Deck 15: The Immune System: Inflammation and Innate Immunity
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Deck 15: The Immune System: Inflammation and Innate Immunity
1
Which of the following is NOT a cardinal sign of inflammation?
A) heat
B) edema
C) pain
D) pus formation
A) heat
B) edema
C) pain
D) pus formation
D
2
All of the following are mechanisms to avoid digestion by phagocytes EXCEPT
A) bacterial capsules.
B) formation of phagolysosomes.
C) escape from the phagolysosome.
D) surviving inside the phagolysosome.
A) bacterial capsules.
B) formation of phagolysosomes.
C) escape from the phagolysosome.
D) surviving inside the phagolysosome.
B
3
Which of the following is NOT an example of a white blood cell (WBC)?
A) mast cell
B) macrophage
C) monocyte
D) erythrocyte
A) mast cell
B) macrophage
C) monocyte
D) erythrocyte
D
4
Macrophages arise from which of the following?
A) neutrophils
B) monocytes
C) eosinophils
D) basophils
A) neutrophils
B) monocytes
C) eosinophils
D) basophils
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5
Lysozyme is an example of a(n)
A) chemical barrier.
B) physical barrier.
C) defensin.
D) adaptive immune response.
A) chemical barrier.
B) physical barrier.
C) defensin.
D) adaptive immune response.
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6
All of the following are true regarding NK cells EXCEPT that they
A) are a type of lymphocyte.
B) have the ability to kill infected host cells.
C) destroy cells via phagocytosis.
D) release toxic substances that induce cellular death.
A) are a type of lymphocyte.
B) have the ability to kill infected host cells.
C) destroy cells via phagocytosis.
D) release toxic substances that induce cellular death.
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7
Once the inflammatory process is complete,neutrophils undergo
A) phagocytosis.
B) oxidative burst.
C) apoptosis.
D) opsonization.
A) phagocytosis.
B) oxidative burst.
C) apoptosis.
D) opsonization.
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8
Bacterial cells may be phagocytized and processed for presentation by
A) erythrocytes.
B) macrophages.
C) T cells.
D) mast cells.
A) erythrocytes.
B) macrophages.
C) T cells.
D) mast cells.
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9
Which of the following is NOT an example of a physical barrier to infection?
A) skin
B) lungs
C) defensins
D) mucosal membranes
A) skin
B) lungs
C) defensins
D) mucosal membranes
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10
Vasodilation promoted by the release of vasoactive factors from macrophages leads to which of the following?
A) stimulation of local nerve endings, causing pain
B) decrease of fluid accumulation at the site
C) loss of heat to the affected area
D) decrease of blood flow to the affected area
A) stimulation of local nerve endings, causing pain
B) decrease of fluid accumulation at the site
C) loss of heat to the affected area
D) decrease of blood flow to the affected area
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11
A consequence of chronic inflammation for the host is the formation of a
A) boil.
B) granuloma.
C) abscess.
D) cyst.
A) boil.
B) granuloma.
C) abscess.
D) cyst.
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12
An immune response that is always on and nonspecific is called ________ immunity.
A) innate
B) adaptive
C) humoral
D) cell-mediated
A) innate
B) adaptive
C) humoral
D) cell-mediated
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13
A child falls and suffers a deep cut on her leg.The cut went through her skin and she is bleeding.Which of the following defense mechanisms will participate in eliminating contaminating microbes?
A) skin normal flora
B) lysozyme
C) Langerhans cells
D) acidic skin secretions
A) skin normal flora
B) lysozyme
C) Langerhans cells
D) acidic skin secretions
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14
Which of the following statements is true?
A) Type I and type II interferons have the same effect on the body.
B) Interferon-alpha promotes phagocytosis.
C) Type II interferons increase MHC antigens on the surface of macrophages.
D) Interferon-gamma is a type I interferon.
A) Type I and type II interferons have the same effect on the body.
B) Interferon-alpha promotes phagocytosis.
C) Type II interferons increase MHC antigens on the surface of macrophages.
D) Interferon-gamma is a type I interferon.
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15
An example of oxygen-dependent killing is
A) lactoferrin.
B) superoxide ion.
C) lysozyme.
D) defensins.
A) lactoferrin.
B) superoxide ion.
C) lysozyme.
D) defensins.
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16
Penicillin interferes with bacterial cell walls.Which of the following interferes with the bacterial cell wall inside the phagolysosome?
A) lactoferrin
B) defensins
C) lysozyme
D) oxygen radicals
A) lactoferrin
B) defensins
C) lysozyme
D) oxygen radicals
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17
Small protein molecules secreted by macrophages are called
A) vasoactive factors.
B) cytokines.
C) selectins.
D) bradykinin.
A) vasoactive factors.
B) cytokines.
C) selectins.
D) bradykinin.
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18
A specialized macrophage located in skin-associated lymphoid tissue (SALT)is called
A) macrophage.
B) alveolar macrophage.
C) a dendritic cell.
D) a Langerhans cell.
A) macrophage.
B) alveolar macrophage.
C) a dendritic cell.
D) a Langerhans cell.
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19
Which of the following statements is true?
A) Macrophages interact with inhibitory glycoproteins to recognize self.
B) Phagocytosis is a specific immune response.
C) Opsonization prevents phagocytosis.
D) Capsules enhance phagocytosis.
A) Macrophages interact with inhibitory glycoproteins to recognize self.
B) Phagocytosis is a specific immune response.
C) Opsonization prevents phagocytosis.
D) Capsules enhance phagocytosis.
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20
The classical,alternative,and lectin complement pathways all converge with the activation of
A) C1.
B) C2.
C) C3.
D) C5.
A) C1.
B) C2.
C) C3.
D) C5.
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21
Which nonspecific defense mechanism is mismatched with its associated body structure or body fluid?
A) lysozyme-tears
B) acidic pH-stomach
C) keratin-skin
D) Langerhans cell-lungs
A) lysozyme-tears
B) acidic pH-stomach
C) keratin-skin
D) Langerhans cell-lungs
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22
All of the following is true regarding a fever EXCEPT that
A) the use of fever reducers helps to speed recovery.
B) a fever creates an unfavorable environment for microbial growth.
C) substances that cause a fever are known as pyrogens.
D) thermoregulation is maintained by the hypothalamus.
A) the use of fever reducers helps to speed recovery.
B) a fever creates an unfavorable environment for microbial growth.
C) substances that cause a fever are known as pyrogens.
D) thermoregulation is maintained by the hypothalamus.
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23
According to the table below,which type of interferon(s)work(s)to create an antiviral state in host cells?

A) Type 1
B) Type 2
C) Both
D) None

A) Type 1
B) Type 2
C) Both
D) None
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24
The figure below displays the process of phagocytosis.What would the result for the pathogen be if the lysosome did not fuse with the phagosome?

A) The pathogen would not be ingested by the phagocyte.
B) The pathogen would be digested in the phagosome.
C) The pathogen would survive unharmed inside the phagosome.
D) The pathogen would render the phagocyte paralyzed.

A) The pathogen would not be ingested by the phagocyte.
B) The pathogen would be digested in the phagosome.
C) The pathogen would survive unharmed inside the phagosome.
D) The pathogen would render the phagocyte paralyzed.
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25
Innate immunity includes all of the following EXCEPT
A) phagocytosis.
B) inflammation.
C) activation of complement.
D) production of antibody.
A) phagocytosis.
B) inflammation.
C) activation of complement.
D) production of antibody.
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26
The figure below highlights the process of complement activation.The classical pathway can be activated in two ways: antibody-dependent binding and by

A) C-reactive protein.
B) cytokines.
C) factor K.
D) lectin.

A) C-reactive protein.
B) cytokines.
C) factor K.
D) lectin.
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27
A series of 20 serum proteins that attack bacterial invaders is called
A) phagocytosis.
B) opsonization.
C) a complement.
D) an interferon.
A) phagocytosis.
B) opsonization.
C) a complement.
D) an interferon.
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28
Which of the following statements about the classical pathway of complement activation is FALSE?
A) The C3 protein is not involved in the classical pathway.
B) C1 is the first protein activated in the pathway.
C) Cleavage of complement proteins increases inflammation.
D) The classical pathway is activated by antibodies binding to bacterial cells.
A) The C3 protein is not involved in the classical pathway.
B) C1 is the first protein activated in the pathway.
C) Cleavage of complement proteins increases inflammation.
D) The classical pathway is activated by antibodies binding to bacterial cells.
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29
The complement cascade produces all of the following outcomes EXCEPT
A) creating pores in bacterial membranes.
B) increasing phagocytosis.
C) attracting white blood cells.
D) decreasing inflammation.
A) creating pores in bacterial membranes.
B) increasing phagocytosis.
C) attracting white blood cells.
D) decreasing inflammation.
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30
Which pathway is the alternative pathway in the figure below?

A) Pathway 1
B) Pathway 2
C) Pathway 3
D) none

A) Pathway 1
B) Pathway 2
C) Pathway 3
D) none
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31
TLRs attach to all of the following EXCEPT
A) flagellin.
B) lipopolysaccharide.
C) peptidoglycan.
D) cytokines.
A) flagellin.
B) lipopolysaccharide.
C) peptidoglycan.
D) cytokines.
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32
All of the following are components of the inflammatory process EXCEPT
A) extravasation.
B) release of cytokines.
C) antibody synthesis.
D) vasodilation.
A) extravasation.
B) release of cytokines.
C) antibody synthesis.
D) vasodilation.
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33
All of the following occur during a fever.What is the first step?
A) Prostaglandins are produced.
B) Pyrogenic cytokines bind to receptors on the hypothalamus.
C) Body temperature is reset to where the body thinks it is cool.
D) Involuntary muscle contractions generate heat.
A) Prostaglandins are produced.
B) Pyrogenic cytokines bind to receptors on the hypothalamus.
C) Body temperature is reset to where the body thinks it is cool.
D) Involuntary muscle contractions generate heat.
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34
Using the data from the differential white blood cell count table below,which patient profile displays a parasitic infection?

A) Patient 1
B) Patient 2
C) Patient 3
D) None

A) Patient 1
B) Patient 2
C) Patient 3
D) None
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35
A differential cell count is used to determine each of the following EXCEPT
A) the total number of white blood cells.
B) the numbers of each type of white blood cells.
C) the number of red blood cells.
D) the presence of cancer.
A) the total number of white blood cells.
B) the numbers of each type of white blood cells.
C) the number of red blood cells.
D) the presence of cancer.
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36
According to the table below,which type of interferons would induce an increase in MHC expression from host cells?

A) Type 1
B) Type 2
C) Both
D) None

A) Type 1
B) Type 2
C) Both
D) None
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37
The figure below shows the process of opsonization.This process belongs to which type of immunity?

A) innate
B) adaptive
C) complement
D) phagocytosis

A) innate
B) adaptive
C) complement
D) phagocytosis
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38
Gut-associated lymphoid tissue (GALT)includes all of the following EXCEPT
A) tonsils.
B) adenoids.
C) M cells.
D) alveolar macrophages.
A) tonsils.
B) adenoids.
C) M cells.
D) alveolar macrophages.
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39
The figure below highlights the mechanism of extravasation in the inflammatory process.What will be the consequence of neutrophils that do NOT produce integrins?

A) Neutrophils will bind to ICAM-1 and VCAM-1.
B) Neutrophils will be able to bind to the vascular wall.
C) Neutrophils will undergo extravasation.
D) Neutrophils will not lock onto endothelial adhesion molecules.

A) Neutrophils will bind to ICAM-1 and VCAM-1.
B) Neutrophils will be able to bind to the vascular wall.
C) Neutrophils will undergo extravasation.
D) Neutrophils will not lock onto endothelial adhesion molecules.
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40
A chill is a sign that
A) body temperature is falling.
B) body temperature is rising.
C) body temperature is not changing.
D) blood vessels are dilating.
A) body temperature is falling.
B) body temperature is rising.
C) body temperature is not changing.
D) blood vessels are dilating.
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41
Movement of neutrophils out of blood vessels and into infected tissue is called ________.
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42
CASE HISTORY
Bobby,an 11-year-old boy from Nebraska,suffered his entire life from recurring life-threatening infections caused mostly by the Gram-positive bacteria Staphylococcus aureus and Streptococcus pneumoniae.His infections included meningitis,osteomyelitis (bone infection),and arthritis caused by S.pneumoniae,as well as episodes of septicemia and osteomyelitis and recurrent boils caused by S.aureus.Tests to find a cause for these recurring infections were initially disappointing.The results of all standard immunological tests were normal,including T-cell lymphocyte responses,blood antibody levels,and antibody responses to injected proteins and polysaccharides.This means his adaptive immune system was functioning.The numbers of monocytes/macrophages in his blood were also normal.However,pro-inflammatory cytokine levels (indicators of innate immunity)measured during the latest infection were considerably lower than expected.Further tests proved that Bobby inherited an innate immune defect in Toll-like receptor signaling.Currently,there is no cure for this immunodeficiency.To stem the tide of infections,Bobby was placed on long-term,preventive antibiotic treatment.
How are NOD-like receptors similar to and different from Toll-like receptors? Would Bobby's immune deficiency manifest identically if he had a deficit in NLRs rather than TLRs?
Bobby,an 11-year-old boy from Nebraska,suffered his entire life from recurring life-threatening infections caused mostly by the Gram-positive bacteria Staphylococcus aureus and Streptococcus pneumoniae.His infections included meningitis,osteomyelitis (bone infection),and arthritis caused by S.pneumoniae,as well as episodes of septicemia and osteomyelitis and recurrent boils caused by S.aureus.Tests to find a cause for these recurring infections were initially disappointing.The results of all standard immunological tests were normal,including T-cell lymphocyte responses,blood antibody levels,and antibody responses to injected proteins and polysaccharides.This means his adaptive immune system was functioning.The numbers of monocytes/macrophages in his blood were also normal.However,pro-inflammatory cytokine levels (indicators of innate immunity)measured during the latest infection were considerably lower than expected.Further tests proved that Bobby inherited an innate immune defect in Toll-like receptor signaling.Currently,there is no cure for this immunodeficiency.To stem the tide of infections,Bobby was placed on long-term,preventive antibiotic treatment.
How are NOD-like receptors similar to and different from Toll-like receptors? Would Bobby's immune deficiency manifest identically if he had a deficit in NLRs rather than TLRs?
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43
CASE HISTORY
Constance,a seven-month-old female,suffered from recurrent infections since the age of two weeks.She was frequently admitted to the hospital for Staphylococcus aureus sepsis (blood infection),hepatosplenomegaly (enlarged liver and spleen),oral thrush caused by Candida albicans,and poor weight gain.Repeated treatments with different antibiotics only temporarily resolved her infections.Two days ago,her alarmed mother and father once again brought Constance to the emergency department at the University of Chicago Medical Center.Constance was lethargic,did not move much,and had a high fever.She also struggled for breath.Her blood work revealed high white blood cell counts (59,000/mm3;normal is 4,000-11,000)with a higher than normal level of neutrophils in her blood (neutrophilia).A chest X-ray showed inflammation in both lungs.It was no surprise,then,when the lab technician reported finding Staphylococcus aureus in Constance's blood.Her doctor ordered intravenous antibiotic therapy and was determined to find the cause of these repeated infections.He suspected a serious defect in Constance's immune system.Laboratory analyses found that her lymphocyte numbers,overall serum immunoglobulin (antibody)levels,and liver and kidney functions were all normal.No help there.Then flow cytometry analysis of surface proteins present on Constance's peripheral blood neutrophils revealed a complete absence of critically important membrane proteins.The doctor's heart sank.It was not good news.
Constance's neutrophils are unable to adhere to the walls of her blood vessels.In the normal process of inflammation,however,describe the next steps for these neutrophils.
Constance,a seven-month-old female,suffered from recurrent infections since the age of two weeks.She was frequently admitted to the hospital for Staphylococcus aureus sepsis (blood infection),hepatosplenomegaly (enlarged liver and spleen),oral thrush caused by Candida albicans,and poor weight gain.Repeated treatments with different antibiotics only temporarily resolved her infections.Two days ago,her alarmed mother and father once again brought Constance to the emergency department at the University of Chicago Medical Center.Constance was lethargic,did not move much,and had a high fever.She also struggled for breath.Her blood work revealed high white blood cell counts (59,000/mm3;normal is 4,000-11,000)with a higher than normal level of neutrophils in her blood (neutrophilia).A chest X-ray showed inflammation in both lungs.It was no surprise,then,when the lab technician reported finding Staphylococcus aureus in Constance's blood.Her doctor ordered intravenous antibiotic therapy and was determined to find the cause of these repeated infections.He suspected a serious defect in Constance's immune system.Laboratory analyses found that her lymphocyte numbers,overall serum immunoglobulin (antibody)levels,and liver and kidney functions were all normal.No help there.Then flow cytometry analysis of surface proteins present on Constance's peripheral blood neutrophils revealed a complete absence of critically important membrane proteins.The doctor's heart sank.It was not good news.
Constance's neutrophils are unable to adhere to the walls of her blood vessels.In the normal process of inflammation,however,describe the next steps for these neutrophils.
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44
Compare and contrast the innate and adaptive immune responses.
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45
Cytokines that have chemotactic properties are called ________.
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46
CASE HISTORY
Bobby,an 11-year-old boy from Nebraska,suffered his entire life from recurring life-threatening infections caused mostly by the Gram-positive bacteria Staphylococcus aureus and Streptococcus pneumoniae.His infections included meningitis,osteomyelitis (bone infection),and arthritis caused by S.pneumoniae,as well as episodes of septicemia and osteomyelitis and recurrent boils caused by S.aureus.Tests to find a cause for these recurring infections were initially disappointing.The results of all standard immunological tests were normal,including T-cell lymphocyte responses,blood antibody levels,and antibody responses to injected proteins and polysaccharides.This means his adaptive immune system was functioning.The numbers of monocytes/macrophages in his blood were also normal.However,pro-inflammatory cytokine levels (indicators of innate immunity)measured during the latest infection were considerably lower than expected.Further tests proved that Bobby inherited an innate immune defect in Toll-like receptor signaling.Currently,there is no cure for this immunodeficiency.To stem the tide of infections,Bobby was placed on long-term,preventive antibiotic treatment.
Which of the following best describes the portion of a pathogen recognized by Toll-like receptors?
A) specific antigens, particularly those on the surface of Gram-positive pathogens such as Streptococci
B) repeating nonself motifs such as peptidoglycan from Gram-positive organisms
C) major histocompatibility complex molecules on the surface of pathogenic cells
D) Toll-like receptors on the surface of pathogens, recognized by MAMPs on our immune cells
Bobby,an 11-year-old boy from Nebraska,suffered his entire life from recurring life-threatening infections caused mostly by the Gram-positive bacteria Staphylococcus aureus and Streptococcus pneumoniae.His infections included meningitis,osteomyelitis (bone infection),and arthritis caused by S.pneumoniae,as well as episodes of septicemia and osteomyelitis and recurrent boils caused by S.aureus.Tests to find a cause for these recurring infections were initially disappointing.The results of all standard immunological tests were normal,including T-cell lymphocyte responses,blood antibody levels,and antibody responses to injected proteins and polysaccharides.This means his adaptive immune system was functioning.The numbers of monocytes/macrophages in his blood were also normal.However,pro-inflammatory cytokine levels (indicators of innate immunity)measured during the latest infection were considerably lower than expected.Further tests proved that Bobby inherited an innate immune defect in Toll-like receptor signaling.Currently,there is no cure for this immunodeficiency.To stem the tide of infections,Bobby was placed on long-term,preventive antibiotic treatment.
Which of the following best describes the portion of a pathogen recognized by Toll-like receptors?
A) specific antigens, particularly those on the surface of Gram-positive pathogens such as Streptococci
B) repeating nonself motifs such as peptidoglycan from Gram-positive organisms
C) major histocompatibility complex molecules on the surface of pathogenic cells
D) Toll-like receptors on the surface of pathogens, recognized by MAMPs on our immune cells
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47
Peyer's patches are located within gut-associated lymphoid tissue (GALT).Explain the function of Peyer's patches in regard to their function in the immune system.
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48
Draw and label the process of phagocytosis.Be sure to speak to the main steps in the pathway (adherence,ingestion,and phagolysome formation/destruction).What would happen if an organism was able to avoid phagocytosis?
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49
Explain how each of the following avoids being killed by phagocytes:
a. Shigella dysenteriae
b. Salmonella typhimurium
c. Listeria monocytogenes
a. Shigella dysenteriae
b. Salmonella typhimurium
c. Listeria monocytogenes
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50
A clinical that counts the total number of white blood cells and identifies their various cell types is called a ________.
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51
Substances that cause fever are known as ________.
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52
There are two general types of interferons,type I and type II.Describe how type I interferons work to prevent the host from infection.
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53
Toll-like receptors recognize ________ on pathogenic microorganisms.
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