacterial residents of the intestines influence influence neurons in the brain
- may infiltrate blood vessels for direct ride to the brain
- promote neuropod cells in the gut lining, stimulate the vagus nerve which connects to the brain
- indirectly activate enteroendocrine cells which send hormones throughout the body
- influence immune cells and inflammation which can affect the brain
37
shape of RBCs
- concave due to cytoskeleton
- flexible: swell in hypotonic medium and shrink in hypertonic medium
38
what is the total arterial O2 carrying capacity in the blood?
O2 bound to Hb + unbound O2
total = ~200mL O2/L blood
39
O2 saturation depends on location...
blood entering tissues: 200mL O2/L
blood leaving tissues: 155mL O2/L
- therefore, 45mL of O2 out of the 200mL is unloaded to the tissues
40
O2 saturation expressed in %...
- in systemic arteries 97% of Hb is in oxyhemoglobin form
- blood leaving the systemic veins has an oxyhemoglobin saturation of ~75%
- ~ 22% of the oxygen is unloaded to the tissues
41
the extent to which deoxyhemoglobin and hemoglobin exchange will happen depends on...
1. the partial pressure of O2 of the environment
2. the affinity (bond strength) between Hb and O2
- partially temperature as well
42
the oxyhemoglobin dissociation curve
- top of the curve shows arterial blood saturation
- Plato point shows how the % oxyhemoglobin decreases by ~22% as blood passes through the tissues from arteries to the veins
- the steepest point (from 0 and up) shows oxyhemoglobin that remains in venous blood (oxygen reserve) - doesn't get exchanged unless emergency
43
how does pH affect the oxyhemoglobin dissociation curve
- changing Hb conformation may affect O2 binding affinity
- when pH decreases, decreased Hb affinity for O2
- dissociation curve shifts right
- allows skeletal muscles receive more O2 when active than at rest
44
how does temperature affect the oxyhemoglobin dissociation curve
- changing Hb conformation may affect O2 binding affinity
- when temperature increases, decreased Hb affinity for O2
- dissociation curve shifts right
- allows skeletal muscles receive more O2 when active than at rest
45
how does a decreased pH affect O2 unloading to tissues
- body pH changes with activity - muscle fibres produce lactic acid which releases H+
- [H+] increase causes blood acidity to rise and the affinity of Hb for O2 decreases and more O2 is unloaded to tissues
46
what is the Bohr effect
- a shift in the Hb saturation curve due to a pH change
- shoot right = greater unloading of oxygen in tissues
47
oxyhemoglobin dissociation curve axis labels
y axis = % oxyhemoglobin saturation
x axis = PO2 (mmHg)
48
how does increased temperature affect unloading onto tissues
- Hb's affinity for O2 is decreased
- increasing the temperature weakens the bond between O2 and Hb allowing more to be unloaded to tissues
- curve shifts right
- similar effects to a decrease in pH
49
how do RBCs obtain energy through anaerobic metabolism of glucose
- during the glycolytic pathway, a side reaction occurs in the RBCs that result in the production of 2,3-DPG
50
how does low PO2 in RBCs (at high altitude) result in increased O2 unloading to tissues
- low PO2 = less oxyhemoglobin
- less inhibition of 2,3-DPG production
- increased 2,3-DPG
- lower affinity of hemoglobin for oxygen
- increased O2 unloading
DISSOCIATION CURVE SHIFTS RIGHT
51
what is 2,3-DPG
- a molecule that binds to deoxyhemoglobin to make it more stable
- more oxyhemoglobin unloads its O2 and be converted to deoxyhemoglobin at each PO2 - shifts curve
- similar effect to increased temperature
52
when does production of 2,3-DPG increase
- when oxyhemoglobin concentration decreases
- when lots of oxyhemoglobin is present, it inhibits the enzyme that produces 2,3-DPG
53
How do RBCs die
- removed from circulation after 120 days by phagocytic cells in the liver, spleen and bone marrow
- Hb gets broken down into heme and globulins
- the heme Fe from these RBCs will be recycled back to bone marrow (by transferrin)
- broken down heme becomes biliverdin then bilirubin in the spleen and liver
- bilirubin is transported to the liver bound to albumin
- bilirubin is then conjugated with glucuronic acid (now water-soluble)
- secreted into bile and eliminated in feces
54
What is Jaundice
- associated with high concentrations of bilirubin (from death of RBCs)
- physiological jaundice is the yellowing of the skin, sclera, and mucosal membranes
- common in babies - lack conjugating enzymes
- in adults associated with liver or gallbladder diseases
55
what is Thalassemia
inherited recessive disease, defect in hemoglobin
alpha: impaired synthesis of a-Hb (more common)
beta: impaired synthesis of B-Hb (come serious)
- excessive distraction of RBCs leading to anemia, growth abnormalities, iron overloading - can lead to heart failure
- iron is stored in places it shouldn't be (have ineffective erythropoiesis)
56
What is sickle cell anemia
- inherited recessive disease: production of HbS instead of HbA
- single amino acid substitution in the B-chain of Hb
- when Hb is deoxygenated HbS polymerizes into long fibres which creates a sickle shape
- reduces blood flow through organs and promotes hemolysis
57
What is unique about individuals that carry the sickle trait (heterozygotes)
- have 50-90% reduction in malarial parasite density compared to normal people
- malaria usually invades healthy RBCs, synthesizes proteins and cause hemolysis
- HbAS people with the parasite -> hypoxia -> sickling
-
58
characteristics of blood type O
- no A or B antigens
- both anti-A and anti-B antibodies
universal donors
59
characteristics of blood type AB
- both A and B antigens
- no anti-A and anti-B antibodies
universal acceptors
60
what is the basis for assigning blood types
- what will cause agglutination (clumping)
- occurs when type A RBCs are miked with anti-A antibodies
- same for type B and anti-B antibodies
61
why can type O blood be used for emergencies
- type O blood cells lack surface antigens so the recipient's antibodies will not attack the foreign blood
62
why can people with type AB blood accept any other blood type
- they lack anti-A and anti-B antibodies so they won't attack any antigens on new blood coming in
63
what is the Rh factor
- another component of blood type that assigns a negative or positive
- if Rh I is present the individual is positive (more common)
- If Rh is absent the individual is negative
64
what is the can rise with the Rh factor and pregnancy
If the mother is Rh+ and gives birth to an
Rh- baby
- fetal and maternal blood are separate so during pregnancy all is good
- AT BIRTH the mother may become sensitized and produce antibodies agains the Rh+ antigen
- Problem: in the next pregnancy these antibodies can cross the placenta and cause hemolysis of Rh+ RBCs in the fetus
- causes hemolytic disease of the newborn
65
Treatment to prevent hemolytic disease of the newborn
Rh- mom is injected with antibody preparation against Rh factor (RhoGAM) within 72 hours of birth of the Rh+ baby
- passive immunization that destroys fetal cells in circulation before they cause an immune response
66
what happens when there is injury to blood vessels
- activates a number of physiological mechanisms to primer hemostasis (stop bleeding)
- Breakage of the endothelial lining of a vessel exposes collagen to the blood which initiates 3 hemostatic mechanisms
67
at are the 3 hemostatic mechanisms to stop bleeding from injured blood vessels
1. vasoconstriction
2. formation of the platelet plug
3. production of a web of fibrin proteins that surround the platelet plug and stabilize it
68
In healthy blood vessels how are platelets repelled from each other and the blood vessel endothelium
- prostacyclin
- nitric oxide
- CD39 (PM: breaks down ADP since it promotes platelet aggregation)
69
what is the first step to forming the platelet plug
- the platelet PM binds to exposed collagen fibres via von Willebrand's factor (VWF)
70
what is the second step to forming the platelet plug
- after platelet collagen binding, we get degranulation of the platelets which releases ADP and thromboxane A2 (TXA2)
- platelets get shrivelled
71
what is the third step to forming the platelet plug (platelet release reaction)
- ADP and TXA2 attract new platelets that stick to the collagen
- the second layer of platelets release ADP and TXA2 which attracts more platelets to the site of injury
- platelet plug os formed
72
what do clotting factors do
- after being activated by platelets, clotting factors will convert fibrinogen (soluble plasma protein) to fibrin (insoluble)
- Platelets have membrane receptors for fibrinogen and fibrin to stabilize the platelet plug
73
what are blood clots composed of
platelets and fibrin with trapped RBCs
74
What is coagulation
a biochemical process that produces blood clots or thrombi
- the conversion of fibrinogen to fibrin can occur by the intrinsic or extrinsic pathway
75
Intrinsic coagulation pathway
- initiated by exposure to collagen in wound tissue or hydrophilic surfaces (like glass)
- the contact pathway activates factor XII (a protease) which goes on to activate a clotting factor cascade to eventually activate factor X
- from here converges with the extrinsic pathway
76
Extrinsic coagulation pathway
- initiated by tissue factor III (a membrane glycoprotein)
- when blood vessels are injured tissue factor becomes exposed to factor VII
- VII complex activates factor X
- from here converges with the intrinsic pathway
77
common coagulation pathway (where intrinsic and extrinsic converge)
- active factor X results in the conversion or prothrombin (inactive glycoprotein) into thrombin (the active enzyme)
- thrombin then converts fibrinogen to fibrin
78
what are the different effects of the intrinsic and extrinsic coagulation pathways
extrinsic: initiates clot formation in vivo (initiated by a chemical not part of the body)
intrinsic: amplifies the clotting cascade (all components are present in blood)
79
negative feedback of blood coagulation
ensures the clotting reaction doesn't spread systemically
- fibrin can bind thrombin to limit the positive feedback loop
- basophils and mast cells involved in tissue repair secrete heparin to prevent the formation of thrombin and limit the size of blood clot formation
80
how does clot dissolution happen
- plasminogen is converted to plasmin
- plasmin is an enzyme that digests fibrin and promotes the breakdown of clots
81
main categories of defence in the immune system
1. innate (non-specific): identifies self from non-self
2. adaptive (specific): identifies antigens and has good memory if exposed again
- some overlap between the mechanisms
82
what is an antigen
a molecule (usually on pathogen) that elects an immune response - particularly the production of antibodies
83
what are antibodies
immunoglobin proteins released by immune cells (plasma cells) in response to a foreign pathogen - only reacts to a specific antigen
84
which cells produce antibodies
plasma cells
85
characteristics of basophils
- lobed nucleus
- granules stain blue
- less than 1% of the WBCs found in circulation
- released as mature
86
characteristics of mast cells
- round nucleus
- similar to basophils but found in the tissues
- released as immature - mature once they enter a tissue
87
functions of basophils and mast cells
- release the anticoagulant heparin (slow blood clotting)
- releases histamine - binds to H1 receptors to induce bronchoconstriction and vasodilation
- releases serotonin, vasoactive molecules and pro-inflammatory cytokines
88
what does heparin do
anticoagulation protein that slows down blood clotting by preventing the prothrombin to thrombin conversion
89
how do basophils and mast cells provide an allergic reaction
when exposed to an allergen for the first time...
- you get an abnormal response from B cells - they differentiate into plasma cells and release IgE antibodies which go to the mast cell
when exposed a second time...
- the allergen is recognized by IgE antibodies on mast cells which cause it to release histamine
- the memory reves up this allergy response every time you are exposed
90
what are allergies
an abnormal immune response to antigens called allergens
B-cells: respond immediately
T-cells: respond a while after exposed
91
characteristics of neutrophils
- immature: sausage-shaped nuclei (band cells)
- mature: segmented nucleus with 2-5 lobes
- granules stain pink (neutral)
- most abundant leukocyte in the body (54-62% of WBCs)
92
what are the functions of neutrophils
- PHAGOCYTOSIS: ingest and kill bacteria, remove foreign substances (via lysosomes) as blood flows and chemically inactivates them (innate)
- clear remnants of cells that died by apoptosis
- early first responders to site of infection
93
extravasation of neutrophils
- neutrophil in the blood binds to a receptor on the vessel wall which causes it to spread and penetrate out of the vessel
- once out of the vessel it releases its bacteria via phagocytosis
94
characteristics of eosinophils
- bilobed nucleus
- granules stain red
- 1-3% of WBCs
95
functions of eosinophils
- help detoxify foreign substances
- secrete enzymes to dissolve clots
- FIGHT PARASITIC INFECTIONS
- e.g. attach to antibody-coated parasites and release substances from granules to damage/kill
96
characteristics of monocytes and macrophages
- agranulocytes (no granules)
- 2-3x larger than RBCs
- nuclear shape varies
- 3-6% of WBCs
- monocytes are present in the blood (immature)
- macrophages are present in tissues (mature)
- both have phagocytic function
97
from monocyte to macrophage
- monocytes are precursors for tissue macrophages
- they circulate the bloodstream for a day then distribute to various tissues and differentiate into distinct macrophage populations
98
how do macrophages replenish themselves
- when they recognize pathogenic signals they become activated and secrete pro-inflammatory cytokines
- cytokines attract neutrophils (chemotaxis)
- neutrophils attack blood monocytes
- monocytes are transformed into tissue-specific macrophages
99
true or false: macrophages are larger and more effective at ingesting bacteria than neutrophils
true
- able to ingest 100 bacteria/lifespan and also remove debris
100
role of monocytes and macrophages in atherosclerosis
- monocytes are recruited to the intima and may differentiate into macrophages
- the macrophages can accumulate lipids and cholesterol derivatives to form foam cells in the subintima
- foam cells secrete pro-inflammatory cytokines and chemicals leading to atherosclerosis
101
characteristics of lymphocytes
- makes up 25-33% of WBCs: most in tires, small amount in circulation
- nucleus nearly fits the cell
- includes Natural killer, B and T cells
- function is to provide SPECIFIC immune response
102
types and structure of antibodies
5 types: IgG, IgA, IgM, IgD, IgE
- IgG is the most common
- consist of 2 heavy and 2 light polypeptide chains
103
what type of immunity is each lymphocyte involved in
NK cells: innate immunity
T-lymphocytes: cell-mediated immunity
B-lymphocytes: humoral immunity
104
what makes NK cells part on non-specific (innate) immunity
- lack receptor diversity of specific antigens (T-cells)
- inherit receptors that allow them to target malignant cancer cells and viral cells
- act in initial stages of immunity prior to T-cell differentiation
105
how do Natural killer (NK) cells kill
1. NK cells are activated by cytokines (IFN-a and IFN-B)
2. activated NK cells then release INF-y to activate macrophages and other immune cells and enhance the immune response
3. they destroy target cells by cell-cell contact (NOT attack pathogen itself, attack the CELL with the virus)
- perforin then enters the PM of victim cells and polymerize to form a pore - osmotic distruction
- granzymes activate caspases involved in apoptosis
106
What are T-cells
- have specific receptors that antigens can be presented to by antigen present cells (APCs) to activate T-cells
107
2 main types of T-cells
Cytotoxic T-cells (CD8+): cause cell-mediated destruction of specific victim cells
Helper T-cells (CD4+): enhance the immune response of B-cells AND cytotoxic T-cells
108
what are antigen-presenting cells (APCs)
- cells that present the antigen on MHC class II molecules to helper T-cells
- concentrated at sites where antigen-bearing microorganisms may enter
- dendritic cells (main), macrophages, monocytes and B-cells are all APCs
109
what are Major histocompatibility complexes (MHCs) class I and II
MHC II: display antigens from outside the cell to helper T-cells
- found mostly on dendritic cells
- trigger helper-T cell response
MHC I: displays "self" antigens, or antigens from within the cell (but can present foreign antigens that entered the cell)
- found on all nucleated cells
-
110
how do APCs do their job
- APCs engulf proteins by pinocytosis
- move the proteins to the cell surface
- present the antigen on MHC class II molecules to helper T-cells
*MHC class II ONLY present to APCs
111
what happens if a helper T-cell encounters an APC with a foreign antigen fragment on the MHC-II
- the T-cell binds the foreign antigen and becomes an activated helper T-cell
- the activated helper T-cell will then secrete cytokines to activate cytotoxic T-cells (CD8) and interact with B-cells to enhance the immune response
112
Summary of how Helper T-cells function
APC presents the antigen on MHC II to helper T-cells. This causes the helper T cell to release cytokines which are a signal for "help" from B-cells and cytotoxic T-cells
113
lymphocyte signalling in lymphatic vessels
- APCs migrate through vessels to lymph tissues and secrete chemokine to attract helper T-cells
- T and B cells concentrate in the lymphatic system
- dendritic cells can process antigens (release cytokines) to activate T-cells which can then travel through the lymphatic system to the site of infection and do its job
114
how do helper T-cells interact with B-cells
- helper T-cells can stimulate B-cells to divide and form more plasma cells (antibody-secreting cells) and memory cells
- this enhances humoral immunity
115
How do infected tissue cells attract cytotoxic T-cells
- the infected tissue cell can put up an MHC class I molecule the cell surface to present the viral antigen
- this message goes to the cytotoxic T-cells (CD8)
- the cytotoxic T-cells bind to MCH I + antigen
116
how do cytotoxic T-cells kill pathogens
- T-cells recognize the antigen presented on the MHC class I molecule, bind to it and directly kill it
- the interaction of cytotoxic T-cells with antigen/MHC II, in combination with IL-2 secreted by helper-T cells stimulates proliferation of those cytotoxic T-cells
117
what is the mechanism that T-cells and NK cells use to kill target cells
- once these cells are activated they release perforin to form pores into the target cell plasma membranes and release GRANZYMES through the perforin channels which sets off apoptosis
118
what is the clonal selection theory of B-cells
B-cells have to "inherit" the ability to produce particular antibodies
- any given B-cell can produce only one type of antibody with specificity to one antigen but they are naive - their inherited specificity is reflected in their antibody receptors
- exposure to their antigen stimulates the B-cell to divide many times until a large population of genetically identical clones is produced
119
first phase of Humoral immunity: Clonal expansion
- antigen binds to the antibody receptor
- as clones develop 2 things happen
1. some become short-lived plasma cells - produce antibodies
2. others become memory cells that continue to reproduce
120
second phase or humoral immunity: Memory cells
- only the memory cells persist, but when re-exposed to the appropriate antigen they rapidly expand to produce more plasma cells (to produce more antibodies) and even more memory cells
121
difference in response time or primary and secondary humoral response
primary: first time meeting the antigen - slower and weaker response
secondary: second time meeting the antigen - clones and memory cells lead to a stronger and faster response
122
how do vaccines work
- expose you to a small amount of a dead virus so that your body can produce antibodies against it. If you ever come into contact with the real thing your body will be able to protect you against the antigen
123
what are autoimmune diseases
- the body attacks its own cells, can't distinguish self from non-self
124
how does your immune system react if you aren't allergic to an antigen
- allergen stimulated cell mediated helper T-cells to secrete IFN-y and IL-2
125
how do B-cells react if you are allergic to an antigen
- allergen stimulates humoral helper T-cells to secrete IL-4 and IL-13
- these stimulate B-cells and plasma cells to secrete IgE antibodies instead of IgG
- IgE binds to mast cells and basophils to stimulate release of histamine to produce an immune reaction
126
how do T-cells react to allergens
- T-cells produce delayed hypersensitivity since reaction is mediated by a cell-mediated T-cell response rather than antibodies
127
how does the Alzheimer's drug Lecanemeb work
- works with the body's immune system to clear amyloid protein buildup from the brain by breaking it down
BIOM 3200
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