BIO 669 Exam 1 Questions And Answers With 100%
Correct Answers (GRADED A+) Latest Update
2024/2025.
Cytokines - ANSWER signaling molecules that regulate innate or adaptive immunity that are
responsible for activating other cells and regulating the inflammatory response; they help stimulate
the response to infection and tissue damage by guiding lymphocytes and leukocytes toward the area
of damage, stimulating healing, and increasing or decreasing inflammation; there are multiple types of
these cells, each with their own different roles in the inflammatory response
Chemokines - ANSWER type of cytokines that are synthesized by many cells in response to
proinflammatory cytokines and induce chemotaxis to promote phagocytosis and wound healing; e.g.
monocyte/macrophage chemotactic proteins, macrophage inflammatory proteins, and neutrophils
Cells that synthesize chemokines - ANSWER macrophages, fibroblasts, endothelial cells
Interleukins - ANSWER type of cytokine made by white blood cells (produced primarily by
macrophages and lymphocytes) in response to stimulation of pattern recognition receptors (PRRs) or
by other cytokines; there are many different types of these cytokines
Interleukin-1 - ANSWER pro-inflammatory cytokine (activates and enhances inflammatory
response) that induces many acute phase proteins and is an endogenous pyrogen
Endogenous pyrogen - ANSWER molecule that stimulates fever by resetting the hypothalamic
set point, setting the body's temperature set point higher so that initially you feel cold as your body
temperature as risen, but then as the fever breaks and your temperature goes back down, you feel hot
Interleukin-10 - ANSWER anti-inflammatory cytokine that is primarily produced by
lymphocytes and suppresses the growth of other lymphocytes and the production of proinflammatory
cytokines of macrophages, which leads to a down-regulation of both inflammatory and acquired
immune response
Tumor necrosis factor-alpha - ANSWER cytokine secreted by macrophages in response to
PAMPs and toll-like receptor recognition that is a strong inflammatory mediator and a key regulatory
molecule for inflammation; induces a multitude of proinflammatory effects
Effects of tumor necrosis factor-alpha - ANSWER - Induces fever by acting as an endogenous
pyrogen (also produces IL-1 and IL-6, which can also both induce/increase fever)
- Increases synthesis of inflammatory serum proteins
- Causes muscle wasting (cachexia) and intravascular thrombosis
- Can cause granuloma formation
TNF-A and biologic agents - ANSWER tumor necrosis factor alpha is the target of many
biologic agents that try to diminish the immune response when it is overexpressed/out of proportion;
since TNF-A enhances inflammation, drugs that target TNF-A will ramp DOWN the inflammatory
,response; e.g. used in treatment of rheumatoid arthritis, psoriatic arthritis, Crohn's disease
(autoimmune conditions where immune system is too active)
Interferon - ANSWER cytokine that protects against viral infections and modulate the
inflammatory response
Interferons alpha and beta - ANSWER Type I interferons that are produced and released by
virally infected host cells in response to viral double-stranded RNA and other viral PAMPs to protect
neighboring healthy cells; don't kill viruses directly
Interferon gamma - ANSWER Type II interferon that is produced primarily by lymphocytes to
activate macrophages, which results in increased capacity to kill infectious agents like viruses (and
bacteria); key cytokine; increases microbicidal activity of macrophages
- Plays important role in how well you can clear infection
Mast cells - ANSWER white blood cells that are the most important cellular activator of the
inflammatory response; cellular bags of granule
- located in the loose connective tissues close to blood vessels (skin, digestive lining, and respiratory
tract)
- their granules contain histamine, cytokines, serotonin, and chemotactic factors that when released,
can lead to a significant inflammatory response
- mediator for pollen, allergic rhinitis, hay fever, etc.
Degranulation of mast cells - ANSWER most common activation of mast cell chemical release
- the release of the contents of the mast cell granules (histamine, serotonin, chemotactic factors,
cytokines, etc.) in response to a receptor being engaged that allows for the stimulation of mast cells
- this receptor is frequently an antibody acting as a receptor (e.g. IgE)
- IgE binds to mast cells, causing them to release and produce a very strong, immediate, acute immune
response (e.g. allergic asthma and other allergic responses)
Basophils - ANSWER granulocyte found in the BLOOD that most likely act the same way as
mast cells
- least prevalent granulocyte
- primary role unknown
Synthesis - ANSWER method of mast cell release in which mast cells produce and release new
mediators in response to a stimulus
Histamine - ANSWER chemical stored in mast cells and is released during degranulation that is
a vasoactive amine (many vascular effects) and causes:
- temporary, rapid constriction of the large blood vessels
- dilation of the postcapillary venules (resulting in increased blood flow into the mcirocirculation)
, - increased vascular permeability due to the retraction of endothelial cells lining the capillaries
- allows fluid and proteins to leave the vasculature, leaking out into tissues, which causes redness,
swelling, pain, loss of function, etc. (inflammation!)
Why do antihistamines not reduce all inflammation? - ANSWER Antihistamines can reduce
some inflammation (the vascular effects caused by histamine), but histamine is not the only mediator
released by mast cells. These mediators also have inflammatory effects, so they cannot treat all of the
effects of inflammation, only the ones caused by histamine.
Neutrophil chemotactic factor and eosinophilic chemotactic factor of anaphylaxis - ANSWER
chemotactic factors contained in mast cell granules and released during degranulation that attract
eosinophils and neutrophils, promoting inflammation
Phopholipase A2 - ANSWER mast cell synthesis can stimulate the production of this enzyme,
which takes the phospholipids from many cell membranes an dconverts them into arachidonic acid
and platelet activating factor
Arachidonic acid - ANSWER molecule that is broken down/metabolized into cyclooxygenase
and 5-lipoxygenase; these metabolites play key roles in inflammation
Cyclooxygenase - ANSWER enzyme that produces prostaglandins from arachidonic acids;
targeted by NSAIDs to stop inflammation due to prostaglandins (e.g. pain, inflammation)
Prostaglandins - ANSWER fatty acids that are produced from arachidonic acid via
cyclooxygenase that cause increased vascular permeability, neutrophil chemotaxis, and pain by direct
effects on nerves
5-lipooxygenase - ANSWER enzyme that produces leukotrienes from arachidonic acid
Leukotrienes - ANSWER - produced from arachidonic acid from 5-lipooxygenase
- play a role in anaphylaxis
- have vascular effects (increased vascular permeability), like histamine
- cause smooth muscle contraction (like histamine)
- affect the bronchial tree and mediate some of the responses seen in asthma
Why don't NSAIDs treat asthma/swelling in bronchi? - ANSWER NSAIDs do not affect swelling
in the bronchi (i.e. in asthma) because bronchial swelling is caused by leukotrienes, NOT
prostaglandins! So, NSAIDs could actually make bronchial swelling worse because when they block
cyclooxygenase from converting arachidonic acid into prostaglandins, they allow more archidonic acid
to be converted into leukotrienes! = increased bronchial swelling
H1 receptor - ANSWER one of the receptors histamine can bind to that is proinflammatory
and located in the smooth muscle cells of the bronchi
- when histamine binds to these receptors, it causes hay fever, swelling, inflammation, drainage
Correct Answers (GRADED A+) Latest Update
2024/2025.
Cytokines - ANSWER signaling molecules that regulate innate or adaptive immunity that are
responsible for activating other cells and regulating the inflammatory response; they help stimulate
the response to infection and tissue damage by guiding lymphocytes and leukocytes toward the area
of damage, stimulating healing, and increasing or decreasing inflammation; there are multiple types of
these cells, each with their own different roles in the inflammatory response
Chemokines - ANSWER type of cytokines that are synthesized by many cells in response to
proinflammatory cytokines and induce chemotaxis to promote phagocytosis and wound healing; e.g.
monocyte/macrophage chemotactic proteins, macrophage inflammatory proteins, and neutrophils
Cells that synthesize chemokines - ANSWER macrophages, fibroblasts, endothelial cells
Interleukins - ANSWER type of cytokine made by white blood cells (produced primarily by
macrophages and lymphocytes) in response to stimulation of pattern recognition receptors (PRRs) or
by other cytokines; there are many different types of these cytokines
Interleukin-1 - ANSWER pro-inflammatory cytokine (activates and enhances inflammatory
response) that induces many acute phase proteins and is an endogenous pyrogen
Endogenous pyrogen - ANSWER molecule that stimulates fever by resetting the hypothalamic
set point, setting the body's temperature set point higher so that initially you feel cold as your body
temperature as risen, but then as the fever breaks and your temperature goes back down, you feel hot
Interleukin-10 - ANSWER anti-inflammatory cytokine that is primarily produced by
lymphocytes and suppresses the growth of other lymphocytes and the production of proinflammatory
cytokines of macrophages, which leads to a down-regulation of both inflammatory and acquired
immune response
Tumor necrosis factor-alpha - ANSWER cytokine secreted by macrophages in response to
PAMPs and toll-like receptor recognition that is a strong inflammatory mediator and a key regulatory
molecule for inflammation; induces a multitude of proinflammatory effects
Effects of tumor necrosis factor-alpha - ANSWER - Induces fever by acting as an endogenous
pyrogen (also produces IL-1 and IL-6, which can also both induce/increase fever)
- Increases synthesis of inflammatory serum proteins
- Causes muscle wasting (cachexia) and intravascular thrombosis
- Can cause granuloma formation
TNF-A and biologic agents - ANSWER tumor necrosis factor alpha is the target of many
biologic agents that try to diminish the immune response when it is overexpressed/out of proportion;
since TNF-A enhances inflammation, drugs that target TNF-A will ramp DOWN the inflammatory
,response; e.g. used in treatment of rheumatoid arthritis, psoriatic arthritis, Crohn's disease
(autoimmune conditions where immune system is too active)
Interferon - ANSWER cytokine that protects against viral infections and modulate the
inflammatory response
Interferons alpha and beta - ANSWER Type I interferons that are produced and released by
virally infected host cells in response to viral double-stranded RNA and other viral PAMPs to protect
neighboring healthy cells; don't kill viruses directly
Interferon gamma - ANSWER Type II interferon that is produced primarily by lymphocytes to
activate macrophages, which results in increased capacity to kill infectious agents like viruses (and
bacteria); key cytokine; increases microbicidal activity of macrophages
- Plays important role in how well you can clear infection
Mast cells - ANSWER white blood cells that are the most important cellular activator of the
inflammatory response; cellular bags of granule
- located in the loose connective tissues close to blood vessels (skin, digestive lining, and respiratory
tract)
- their granules contain histamine, cytokines, serotonin, and chemotactic factors that when released,
can lead to a significant inflammatory response
- mediator for pollen, allergic rhinitis, hay fever, etc.
Degranulation of mast cells - ANSWER most common activation of mast cell chemical release
- the release of the contents of the mast cell granules (histamine, serotonin, chemotactic factors,
cytokines, etc.) in response to a receptor being engaged that allows for the stimulation of mast cells
- this receptor is frequently an antibody acting as a receptor (e.g. IgE)
- IgE binds to mast cells, causing them to release and produce a very strong, immediate, acute immune
response (e.g. allergic asthma and other allergic responses)
Basophils - ANSWER granulocyte found in the BLOOD that most likely act the same way as
mast cells
- least prevalent granulocyte
- primary role unknown
Synthesis - ANSWER method of mast cell release in which mast cells produce and release new
mediators in response to a stimulus
Histamine - ANSWER chemical stored in mast cells and is released during degranulation that is
a vasoactive amine (many vascular effects) and causes:
- temporary, rapid constriction of the large blood vessels
- dilation of the postcapillary venules (resulting in increased blood flow into the mcirocirculation)
, - increased vascular permeability due to the retraction of endothelial cells lining the capillaries
- allows fluid and proteins to leave the vasculature, leaking out into tissues, which causes redness,
swelling, pain, loss of function, etc. (inflammation!)
Why do antihistamines not reduce all inflammation? - ANSWER Antihistamines can reduce
some inflammation (the vascular effects caused by histamine), but histamine is not the only mediator
released by mast cells. These mediators also have inflammatory effects, so they cannot treat all of the
effects of inflammation, only the ones caused by histamine.
Neutrophil chemotactic factor and eosinophilic chemotactic factor of anaphylaxis - ANSWER
chemotactic factors contained in mast cell granules and released during degranulation that attract
eosinophils and neutrophils, promoting inflammation
Phopholipase A2 - ANSWER mast cell synthesis can stimulate the production of this enzyme,
which takes the phospholipids from many cell membranes an dconverts them into arachidonic acid
and platelet activating factor
Arachidonic acid - ANSWER molecule that is broken down/metabolized into cyclooxygenase
and 5-lipoxygenase; these metabolites play key roles in inflammation
Cyclooxygenase - ANSWER enzyme that produces prostaglandins from arachidonic acids;
targeted by NSAIDs to stop inflammation due to prostaglandins (e.g. pain, inflammation)
Prostaglandins - ANSWER fatty acids that are produced from arachidonic acid via
cyclooxygenase that cause increased vascular permeability, neutrophil chemotaxis, and pain by direct
effects on nerves
5-lipooxygenase - ANSWER enzyme that produces leukotrienes from arachidonic acid
Leukotrienes - ANSWER - produced from arachidonic acid from 5-lipooxygenase
- play a role in anaphylaxis
- have vascular effects (increased vascular permeability), like histamine
- cause smooth muscle contraction (like histamine)
- affect the bronchial tree and mediate some of the responses seen in asthma
Why don't NSAIDs treat asthma/swelling in bronchi? - ANSWER NSAIDs do not affect swelling
in the bronchi (i.e. in asthma) because bronchial swelling is caused by leukotrienes, NOT
prostaglandins! So, NSAIDs could actually make bronchial swelling worse because when they block
cyclooxygenase from converting arachidonic acid into prostaglandins, they allow more archidonic acid
to be converted into leukotrienes! = increased bronchial swelling
H1 receptor - ANSWER one of the receptors histamine can bind to that is proinflammatory
and located in the smooth muscle cells of the bronchi
- when histamine binds to these receptors, it causes hay fever, swelling, inflammation, drainage
