Exam 3 Practice Set 2 Flashcards by Kim Wong

Extracellular bacteria are optimally killed by:
A Macrophages.
B Complement.
C Antibody.
D Macrophages plus complement.
E Macrophages plus antibody plus complement.

E Macrophages plus antibody plus complement.

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Opsonization of bacteria occurs through coating bacteria just with:
A C3b
B C8
C Membrane attack complex D F(ab')2 IgG
E IgM

A C3b

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Extracellular bacteria try to avoid killing by:
A Activating neutrophils.
B Accelerating complement activation.
C Synthesizing capsules.
D By deviating complement deposition to the cell membrane.
E Limiting variation in their antigens.

D By deviating complement deposition to the cell membrane.

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CR1 complement receptors on phagocytic cells bind:
A Factor H
B Factor I
C C3d
D Only inactive C3b (iC3b) 
E C3b

E C3b

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iC3b binds to:
A Factor H
B C5 convertase 
C CR1
D CR2
E C3 convertase

C CR1

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Individuals lacking C8 or C9 are more prone to infection with the following type of bacteria:
A Haemophilus influenzae. 
B Bacillusanthrax.
C Vibrio cholerae.
D Neisseria.
E Listeria monocytogenes.

D Neisseria.

Ideally, the membrane attack complex generated by complement activation lyses bacteria, especially Neisseria species that are particularly susceptible to lysis because of their thin cell walls, and complement byproducts stimulate inflammatory responses by recruiting and activating leukocytes.

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Neutrophil chemotaxis is mediated by:
A. C5b
B. IL-8
C. C3a
D. CCL2
E. E-selectin

B. IL-8

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The membrane attack complex consists of:
A OH
B Colicins
C C3b3b, Bb
D C5b,6,7,8,9
E Properdin

D C5b,6,7,8,9

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C3b:
A Is chemotactic.
B Is an anaphylatoxin.
C Opsonizes bacteria.
D Directly injures bacteria. 
E Is the inactive form of C3.

C Opsonizes bacteria.

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IgG antibodies:
A Are the earliest class to appear in an immune response.
B Are normally dimeric in mucosal secretions.
C Remain of low affinity.
D Inhibit antibody responses through the Fc gamma receptor FcgRIIB1 on B-cells.
E Augment antibody responses through the Fc gamma receptor FcgRIIB1 on B-cells.

D Inhibit antibody responses through the Fc gamma receptor FcgRIIB1 on B-cells.

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Dendritic cells can be driven from a resting state to an activated state by the T-cell surface molecule:
A TCR
B CD40L
C CD28
D B7
E CD40

B CD40L

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Which is the first of the following genes to be upregulated subsequent to T-cell activation:
A Transferrin receptor 
B Cytokine receptor
C Cytokine
D c-Myc
E VLA-1

D c-Myc

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Cytokines always act:
A By binding to specific receptors.
B In an autocrine fashion.
C At long range.
D Antagonistically with other cytokines
E Synergistically with other cytokines

A By binding to specific receptors.

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A cytokine receptor which is a member of the hematopoietic receptor family is:
A IL-8 receptor
B IFN gamma receptor
C TNF (TNF-alpha) receptor
D IL-1 receptor
E IL-2 receptor

E IL-2 receptor

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IFN-gamma and TNF (TNF alpha) can act synergistically:
A To downregulate expression of MHC class I
B Because IFN-gamma downregulates expression of TNF receptors
C To upregulate expression of MHC class II
D Because they both bind to the same receptor
E Because they cross-link IFN-gamma and TNF beta receptors

C To upregulate expression of MHC class II

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Which of the following is characteristically produced by the Th2 CD4 cells which provide help for antibody production, but not by Th1 cells?
A IFN-gamma
B Lymphotoxin (TNF-beta)
C GM-CSF
D IL-4
E IL-1

D IL-4

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In the germinal center, B-cells become memory cells under the influence of:
A CD40
B CD23
C IL-1 alpha
D IL-4
E TGF beta

A CD40

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High affinity B-cell clones in mammals are usually generated by:
A Somatic hypermutation
B Expression of high affinity precursors in the virgin (naive) B-cell population
C Class switching
D Apoptosis
E Gene conversion

A Somatic hypermutation

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Prior to class switching, B-cells express:
A IgA alone
B IgA and IgG
C IgM and IgD
D IgD alone
E No surface Ig

C IgM and IgD

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The specificity of antibody secreted by a B-cell may not be the same as that of the surface Ig of the clonal parent because of:
A Class switching
B Somatic hypermutation
C Allelic exclusion
D Alternative splicing
E Different heavy:light pairing

B Somatic hypermutation

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In the thymic medulla, the majority of gamma delta T-cells are:
A CD4+CD8+
B CD4+CD8-
C CD4-CD8+
D CD4-CD8-
E Surface Ig+

D CD4-CD8-

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The major long term source of a foreign antigen in the body is:
A Anti-idiotype
B Complexes on the surface of follicular dendritic cells
C Antigen bound to the surface of B-cells
D Antigenic peptides in the groove of MHC molecules
E There are no long term sources of foreign antigen in the body

B Complexes on the surface of follicular dendritic cells

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Cytokines:
A Are usually around 150-200 kDa
B Have glycosyl phosphatidylinositol (GPI) anchors
C Can be pleiotropic
D Generally act at long range
E Produce very stable long-lived messenger RNA

C Can be pleiotropic

Pleiotropy occurs when one gene influences two or more seemingly unrelated phenotypic traits. Consequently, a mutation in a pleiotropic gene may have an effect on some or all traits simultaneously. An example is phenylketonuria, a human disease that affects multiple systems but is caused by one gene defect. (Wikipedia)

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Th1 cell secrete:
A CD4
B IL-4
C IL-5
D IL-6
E IFN-gamma

E IFN-gamma

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``` Which one of the following cytokines can mediate release of acute phase proteins from the liver? A IL-10 B TGF-beta C IL-6 D IL-12 E IL-8 ```

C IL-6

``` Which of the following is not a feature of germinal center B-cells: A Immunoglobulin gene class switching B Apoptosis C Initial VDJ rearrangement D Somatic hypermutation E Proliferation ```

C Initial VDJ rearrangement

Low amounts of antigen: A Produce low affinity antibodies B Do not influence the affinity of antibodies C Produce high affinity antibodies D Affect the avidity but not the affinity of antibodies E Preferentially induce class switching

C Produce high affinity antibodies Because the BCR recognizes an epitope of the native protein with high affinity, specific B cells bind and present the antigen much more efficiently (i.e., at much lower concentrations) than do other B cells not specific for the antigen. This is why B cells specific for an antigen respond preferentially to that antigen, compared with other cells.

The level of antigen: A Is unrelated to the intensity of the immune response B Is related to the intensity of the immune response C Never has an effect on the response to a T-independent antigen D Has no effect on the concentration of MHC bound processed antigen E Is constant in the extracellular fluid

B Is related to the intensity of the immune response

Memory T-cells: A Are continuously produced directly from naive progenitors B Express high levels of CD44 C Are only present in primary immune responses D Switch from an alpha beta to gamma delta T cell receptor E. Express germ line Ig V genes

B Express high levels of CD44

``` Activated memory T-cells can be distinguished from naive T-cells on the basis of expression of: A T-cell receptor B Immunoglobulin C MHC class II molecules D CD45RO E IL-1 ```

D CD45RO In humans, most naive T cells express the 200-kD isoform of the surface molecule CD45 called CD45RA (for “restricted A”) and most memory T cells express a 180-kD isoform of CD45 called CD45RO

``` A major factor regulating the adaptive immune response is: A The neutrophil B Complement membrane attack complex C C-reactive protein D Antigen concentration E Haptoglobin ```

D Antigen concentration

Antigenic competition: A Involves competition between T-cell epitopes for the MHC groove B Involves competition for available soluble antibodies C Is unrelated to the concept of dominant and subdominant epitopes D Can only occur with cryptic epitopes E Refers to the differential immunogenicity of the carbohydrate and protein moieties in a glycoprotein

A Involves competition between T-cell epitopes for the MHC groove

``` Negative feedback on adaptive B-cell responses is mediated by: A Antigen specific IgM B Antigen specific IgG C Just antigen neutralization D Fc gamma receptors on macrophages E F(ab') 2 anti-mu ```

B Antigen specific IgG

``` An example of an anti-apoptotic molecule is: A Bcl-2 B TRAIL C Bax D FADD E Caspase 8 ```

A Bcl-2

``` Suppression of Th2 by Th1 cells may be mediated by: A IL-1 B IL-3 C IL-4 D GM-CSF E IFN-gamma ```

E IFN-gamma

``` Cells bearing MHC class I plus peptide are targets for specific: A B-cells B Cytotoxic T-cells C Th1 cells D Th2 cells E Interdigitating dendritic cells ```

B Cytotoxic T-cells

Natural antibodies: A Are mostly IgG B Are mostly high affinity autoantibodies C Are produced spontaneously by B-1 B-cells D Are acquired by transplacental passage from the mother E Do not arise in thymectomized mice

C Are produced spontaneously by B-1 B-cells TI antigens also contribute to the generation of natural antibodies, which are present in the circulation of normal individuals and are apparently produced without overt exposure to pathogens. Most natural antibodies are low-affinity anti-carbohydrate antibodies, postulated to be produced by peritoneal B-1 cells stimulated by bacteria that colonize the gastrointestinal tract and by marginal zone B cells in the spleen. A remarkably large proportion of the natural antibodies in humans and mice are specific for oxidized lipids, including phospholipid head groups such as lysophosphatidylcholine and phosphorylcholine, which are found on bacterial membranes and on apoptotic cells but are not exposed on the surface of healthy host cells. Some experimental evidence indicates that the natural antibodies specific for these phospholipids provide protection against bacterial infections and facilitate the phagocytosis of apoptotic cells. The anti-ABO blood group antibodies, another example of natural antibodies, recognize certain glycolipids (blood group antigens) expressed on the surface of many cell types, including blood cells. Blood group antigens and antibodies are important for blood transfusions and transplantation but not for host defense.

``` Natural antibodies are: A IgG B IgE C IgD D IgM E IgA ```

D IgM

``` Which of the following is never related to poor MHC-linked immune response: A Defective T-cell repertoire B T-suppression C Inadequate antigen processing D Poor binding of peptide epitope to MHC E Defective V gene rearrangement ```

E Defective V gene rearrangement

IgG antibodies: A Are the earliest class to appear in an immune response B Are normally dimeric in mucosal secretions C Remain of low affinity D Inhibit antibody responses through Fc gamma receptor FcgRIIB1 on B-cells E Augment antibody responses through the Fc gamma receptor FcgRIIB1 on B-cells

D Inhibit antibody responses through Fc gamma receptor FcgRIIB1 on B-cells

T-cell mediated suppression: A Is always mediated by CD8+ T-cells B Is always mediated by CD4+ T-cells C Can be due to Th2 cells suppressing Th1 by IL-4 or IL-10 D Does not exist E Cannot transfer suppression to another animal

C Can be due to Th2 cells suppressing Th1 by IL-4 or IL-10

High antibody responses linked to MHC class II genes: A Are independent of MHC haplotype B Depend on good T-helper cell recognition of class II/antigen peptide complex C Depend on defective antigen presentation by MHC molecules D Result from tolerance to MHC/self-peptide complexes E Require suppression of Th2 cells

B Depend on good T-helper cell recognition of class II/antigen peptide complex

Cell-mediated immunity: A Is unaffected by exercise B Is unaffected by surgical trauma C I unaffected by diet D May be grossly impaired by protein-calorie malnutrition E Is unaffected by protein-calorie malnutrition

D May be grossly impaired by protein-calorie malnutrition

``` NKT cells: A Have rearranged TCR alpha beta genes B Express a gamma delta TCR C Have rearranged immunoglobulin genes D Lack NK1.1 E Can only recognize antigens presented by CD1 ```

A Have rearranged TCR alpha beta genes The TCR α chains expressed by a subset of NKT cells have limited diversity, and, in humans, these cells are characterized by a V region encoded by a rearranged Vα24-Jα18 gene segment, with little or no junctional diversity, associated with one of three β chains.

CD8+ T-cells bearing an alpha beta TCR: A Always co-express CD4 B Will have expressed terminal deoxynucleotidyl transferase (TdT) during early development C Do not require the presence of a thymus for their development D Recognize native antigen E Recognize MHC class II molecules

B Will have expressed terminal deoxynucleotidyl transferase (TdT) during early development

Alpha beta T-cells: A Initially express a pre-TCR bearing an invariant pre-beta chain. B Arise earlier in ontogeny than gamma delta T-cells. C Can be CD4+CD8– but not CD4–CD8+. D Unlike gamma delta T-cells, do not rely on Notch-1 signaling pathways during their development E Express RAG-1 and RAG-2 at the pre-T stage

E Express RAG-1 and RAG-2 at the pre-T stage

``` Allelic exclusion is not seen for: A T-cell receptor alpha genes B T-cell receptor beta genes C T-cell receptor gamma genes D T-cell receptor delta genes E T-cell receptor gene D region segments ```

A T-cell receptor alpha genes These signals also inhibit further rearrangement of the TCR β chain locus largely by limiting accessibility of the other allele to the recombination machinery. This results in β chain allelic exclusion (i.e., mature T cells express only one of the two inherited β chain alleles). As in pre-B cells, it is not known what, if any, ligand the pre-TCR recognizes. p. 193

``` Positive selection in the thymus is mediated by: A Thymic epithelial cells B Macrophages C Dendritic cells D B-cells E T-cells ```

A Thymic epithelial cells

``` Which immunoglobulin class crosses the placenta to provide a high level of passive immunity at birth? A IgA B IgD C IgE D IgG E IgM ```

D IgG

``` Which of the following molecules does not belong to the Ig gene superfamily? A Immunoglobulin B T-cell receptor C Beta2-microglobulin D Thy-1 E LFA-1 ```

E LFA-1 Integrin! Thy-1 is part of Ig superfamily as well as TCRs and beta2-microglobulin.

``` LFA-1 pairs with: A LFA-3 B P-selectin C ICAM-1 D Sialyl Lewisx E Beta2 integrin molecules ```

C ICAM-1

``` Toxins are neutralized by: A Complement B Antibody C Toxoids D PGE2 E Proteolytic enzymes ```

B Antibody

Secretory IgA protects external mucosal surfaces by: A Triggering mast cells B Recruiting phagocytic cells C Preventing microbial adherence to the mucosa D Binding to epithelial cells E Its secretory piece

C Preventing microbial adherence to the mucosa

The streptococcal pyrogenic exotoxins SPE, A, B, and C: A. Are M proteins B. Cause post-streptococcal autoimmune disease C. Produce high titers of anti-streptolysin O D. Have hyaluronidase activity E. Are superantigens

E. Are superantigens

Classical NK cells: A Have rearranged T-cell receptor genes B Are unaffected by IFN-alpha C Are more active against targets with unregulated MHC class I D Can kill certain virally-infected cells E Can kill all virally-infected cells

D Can kill certain virally-infected cells

Inflammation is a defensive reaction initiated by infection or tissue injury which first causes: A Upregulation of adhesion molecules on endothelial cells and leukocytes B Chemotaxis C IL-8 release D Phagocytosis E Bacterial killing

A Upregulation of adhesion molecules on endothelial cells and leukocytes

``` Extracellular bacteria are killed by: A Secreting exotoxins B Impeding inflammatory reactions C Phagocytosis and complement D Toxin neutralization E C-reactive protein ```

C Phagocytosis and complement

``` The mucosal surfaces of the body are initially protected by free: A IgG B IgM C IgE D Secretory IgA E IgD ```

D Secretory IgA

Bacteria growing within macrophages are killed by: A Complement B Reactive oxygen and nitrogen intermediates C Antibody D Cytotoxic T-cells E Directly by cytokines released from Th1 cells

B Reactive oxygen and nitrogen intermediates

``` Protection against worm infestations is particularly associated with an increase in: A IgD B IgE C IgG D IgA E IgM ```

B IgE

``` Which of the following does not protect body surfaces: A Skin B Mucus C Gastric acid D Salivary amylase E Gut microflora ```

D Salivary amylase

``` Pattern recognition receptors (PRR) include: A LPS B PAMPs C Lipoteichoic acid D Lectin-like molecules E Unmethylated CpG sequences ```

D Lectin-like molecules

``` The mononuclear phagocyte system does not include: A Monocytes B Kupffer cells C Kidney mesangial cells D Lymph node medullary macrophages E Endothelial cells ```

E Endothelial cells

``` A polymorphonuclear neutrophil (PMN): A Is a bone marrow stem cell B is closely similar to a mast cell C contains microbicidal cytoplasmic granules D is not a professional phagocytic cell E has granules which stain with eosin ```

C contains microbicidal cytoplasmic granules

``` Which of the following is not produced following activation of the NADPH oxidase microbicidal pathway? A O2- B O2 C H2O2 D NO E OH ```

D NO

``` Neutrophil defensins are: A Anti-toxins B Oxygen-dependent C Enzymes D Glycolipids E Peptide antibiotics ```

E Peptide antibiotics

``` The TLR9 pattern recognition receptor recognizes: A CpG motifs B Gram + peptidoglycan C Mycobacterial lipoarabinomannan D Gram - LPS E dsRNA ```

A CpG motifs

``` Complement component C3 is cleaved by: A C3b B C3bBb C Factor B D Factor D E Factor H ```

B C3bBb

``` Acute inflammation characteristically involves: A Constriction of arterioles B Capillary endothelial cell enlargement C Influx of macrophages D Influx of mast cells E Influx of neutrophils ```

E Influx of neutrophils

``` Lysozyme: A Is a cytoplasmic organelle B Activates complement C Is a proteolytic enzyme D Splits peptidoglycan E Is released by mast cells ```

D Splits peptidoglycan

``` Which of the following is not an acute phase protein: A Serum amyloid P component B Chondroitin sulfate C C-reactive protein D Mannose binding lectin E Fibrinogen ```

B Chondroitin sulfate

``` A complement component which is strongly chemotactic for neutrophils is: A C9 B C5a C C3 D C3b E C5b ```

B C5a

``` Acute inflammation can be initiated by: A Mast cell activation B Influx of neutrophils C An increase in vascular permeability D C3 E Lysozyme ```

A Mast cell activation These changes include increased blood flow into the tissue due to arteriolar dilation, increased adhesiveness of circulating leukocytes to the endothelial lining of venules, and increased permeability of the capillaries and venules to plasma proteins and fluid. All of these changes are induced by cytokines and small-molecule mediators initially derived from resident cells in the tissue, such as mast cells, macrophages, and endothelial cells, in response to PAMP or DAMP stimulation. As the inflammatory process develops, the mediators may be derived from newly arrived and activated leukocytes and complement proteins.