Basic Immunology: Functions and Disorders of the Immune System 4th Edition Test Bank

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Abbas: Basic Immunology,4thEditionChapter 01:Introduction to the Immune SystemTest BankMULTIPLE CHOICE1.The principal function of the immune system is:A.Defense against cancerB.Repair of injured tissuesC.Defense against microbial infectionsD.Prevention of inflammatory diseasesE.Protection against environmental toxinsANS: CThe immune system has evolved in the setting of selective pressures imposed bymicrobial infections. Although immune responses to cancer may occur, the concept that“immunosurveillance” against cancer is a principal function of the immune system iscontroversial. Repair of injured tissues may be a secondary consequence of the immuneresponses and inflammation. Although the immune system has regulatory features thatare needed to prevent excessive inflammation, prevention of inflammatory diseases is nota primary function. The immune system can protect against microbial toxins, but itgenerally does not offer protection against toxins of nonbiologic origin.2.Which of the following infectious diseases was prevented by the first successfulvaccination?A.PolioB.TuberculosisC.SmallpoxD.TetanusE.RubellaANS: CIn 1798, Edward Jenner reported the first intentional successful vaccination, which wasagainst smallpox in a boy, using material from the cowpox pustules of a milkmaid. In1980, smallpox was reported to be eradicated worldwide by a vaccination program.Effective vaccines against tetanus toxin, rubella virus, and poliovirus were developed inthe 20th century and are widely used. There is no effective vaccine againstMycobacterium tuberculosis.3.A previously healthy 8-year-old boy is infected with an upper respiratory tract virusfor the first time. During the first few hours of infection, which one of the followingevents occurs?A.The adaptive immune system responds rapidly to the virus and keeps the viralinfection under control.B.The innate immune system responds rapidly to the viral infection and keeps theviral infection under control.

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C.Passive immunity mediated by maternal antibodies limits the spread of infection.D.B and T lymphocytes recognize the virus and stimulate the innate immuneresponse.E.The virus causes malignant transformation of respiratory mucosal epithelial cells,and the malignant cells are recognized by the adaptive immune system.ANS: BThe innate immune response to microbes develops within hours of infection, well beforethe adaptive immune response. B and T lymphocytes are components of the adaptiveimmune response, and they would not be able to respond to a newly encountered virusbefore the innate immune response. An 8-year-old boy would no longer have maternalantibodies from transplacental passive transfer and is unlikely to be breast-feeding, whichis another potential source of maternal antibodies. Malignant transformation takes monthsor years to develop.4.Which of the following is a unique property of the adaptive immune system?A.Highly diverse repertoire of specificities for antigensB.Self-nonself discriminationC.Recognition of microbial structures by both cell-associated and soluble receptorsD.Protection against viral infectionsE.Responses that have the same kinetics and magnitude on repeated exposure to thesame microbeANS: AHighly diverse repertoires of specificities for antigens are found only in T and Blymphocytes, which are the central cellular components of the adaptive immune system.Both the innate and the adaptive immune systems use cell-associated and solublereceptors to recognize microbes, display some degree of self-nonself discrimination, andprotect against viruses. On repeated exposure to the same microbe, the adaptive immuneresponse becomes more rapid and of greater magnitude; this is the manifestation ofmemory.5.Antibodies and T lymphocytes are the respective mediators of which two types ofimmunity?A.Innate and adaptiveB.Passive and activeC.Specific and nonspecificD.Humoral and cell-mediatedE.Adult and neonatalANS: DBoth B and T lymphocytes are principal components of adaptive immunity. Blymphocytes produce antibodies, which are the recognition and effector molecules ofhumoral immune responses to extracellular pathogens. T cells recognize and promoteeradication of intracellular pathogens in cell-mediated immunity. Passive and activeimmunity both can be mediated by either B or T lymphocytes.Specific immunityisanother term for adaptive immunity. Both B and T lymphocytes participate in adultadaptive immunity but are still developing in the neonatal period.

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6.A standard treatment of animal bite victims, when there is a possibility that theanimal was infected with the rabies virus, is administration of human immunoglobulinpreparations containing anti–rabies virus antibodies. Which type of immunity would beestablished by this treatment?A.Active humoral immunityB.Passive humoral immunityC.Active cell-mediated immunityD.Passive cell-mediated immunityE.Innate immunityANS: BHumoral immunity is mediated by antibodies. The transfer of protective antibodies madeby one or more individuals into another individual is a form of passive humoralimmunity. Active immunity to an infection develops when an individual’s own immunesystem responds to the microbe. Cell-mediated immunity is mediated by T lymphocytes,not antibodies, and innate immunity is not mediated by either antibodies or Tlymphocytes.7.At 15 months of age, a child received a measles-mumps-rubella vaccine (MMR). Atage 22, she is living with a family in Mexico that has not been vaccinated and she isexposed to measles. Despite the exposure, she does not become infected. Which of thefollowing properties of the adaptive immune system is best illustrated by this scenario?A.SpecificityB.DiversityC.SpecializationD.MemoryE.Nonreactivity to selfANS: DProtection against infections after vaccination is due to immunologic memory of theadaptive immune system. Memory is manifested as a more rapidly developing andvigorous response on repeat exposure to an antigen compared with the first exposure.Specificity and diversity are properties related to the range of antigenic structuresrecognized by the immune system, and specialization is the ability of the adaptiveimmune system to use distinct effector mechanisms for distinct infections.8.A vaccine administered in the autumn of one year may protect against the prevalentstrain of influenza virus that originated in Hong Kong that same year, but it will notprotect against another strain of influenza virus that originated in Russia. Thisphenomenon illustrates which property of the adaptive immune system?A.SpecificityB.AmnesiaC.SpecializationD.Cultural diversityE.Self-toleranceANS: A

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Adaptive immune responses are highly specific for distinct molecular structures, whichmay be present in a vaccine and be produced by one strain of virus but not by a closelyrelated strain. Amnesia, although generally not used in immunology, implies lack ofmemory, but the efficacy of the vaccine against the Hong Kong strain implies it hasinduced memory. The same effector mechanisms would be required to combat differentstrains of influenza, and therefore failure of a vaccine to protect against two differentstrains of virus is not related to specialization of effector functions.9.The two major functional classes of effector T lymphocytes are:A.Helper T lymphocytes and cytotoxic T lymphocytesB.Natural killer cells and cytotoxic T lymphocytesC.Memory T cells and effector T cellsD.Helper cells and antigen-presenting cellsE.Cytotoxic T lymphocytes and target cellsANS: AT cells can be classified into effector subsets that perform different effector functions.Most effector T cells are either helper T lymphocytes, which promote macrophage and Bcell responses to infections, or cytotoxic T lymphocytes, which directly kill infected cells.Natural killer cells are not T lymphocytes. Antigen-presenting cells usually are not Tcells. Memory T cells are not effector T cells.10.Which of the following cell types is required for all humoral immune responses?A.Natural killer cellsB.Dendritic cellsC.Cytolytic T lymphocytesD.B lymphocytesE.Helper T lymphocytesANS: DHumoral immune responses are antibody-mediated immune responses, and all antibodiesare made by B lymphocytes and by no other cell type.11.During a humoral immune response to a newly encountered bacterial infection, Bcells are first stimulated to proliferate and then secrete antibodies specific for thebacterium. The antibodies may then bind to the bacteria and facilitate ingestion of themicrobes by phagocytic cells. In what phase of the humoral immune response does thebinding of secreted antibodies to bacteria occur?A.Recognition phaseB.Activation phaseC.Effector phaseD.Homeostatic phaseE.Memory phaseANS: CThe effector phase of an immune response occurs when cells or molecules eliminate themicrobe or microbial toxin. In a humoral immune response, the effector phase includessecretion of antibody, binding of the antibody to the microbe or toxin, and subsequent

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antibody-dependent elimination of the microbe or toxin. The recognition phase is theinitial binding of the antigen by the naive lymphocyte. The activation phase includesproliferation and differentiation of lymphocytes in response to antigen recognition. Thehomeostatic phase follows the effector phase, during which the response wanes. In thememory phase, memory B cells and antibodies secreted by long-lived antibody-secretingcells are “waiting” for a repeat exposure to the microbe.12.Which of the following statements is consistent with the process of clonal selection?A.The specificity of a lymphocyte antigen receptor changes to accommodate thestructure of an antigen that binds to it.B.Many different antigen receptors with different specificities are expressed on eachlymphocyte.C.Lymphocytes do not express antigen receptors on their cell surfaces until afterexposure to antigen.D.The diversity of the lymphocyte repertoire for antigens is very small beforeexposure to antigen but increases significantly after antigen exposure.E.The diversity of the lymphocyte repertoire for antigens is very large beforeexposure to antigen, with millions of different clones of lymphocytes, each having adifferent specificity.ANS: EThe clonal selection hypothesis accurately predicted that individuals possess largenumbers of different clones of lymphocytes before antigen exposure, with cells in eachclone expressing antigen receptors with a single identical specificity, but with differentspecificities from other clones. Thus, the diversity of the lymphocyte repertoire is verylarge even before antigen exposure. These receptors are expressed before antigenexposure, and their specificities generally do not change in response to antigen.13.Which of the following best describes clonal expansion in adaptive immuneresponses?A.Increased number of different lymphocyte clones, each clone specific for adifferent antigen during the course of an infectionB.Increased number of different lymphocyte clones, each clone specific for adifferent antigen during development of the immune system, before exposure toantigenC.Increased number of lymphocytes with identical specificities, all derived from asingle lymphocyte due to nonspecific stimuli from the innate immune systemD.Increased number of lymphocytes with identical specificities, all derived from asingle lymphocyte stimulated by a single antigenE.Increased size of the lymphocytes of a single clonedue to antigen-inducedactivation of the cellsANS: DClonal expansion occurs during the activation phase of an adaptive immune response. Asingle lymphocyte is stimulated to divide by antigen, and the progeny go through severalrounds of division until there are many lymphocytes, all with identical specificities, allderived from one cell. The number of different clones is not influenced by antigen

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exposure. Expansion does not refer to the size of the cells, although activatedlymphocytes are larger than their naive precursors.14.The estimated number of distinct structures that can be recognized by the mammalianadaptive immune system isA.1-10B.102-103C.103-105D.107-109E.∞ANS: DAlthough the theoretical number of antigen specificities of the adaptive immune system ishigher, estimates of the actual number ofdifferent antibody and T cell antigen receptorspecificities are in the range of 107-109. This number is large enough to accommodatemost of the diversity in molecular structures that the microbial world is capable ofproducing.15.Which of the following statements best describes the “two-signal requirement” fornaive lymphocyte activation?A.Lymphocytes must recognize two different antigens to become activated.B.Lymphocytes must recognize the same antigen at two sequential times to becomeactivated.C.Lymphocytes must recognize antigen and respond to another signal generated bymicrobial infection to become activated.D.Both naive B and naive T lymphocytes must simultaneously recognize antigen foreither to be activated.E.When lymphocytes recognize antigen, the antigen receptors must activate two-signal transduction pathways to become activated.ANS: CNaive lymphocytes will not become activated by antigen alone (signal 1). In addition,they require “costimulatory” signals (signal 2), which are either microbial products ormolecules on host cells induced by microbial infection. The molecules that provide signal2 bind to receptors on the lymphocytes that are distinct from the clonally distributedantigen receptors. Each lymphocyte cannot generally recognize more than one antigen.Although lymphocyte activation may require recognition of antigen molecules by morethan one antigen receptor, the two-signal requirement does not refer to this. There is nogeneral requirement for both T and B cells to recognize the same antigen for activation ofeither to occur. The two-signal requirement does not refer to antigen receptor–associatedsignal transduction pathways.16.In addition to T cells, which cell type is required for initiation of all T cell–mediatedimmune responses?A.Effector cellsB.Memory cellsC.Natural killer cells

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D.Antigen-presenting cellsE.B lymphocytesANS: DT cell–mediated immune responses are initiated when naive T cells are activated.Antigen-presenting cells, such as dendritic cells, are required to display antigens(peptide-MHC molecule complexes) for naive T cell recognition and to expresscostimulatory molecules also needed for T cell activation. Memory cells, cytotoxic Tcells, and B lymphocytes are not involved in the initial activation of naive Tlymphocytes.

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Abbas: Basic Immunology,4thEditionChapter 02: Innate ImmunityTest BankMULTIPLE CHOICE1.Which of the following statements about the innate immune system is NOT true?A.Innate immunity is present in all multicellular organisms, including plants andinsects.B.Deficiencies in innate immunity markedly increase host susceptibility to infection,even in the setting of an intact adaptive immune response.C.Innate immunity is better suited for eliminating virulent, resistant microbes than isadaptive immunity.D.The innate immune response can be divided into recognition, activation, andeffector phases.E.The innate immune response against microbes influences the type of adaptiveimmune response that develops.ANS: CInnate immunity is the first line of defense against infections, yet many pathogenicmicrobes have evolved strategies to resist innate immunity. Adaptive immunity, beingmore potent and specialized, plays a critical role in defending against these virulentmicrobes. Innate immunity is the phylogenetically oldest mechanism of microbialdefense, and it is present in all multicellular organisms, including plants and insects.Studies have shown that hampering effector mechanisms of innate immunity rendershosts much more susceptible to infection, even with a functional adaptive immunesystem. It is also true that, like the adaptive response, the innate immune responseconsists of recognition, activation, and effector phases. Although it provides the initial,rapid response against microbes, innate immunity can influence adaptive immuneresponses to tailor them against particular microbes.2.A 4-year-old girl stepped on a rusty nail in her backyard. Two days later, she is takento the pediatrician because her heel is painful, red, and swollen and is warm to the touch.All of the following are mechanisms of innate immunity that may be protecting thepatient against pathogenic microbes in the heel wound EXCEPT:A.Epithelial barrier function of the skin of her footB.Intraepithelial lymphocytes present in the skinC.Circulating neutrophils migrating to the site of the woundD.Soluble cytokines that induce a local inflammatory responseE.Circulating anti-tetanus toxin antibodiesANS: ESecreted antibodies against protein antigens are effectors of humoral immunity, acomponent of the adaptive immune system. All other mechanisms listed are part of theinnate immune system. Intact epithelial surfaces prevent microbial entry, and epithelialcells express anti-microbial factors, such as defensins. Neutrophils are effector cells that

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function in early phagocytosis and killing of microbes. Cytokines that mediateinflammation (e.g., tumor necrosis factor, interleukin-1, chemokines) are components ofinnate immunity. Intraepithe-lial T lymphocytes present in the epidermis and mucosalepithelia express a limited diversity of antigen receptors; as such, they are consideredeffector cells of innate immunity and function in host defense by secreting cytokines,activating phagocytes, and killing infected cells.3.Which of the following comparisons of the innate and adaptive immune systems isFALSE?A.The innate immune system is more likely to recognize normal self, and thereforecause autoimmunity, than is the adaptive immune system.B.Receptors used for recognition in innate immunity are encoded in the germline,whereas those of the adaptive immune system are encoded by genes generated viasomatic recombination of germline receptor gene loci.C.The innate and adaptive immune systems share some of the same effectormechanisms.D.Both the innate and adaptive immune systems can recognize nonmicrobialsubstances.E.The innate immune system does not have memory but the adaptive immunesystem does.ANS: AInnate immune system receptors are encoded by germline genes that have evolved torecognize microbial structures or molecules produced by stressed self, and therefore thereis little chance of innate immune responses to normal self. Because the specificities ofadaptive immune system receptors (Ig or T cell receptor molecules) are randomlygenerated by somatic recombination and junctional-diversity mechanisms, there is agreater chance that the adaptive immune system receptors may recognize normal selfmolecules, leading to autoimmunity. Mechanisms of tolerance minimize this possibility,but these mechanisms can fail. The adaptive immune system receptors can recognizenonmicrobial structures. Although most innate immune system receptors recognizemicrobial structures, some Toll-like receptors and activating receptors of natural killercells do recognize nonmicrobial self proteins expressed by stressed, damaged, or infectedcells. Memory is a unique property of the adaptive and not the innate immune system.4.Toll-like receptors (TLRs) are a family of homologous receptors expressed on manycell types and are involved in innate immune responses. Ten different mammalian TLRshave been identified, and several ligands for many of these receptors are known. Whichof the following is a TLR ligand?A.Single-stranded RNAB.Transfer RNAC.Double-stranded DNAD.Unmethylated CpG DNAE.HeterochromatinANS: DMore than 10 mammalian Toll-like receptors (TLRs) have been identified, and eachappears to recognize a different set of structures that are found in pathogenic microbes

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but not in mammalian cells. Such structures are called pathogen-associated molecularpatterns (PAMPs). Unmethylated cytosine guanosine (CpG) motifs are typical ofbacterial and protozoan DNA, but not mammalian DNA, and are therefore PAMPs.TLR9 binds CpG DNA. Transfer RNA, single-stranded RNA, double-stranded DNA, andheterochromatin are all normal components of mammalian cells and are not recognizedby TLRs. Double-stranded RNA is produced by some viruses but not by mammalian cellsand is recognized by TLR3.5.A 67-year-old homeless man is brought to the emergency department after beingfound behind a neighborhood bar in freezing weather. On arrival, he has a shaking chill,fever, and cough productive of blood-tinged sputum. A chest radiograph shows lobarconsolidations consistent with bacterial pneumonia. Blood cultures are positive forStreptococcus pneumoniae.Which of the following molecular patterns recognized byToll-like receptors expressed on the surface of this patient’s phagocytes is important foractivating his innate immune system against this gram-positive bacterial infection?A.PeptidoglycanB.Double-stranded RNAC.Lipopolysaccharide (LPS)D.LipoarabinomannanE.Phosphatidylinositol dimannosideANS: AGram-positive bacteria contain cell walls rich in peptidoglycan. When shed by bacteriasuch asStreptococcus pneumoniae,peptidoglycan serves as a ligand that binds Toll-likereceptor 2 (TLR2), stimulating an innate immune response. The other choices listed arealso ligands that stimulate TLRs, but they are not present in gram-positive bacteria.Double-stranded RNA is found in replicating viruses, lipopolysaccharide (LPS) is acomponent of the outer cell wall of gram-negative bacteria, and both lipoarabinomannanand phosphatidylinositol dimannoside are present in mycobacteria.6.The signaling pathways triggered by Toll-like receptors typically result in activationof which of the following pairs of transcription factors?A.NFAT and T-betB.AP-1 and GATA-3C.Fos and STAT-6D.NFBand AP-1E.Lck and JunANS: DThe predominant signaling pathway used by Toll-like receptors (TLRs) results in theactivation of the NF-B transcription factor. Ligand binding to the TLR at the cell surfaceleads to recruitment of several cytoplasmic signaling molecules through specific domain-domain interactions, resulting in degradation of IB and subsequent activation of NFB.In some cell types, certain TLRs also engage other signaling pathways, such as the MAPkinase cascade, leading to activation ofthe AP-1 transcription factor. T-bet and GATA-3are transcriptional regulators involved in helper T cell differentiation. Fos is a componentof AP-1, and STAT-6 is a transcription factor activated by IL-4 binding to cells. Lck is

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not a transcription factor, but rather a tyrosine protein kinase involved in antigen-receptorsignaling in T cells.7.Toll-like receptors and other receptors are potent activators of various components ofthe innate immune system. All of the following proteins are expressed in response tosignaling by these receptors EXCEPT:A.Interleukin-12B.E-selectinC.Tumor necrosis factorD.Inducible nitric oxide synthase (iNOS)E.CD28ANS: ECD28, the activating receptor for B7-1 and B7-2 costimulatory molecules, isconstitutively expressed on the surface of many T cells and is not induced by Toll-likereceptor (TLR) signaling. TLR signaling does induce expression of B7-1 and B7-2 onantigen-presenting cells. Other genes expressed in response to TLR signaling encodeproteins importantin many different components of innate immune responses. Theseinclude inflammatory cytokines such as tumor necrosis factor-(TNF-), interleukin-1(IL-1), and IL-12; endothelial adhesion molecules such as E-selectin; and proteinsinvolved in microbial killing mechanisms, including inducible nitric oxide synthase(iNOS). The specific genes expressed depend on the cell type of the responding cell.8.Which of the following is a receptor on macrophages that is specific for a structureproduced by bacteria but not by mammalian cells?A.CD36 (scavenger receptor)B.Fc receptorC.Complement receptorD.Mannose receptorE.ICAM-1ANS: DThe macrophage mannose receptor binds to terminal mannose and fucose residues onbacterial glycoproteins and glycolipids. Mammalian cells do not typically contain theseresidues. CD36 binds many different ligands, including microbial and self molecules. Fcreceptors, complement receptors, and ICAM-1 are receptors for mammalian complementfragments, Ig, and LFA-1, respectively.9.Which one of the following comparisons between neutrophils and macrophages istrue?A.Neutrophils that enter inflammatory sites can survive for days, but macrophagesare very short lived and only survive for hours.B.Both neutrophils and macrophagesare phagocytic and can kill internalizedmicrobes.C.Neutrophils proliferate at inflammatory sites, but macrophages are terminallydifferentiated and cannot proliferate.D.Neutrophils, but not macrophages, express the high-affinity FcRI receptor, whichrecognizes specific opsonins bound to microbes and facilitates phagocytosis.

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E.Both neutrophils and macrophages contain abundant cytoplasmic granulescontaining lysozyme, collagenase, and elastase.ANS: BNeutrophils and macrophages can both actively phagocytose and kill microbes, and bothexpress opsonin receptors, such as FcRI or complement receptors that enhancephagocytosis. Neutrophils are short lived, whereas macrophages can survive for days orweeks. Macrophages are not terminally differentiated and can undergo cell division atinflammatory sites, but neutrophils cannot. Only neutrophils have cytoplasmic granulesfilled with enzymes, including lysozyme, collagenase, and elastases; these are calledspecific granules.10.A 43-year-old man with a history of kidney transplantation is on immunosuppressivedrugs. He presents to the emergency department 84 days after transplantation with aslight fever, accompanied by violent shaking chills, rapid heart rate, and dangerously lowblood pressure. Blood cultures are positive for gram-negative bacteria, includingKlebsiellaandPseudomonas.Although the patient was initially alert and responsive tofluids and antibiotic therapy, his condition rapidly deteriorates into disseminatedintravascular coagulation (DIC), hypoglycemia, and cardiovascular failure. Which of thefollowing is an essential mediator of this patient’s condition?A.Transforming growth factor-B.Tumor necrosis factor-C.Interleukin (IL)-2D.IL-10E.IL-3ANS: BThis patient is suffering from septic shock, characterized by the clinical triad ofdisseminated intravascular coagulation (DIC), hypoglycemia, and cardiovascular failure.This condition is most often initiated by endotoxin, also known as lipopolysaccharide(LPS), a component of the outer cell walls of gram-negative bacteria. LPS is a potentstimulus for tumor necrosis factor (TNF)-secretion by mononuclear phagocytes andother cell types. Most of the biologic effects of LPS are mediated through TNF-.Transforming growth factor-(TGF-) and interleukin (IL)-10 are anti-inflammatorycytokines, IL-2 is a T cell growth factor, and IL-3 is a hematopoietic cytokine. Thesecytokines are not mediators of septic shock.11.Macrophages and neutrophils express several enzymes that are involved inbiochemical mechanisms that kill ingested microbes. Which of the following is NOT anenzyme expressed by these cells?A.Inducible nitric oxide synthase (iNOS)B.Granzyme BC.Phagocyte oxidaseD.MyeloperoxidaseE.LysozymeANS: B

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Granzyme B, a proteolytic enzyme component of cytolytic T lymphocyte (CTL) andnatural killer (NK) cell granules, is involved in initiating caspase-dependent CTL killingof target cells. Granzyme B is not involved in phagocyte killing of ingested microbes.Inducible nitric oxide synthase (iNOS) generates NO in macrophages, and NO is toxic tomicrobes. Phagocyte oxidase and myeloperoxidase are involved in generating free radicalspecies that kill ingested microbes in phagocytes. Lysozyme is a proteolytic enzyme inneutrophil granules that contributes to microbial killing.12.All of the following molecules are opsonins that facilitate efficient phagocytosis ofmicrobes by neutrophils and macrophages EXCEPT:A.C3bB.C5aC.C-reactive proteinD.IgGE.Mannose-binding lectinANS: BC5a is a peptide released after cleavage of C5 protein during the complement cascade. Itstimulates the influx of neutrophils to the site of infection, thus acting as achemoattractant, not as an opsonin. C3b (covalently bound to microbes on whichcomplement activation has taken place) and IgG bound to antigen, are particularly potentopsonins, because phagocytes have receptors for both C3b and the Fc region of IgG. C-reactive protein and mannose-binding lectin also can coat microbes and be recognized byphagocyte receptors; thus they serve as opsonins.13.A 3-year-old boy, who is small for his age, has a history of pyogenic (pus-producing)infections and cutaneous skin abscesses. Physical examination is remarkable for highfever, enlarged liver and spleen, and swollen cervical lymph nodes. A culture from anabscess on his arm revealsStaphylococcus aureus,a gram-positive bacteria that is alsocatalase-positive. Immunoglobulin and complement levels are normal. Results of thenitroblue tetrazolium test are consistent with a diagnosis of chronic granulomatousdisease (CGD). The boy’s immunodeficiency involves impaired generation of which ofthe following?A.C5aB.C-reactive proteinC.Mannose-binding lectinD.Reactive oxygen intermediatesE.Membrane attack complexANS: DChronic granulomatous disease (CGD) is a rare, inherited immunodeficiency diseaseassociated with a defective intracellular respiratory burst in phagocytes. It consists of agroup of heterogeneous disorders of oxidative metabolism in which the pathwaysrequired for generation of toxic reactive oxygen species (ROIs) are impaired. In patientswith CGD, phagocytosis occurs normally, but the engulfed microbes are not killed andthey multiply within the cell. In this way, patients are susceptible to recurrent infectionswith organisms such asStaphylococcus,which are of low virulence in normal hosts.

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14.A 4-year-old-girl sees her physician because of a severe necrotizing, oropharyngealherpes simplex viral (HSV) infection. She has a past medical history of cytomegalovirus(CMV) pneumonitis and cutaneous HSV infection. Phenotypic analysis of her blood cellsshows an absence of CD56+and CD16+cells. There are normal numbers of CD4+andCD8+cells in the blood, and serum antibody titers are normal. The patient’s CD8+Tcells were able to kill virally infected target cells in vitro. Which of the following is NOTcharacteristic of this girl’s immunodeficiency disease?A.Lack of cells whose activation is normally inhibited by self class I majorhistocompatibility complex (MHC)B.Impaired granzyme B–dependent killing of virally infected target cellsC.Lack of cells that are activated by IL-15D.Impaired interferon (IFN)-production during early phases of viral infectionE.Failure to form viral peptide-class I MHC complexesANS: EThe presence of normal numbers of CD8+T cells and the ability of these cells to killvirally infected target cells indicates that the classI major histocompatibility complex(MHC) pathway of viral peptide antigen presentation is intact. The patient’simmunodeficiency is due to a lack of natural killer (NK) cells. NK cells express CD56and/or CD16. NK cells are activated by interleukin-15 (IL-15) and IL-12, are normallyinhibited by recognizing class I MHC on other cells, kill target cells with altered class IMHC expression through a granzyme B–dependent mechanisms (similar to cytolytic Tlymphocyte killing), and produce interferon-as part of the early innate response to viralinfection.15.Which one of the following statements about inhibitory receptors on natural killer(NK) cells is true?A.Inhibitory receptors on NK cells express ITAM motifs in their cytoplasmic tails.B.Some inhibitory receptors on NK cells recognize HLA-A or HLA-C.C.Some inhibitory receptors on NK cells are members of the integrin family.D.Some inhibitory receptors on NK cells are members of the Toll-like receptorfamily.E.Inhibitory receptors on NK cells are not expressed on the same NK cells thatexpress activating receptors.ANS: BNatural killing (NK) inhibitory receptors recognize class I MHC molecules that arenormally and constitutively expressed, including various alleles of HLA-A and HLA-C.The cytoplasmic tails of NK inhibitory receptors contain immunoreceptor tyrosine-basedinhibitory motifs (ITIMs), but not immunoreceptor tyrosine-basedactivation motifs(ITAMs). Some inhibitory receptors on NK cells are members of the Ig superfamily, butnot the integrin or TLR families. NK cells usually express both activating and inhibitoryreceptors, and activation is regulated by a balance between signals generated from bothtypes of receptors. The inhibitory receptors on NK cells bind to self class I MHCmolecules, which are expressed on most normal cells. When activating and inhibitoryreceptors are simultaneously engaged, the inhibitory receptor signals dominate and theNK cell is not activated.

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16.Complement activation in the innate immune system can be initiated in the absence ofantibody.Which of the following molecular components of the complement system isinvolved in initiation of antibody-independent complement activation?A.C1B.C9C.Mannose binding lectinD.CR2E.Mannose receptorANS: CMannose-binding lectin (MBL) is a soluble serum component that is structurally similarto C1 of the classical complement pathway. MBL binds to mannan residues on microbialsurfaces and triggers proteolytic cleavage and activation of downstream components ofthe complement system. C9 is not involved in initiation of complement activation but ispart of the common final membrane attack complex (MAC) pathway. CR2 is a cellsurface receptor for complement fragments. A mannose receptor is a cell surface receptoron phagocytes that binds mannan residues and promotes phagocytosis of microbes.17.Which of the following is an example of how the innate immune response stimulatesor modifies adaptive immunity?A.Tumor necrosis factor (TNF) secreted by helper T cells enhances adhesionmolecules on endothelial cells and promotes recruitment of inflammatory cells.B.Interferon (IFN)-produced by T helper cells is a potent activator ofmacrophages, allowing killing of phagocytosed microbes.C.B7-1 expression on antigen-presenting cells is up-regulated in response tosignaling through Toll-like receptors, thus enabling costimulation of T cells.D.Infected cells coated by IgG3 are recognized by Fc receptors on natural killercells, allowing efficient killing of the infected cells.E.Double-stranded RNA of replicating viruses potently stimulates IFN-expressionby fibroblasts, inducing an “antiviral state” in neighboring, uninfected cells.ANS: CInnate immune responses are important stimulators of adaptive immunity. Increasedexpression of B7-1 and B7-2 on antigen-presenting cells after microbial activation ofToll-like receptors (innate immunity) is critical in providing costimulatory signals for Tcell activation (adaptive immunity) via binding to CD28 receptors on T cells. T helpercell–mediated endothelial or macrophage activation is an example of adaptive immunityusing the effector mechanisms of innate immunity. Neither IgG3 opsonization facilitatingnatural killer cytolytic activity nor double-stranded RNA stimulating interferon-secretion involve innate immunity enhancing adaptive immunity.

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