Exam 1 Flashcards
The first line of defense against microorganisms that infect the body is referred to as _____.
innate immunity
Which of the following pairs is mismatched?
a. innate immunity: highly specialized defenses
b. secondary immune response: immunological memory
c. hematopoiesis: bone marrow
d. phagocytosis: uptake and killing of microbes
e. lymphocyte recirculation: continuous transport between blood and lymph
innate immunity: highly specialized defenses
When effector lymphocytes secrete _____, an inflammatory response ensues.
Cytokines
The thin layer of cells that makes up the interior lining of the blood vessels is called the _____.
Endothelium
Identify the incorrect statement regarding hematopoiesis.
a. Hematopoiesis is a continuous process that occurs throughout one’s lifetime.
b. The location for hematopoiesis differs with age.
c. Self renewal is necessary to replenish the supply of hematopoietic stem cells.
d. Most hematopoiesis occurs in the bone marrow after birth.
e. Leukocytes, but not erythrocytes, must go through hematopoiesis in order to develop.
Leukocytes, but not erythrocytes, must go through hematopoiesis in order to develop.
Effector cells that secrete antibodies are known as _____.
Plasma Cells
The _____ is (are) the lymphoid organ(s) that filter(s) the blood.
Spleen
_____ cells persist long after an individual has been vaccinated.
Memory
In most cases, adaptive immune responses rely on the initial activation of _____ in secondary lymphoid tissue:
B-Cells
All of the following statements are characteristic of secondary immune responses except _____.
a. Secondary immune responses are activated when primary immune responses fail to completely eradicate an infection.
b. Secondary immune responses are restricted to adaptive immune responses.
c. Memory cells are activated rapidly during secondary immune responses.
d. Secondary immune responses are orders of magnitude greater than primary immune responses.
e. During a secondary immune response to a booster vaccine, it is possible to experience a primary
immune response to an unrelated vaccine component encountered for the first time.
Secondary immune responses are activated when primary immune responses fail to completely eradicate an infection.
An example of an antimicrobial peptide that protects epithelial surfaces from pathogens is _____.
Defensin
Which of the following statements regarding neutrophils is false?
a. Neutrophils are mobilized from the bone marrow to sites of infection when needed.
b. Neutrophils are active only in aerobic conditions.
c. Neutrophils are phagocytic.
d. Neutrophils form pus, which comprises dead neutrophils.
e. Dead neutrophils are cleared from sites of infection by macrophages.
Neutrophils are active only in aerobic conditions.
Primary lymphoid tissues are the sites where lymphocytes _______, whereas secondary lymphoid tissues are the sites where lymphocytes _______.
develop and mature; become stimulated
Which of the following pairs is mismatched?
a. lymphocytes: innate immune response
b. natural killer cell: kills virus-infected cells
c. macrophage: phagocytosis and killing of microorganisms
d. erythrocyte: oxygen transport
e. eosinophil: defense against parasites.
lymphocytes: innate immune response
A term generally used to describe all white blood cells is _____.
leukocytes
Examples of granulocytes include all of the following except:
a. neutrophil
b. monocyte
c. basophil
d. eosinophil
e. All of the above are examples of granulocytes.
monocyte
The most abundant type of leukocyte in human peripheral blood is the _____.
Nuetrophill
Which of the following statements is false?
a. During human development, hematopoiesis takes place at different anatomical locations.
b. The hematopoietic stem cell gives rise to white blood cells, but a different stem cell is the progenitor
of red blood cells.
c. Hematopoietic stem cells are self-renewing.
d. Platelets participate in clotting reactions to prevent blood loss.
e. Megakaryocytes do not circulate and reside only in the bone marrow.
The hematopoietic stem cell gives rise to white blood cells, but a different stem cell is the progenitor
of red blood cells.
Vaccination is best described as prevention of severe disease by _______.
prior exposure to an infectious agent in an attenuated or weakened form
Which of the following explains why immunity to influenza may appear to be relatively short-lived?
New influenza variants able to escape previous immunity appear regularly.
Which of complement pathway(s) becomes activated soonest after an initial infection?
The alternative pathway
_____ are soluble complement fragments that mediate localized and systemic inflammatory responses.
anaphylatoxins
Although activation of the three different pathways (alternative, lectin, and classical) of complement activation converge involves different components, the three pathways converge on a common enzymatic reaction referred to as complement fixation. The reaction involves the cleavage of C3 into C3a and C3b and the covalent bonding of C3b to the pathogen surface.
true
The enzyme responsible for cleaving C3 into C3a and C3b is called C3 convertase, and it differs in composition depending on the particular complement pathway. The classical and lectin pathways use the classical C3 convertase (C3bBb), whereas the alternative pathway uses the alternative convertase (C4b2a).
False -
The steps that take place when a bacterium is opsonized via C3b:CR1 interaction between the bacterium and a resident macrophage in tissues are the following: (1) The CR1 on the macrophage can bind to C3b that is coating a bacterial surface after complement activation, and the macrophage then engulfs the bacterium through receptor-mediated endocytosis. (2) The macrophage membrane invaginates and forms an intracellular vesicle called a phagosome. (3) The phagosome fuses with a lysosome to form a phagolysosome, where toxic mediators and degradative enzymes are localized. (4) The bacterium is destroyed.
True
Regarding the three pathways of complement: (1) The classical pathway requires an activating surface of a pathogen, which stabilizes complement components. (2) The lectin pathway requires the presence of mannose-binding lectin, an acute-phase protein made by the liver in response to interleukin-6 (IL-6) (secreted by activated macrophages) and which accumulates in plasma during infection. (3) The alternative pathway is activated in two ways, either by the presence of antibody bound to the surface of the microorganism (for example IgM bound to lipopolysaccharide of Gram- negative bacteria) or by the presence of C-reactive protein bound to a bacterium.
False
Only the classical pathway is considered part of the adaptive immune response because of the requirement for antibody. However, the classical pathway is also considered part of innate immunity because of the ability of C-reactive protein, an acute-phase protein, to activate it. The other two pathways are considered part of innate immunity because they are initiated independently of antibody.
True
Which of the following does not accurately describe complement components?
a. soluble proteins
b. made by the spleen
c. located in extracellular spaces
d. some function as proteases once activated
e. activated by a cascade of enzymatic reactions
Made by spleen
A genetic deficiency of C3 leads to a type of immunodeficiency characterized by recurrent and severe infections. C3 is a key element in the initiation of the complement cascade in all three pathways of complement activation, namely the alternative, lectin, and classical pathways. Its cleavage into C3a and C3b occurs early in the complement cascade. C3a acts as an inflammatory mediator and recruits inflammatory cells to the site of infection. C3b becomes fixed to the pathogen surface and facilitates the opsonization of pathogens by phagocytes and the assembly of complement components for perforation of the pathogen membrane. In the absence of C3, all three pathways of complement activation would be arrested and extracellular pathogens would escape immune detection until adaptive immune mechanisms develop fully many days later.
True
Which of the following is the membrane-bound form of C3 convertase of the alternative pathway of complement activation?
C3bBb
The alternative C3 convertase on pathogen cell surfaces is formed by spontaneous hydrolysis of C3 without cleavage exposes its highly reactive thioester bond, forming iC3. Factor B binds to iC3, is cleaved by factor D, and consequently releases a small fragment called Ba. The larger fragment, Bb, remains associated with iC3 to form iC3Bb, a soluble C3 convertase, which cleaves C3 into C3a and C3b. The reactive thioester bond of C3b is attacked by R–OH and R–NH2 groups on the surface of the pathogen, where it becomes anchored and binds to factor B. Factor D then cleaves factor B, releasing fragment Ba and forming C3bBb on the pathogen surface. The alternative C3 convertase on pathogen cell surfaces is stabilized by Factor P (properdin) binds to C3 convertase (C3bBb) bound to the pathogen surface, and inhibits the proteolytic degradation of C3bBb. This stabilizes the C3 convertase and enhances the rate of C3b deposition on the pathogen surface.
True
During the formation of the membrane-attack complex, it is important to expose the hydrophobic sites of C7 and C8, because these sites enable anchoring of these two complement components into the membrane of the pathogen. Once anchored in the membrane, the hydrophobic site of C8 facilitates C9 polymerization, which completes the formation of the membrane-attack complex.
True
The plasma proteins that counteract the activity of factor P by inactivating C3 convertase through the cleavage of C3b are _____.
factor H and factor I
The membrane-bound proteins on human cells that dissociate and inactivate alternative C3 convertase to avoid complement activation are _____.
decay-accelerating factor and membrane cofactor protein
Anaphylatoxins C3a and C5a contribute physiologically to inflammation during complement activation. G-protein-coupled receptors for the anaphylatoxins C3a and C5a are found on phagocytes, mast cells, and the endothelial cells of blood vessel walls. Anaphylatoxin bound to mast cells causes them to degranulate, releasing inflammatory mediators such as histamine and leading to increased vascular permeability. Through their action on endothelial cells, anaphylatoxins exert vasoactive effects on blood vessels, contributing to increased vascular permeability and increased blood flow, which facilitate the extravasation of plasma proteins, such as complement proteins and antibodies, and the recruitment of cells to infected tissues through increased adherence and chemotaxis. Phagocytic activity is enhanced by anaphylatoxins, which bring about increased levels of CR1 and CR3 and microbicidal activity. All these activities enhance inflammation.
True