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    Bf answers ID Virus-infected cells are recognized and killed by cytotoxic CDS+ Tells, The ell receptor on the CDS+ T cells binds to the complex of viral peptide and MHC class I mol- ceules displayed on the surface ofthe infected cell. Natural aller (NK) cells also recognize MH class I molecules with sel-peptides, but this sei-ecognition inhibits NK cell Kill ing. Viruses that inhibit MFIC T expression of peptides may hide from cytotoxic cells, but not lrom NK cells. The other listed options are not the major immune response to hepatitis viral infection. 7809 190 BPP 10l-102,104 P8DE207 BPA 109-110 RIC The NLRinflammasome pathway plays a role in the Jimate immune system recognition of urate crystals and pro- ‘ecg the inflaranation sobaciated with gece Thess rap tors may also contibute to inflammation of atherosclerosis. Ciype lectin receptors (CLRs) expressed on the plasma ‘membrane of macrophages and dendritic cells detect fengal tlycans and elicit inflammatory rections to fungi, Mannose Feceptore on phagocytes recognize microbial eugars with a ‘minal mannose residues and induce microbial phagocytosis. RIGelike receptors (RLRs) are located in the cytosel of most cell types and detect nucleic acids of viruses that repliate in the cytoplasm of infected calls to stinalaia producti of antiviral cytokines, Tolike receptors (TLR) in the plasma Iembrane and endosomal vesicles activate transcription factors that stimalate synthesis and secretion of cytokines and expression of adhesion moliles to recruit and activabs leukocytes P09 188 BPD 105, BIB The adaptive immune syste requires presentation of antigen to effector calla. Inracllilar pathogens eich as Viruses are displayed by MHC I molecules to both CD4 and CDS Feels with a cell receptors. Some CDS cells secrete cytokines, bit most are cytotoxic. B ymphocytes express Encwmnoglobulinrecoptors that prinarily react to extracel larantigens such a those derived from bacteria as an adap- tive humoral immune response. Dendritic cells are a typeof antigen-presening cell Natura killer cells are part of innate imnmunity and react against cells when they do not display MHC molecules. A subset of T cells beneath epithelia display x eceptos that are part of an innate immune response PRD9 190-191 BPP 10I-103 OB 186-187 BPE 10-112 [ID Natural killer (NK) cells have the ability to respond without prior sensitization. They carry receptors for MHC class 1 molecules, which inhibit thei Iytc function, When expression of class I MHC molecules is reduced on a cell surface by viral interference the inhibitory receptors on NK cells do not receive a negative signal, and the targeted cel is kalled. NK cells are often the first line of defense against viral infection. CD4+ cells are helper T cells that assist other cells, such as NK cells, macrophages, and B cells, in the immune response. Dendritic cells aid in antigen presentation. Mac- rophages can phagocytize necrotic cells, then process and CHAPTER 6 Immune System Diseases display any foreign antigens within those cells. Neutrophils, provide a nonspecific immune response, primarily to bacte- rial infections and not to intracellular viral infections PDS 186,192 BP9 104 PBDE I88 878 108,113, [ISIF Natural killer (NK) cells have CDI6,an Fe receptor that allows them to bind te opsonized cells and lyse them. This is 8 form of type If hypersensitivity with antibody-mediated disease, NK cell comprise 10% to 15% of circulating Iym- phocytes. NK cells also may lyse human cells that have lost (MHC class I expression as a result of viral infection or neo- plastic transformation B cells have surface immunoglobulin, are CDIY positive, and participate in humoral immunity. CDA+ cells are T Iymphocytes that are “helper” cells; they have T cel receptors and are CD3 positive. Likewise, CDS cells have T cell receptors and mark with CD3, but they aet a8 cytotoxic T lymphocytes. Dendritic ces are a form of antigen-presenting, cell that expresses large amounts of (MHC class II molecules. Macrophages express MHC Il and actasantigen-presenting cells to CD4* cells they ean phago- ctize opsonized cells aD 192. BPP 104115 PBDE 168 88 108,113,125, BEBE IDenasitc cele are form of antigen-preseting cell Dendrite cells in epithelia are Known as Langerhans cll and those within germinal centers are called flcuarden- “nic ells (EDCS) The FDCs may become infected but not killed by FIV. They have cell surface Fe receptors that cap- ture antibody-coated HIV virions through the Fe portion of the antibody. These virions attached to the FDCs can infect passing CDs Iymphocytes Dendrite cells elaborate type | Eicervna that ap rogeate antiviral probe in wight: ing calls B cells are a component of humoral immunity, and antibody to HIV does not serve a protective function, but al lov serologic detection of infection, CD8+ cells are cytotoxic lymphocytes that lack the receptor necesary for infection by FIV, Because they survive selectively, the CD4#;CD8¢ ratio is reversed so that itis typically less than 1 with advanced HIV infection, Innate lymphoid cells resemble NK cll, but shape further Iymphoid reactions, Langhans giant cells sre “committees” of activated macrophages that are part of a sfanulomatous response, Macrophages area type of antigen Presenting cell that can become infected by HIV without de- struction, Mast cells have surface-bound IgE, which can be crosslinked by antigens (allergens) to cause degrantlation and release of vasoactive amines, such as histamine, as part of anaphylaxis with type hypersensitivity, RDP 1619-192. BP 104 145-147 PROB Ia7.248 BPE 113 TIC Blood monocytes expressing MHC lassi antigenscan migrate into tissues and become longerlived macrophages. In tuberculosis, these macrophages further transform into epithelia evils that can contribute to granslomatots in- #ammation. Macrophages play an important role in delayed hypersensitivity reactions associated with celtmediated tm- unity. Basophils are circlating counterparts of mast cells UNIT | General Pathology and may play a role in IgE-mediated immune responses. B cells form plastna cells that secrete immunoglobulin on stimulation and are essential to humoral immunity. Natural killer cells ean function without prior sensitization. Newtro- phils are important mainly in acute inflammatory responses, although some neutrophils may be present within a granulo- ‘matous reaction, PRD? 187 BPS 104,120 PBDE208 8P8 116-117 (IBIB Her systemic anaphylactic reaction results from an immediate type I hypersensitivity reaction with antigen tig- gering mast cell-bound IgE with release of preformed me- Giators sch as histamine. Epinephrine isthe fastest acting ‘agent to treat ths ile threatening condition. Cyclosporine is used to minimize Iymphocyte-mediated transplant rejection lucocortcoids can reduce irarune inflammatory reactions, although this occurs over days to weeks, not rinutes, Metho- ‘rexate is useful in the treatment of graft-verss-host disease and for some malignancies, Penicilin is an antibiotic that can induce a type I hypersensitivity eaction in sensitized persons PED? 201-205 9111-112 PBDBI01 BPe 122-124 BIBI This history is typical of the late-phase reaction in type I hypersensitivity. The inital rapid response is largely cats by degrantlation of mast cll, The late-phase reac tion follows wittenit additonal exposure to untgen and ia characterized by mote intense infiltration by inflammatory cells sich as neutrophil, eosinophils, basophils, monocytes, and T,2CDi+ lymphocytes, There is more tissue destruction inthis late phase. The most characteristic cll in secretions from an allergic response isthe eosinophil. Dendrite cells, Iymphocytes, and mast ells remain in the epithelium. NK cells are no part ofthe typical allergic response RDO 201-204 BPP III-113. PDB 198-200 BPE 120-124 HHO.A He has Goodpasture syndrome, in which an auto- antibody is directed against {ype IV collagen in basemnent ‘membranes ofthe glomnerl and inthe kang This i form of type Il Ryperserstivity reaction. The antvodie attach to the basement membrane and ix complement, damaging the glomeruli. Anticardioipin, along with ant-Byelycoprotein lupus anticoagulant” are found with antiphospholipid syn- rome, which may appear in systemic hips erythemators (GLE), These patients have coagulopathies with thrombosis or bleeding, or both. Anti-double-strnded DNA antibod- jes have specificity for SLE, whereas anthistone antibodies ae characteristic of drugrinduced SLE. Anti-SS-A antibody is econ in Sgren eyndrome, The an-Ul-rlbonueleoprotain antibody is seen in mixed connective issue disease (MCTD). PRD? 701,205.206 8°9114.532.FBDE202. B78 25,14 [BA A major transfusion reaction results from a type TL hypersensitivity reaction. The patents serum contains nat rally occurring antibodies to the incompatible donor RBCS. They attach to the donor RBCs and induce complement activation that results in generation ofthe C5.9 membrane attack complex. Major transfusion reactions are rare, and ‘most result from clerical errors. Natural killer cell Lysis is, seen with antibody-mediated diseases, Antigen-antibody complex formation is typical of a type II] hypersensitivity reaction. Mast cells degranulate with antigen attachment to IgE in type I hypersensitivity reactions. Tumor necrosis, factor «is not part of hypersensitivity reactions, D9 205-206 BPP |4-115 PBDE 202 BPS 124-125 2A Myasthenia gravis isa form of type I! hypersenstiv- ity reaction in which antibody is directed against cell s- face receptors, Thymic hyperplasia or thymoma is likely to be present. Antibodies to acetylcholine receptors impair the function of skeletal muscle motor end plates, leading to muscular weakness. B els produce these antibodies; macro- phages are nota significant part of this hypersensitivity reae- tion, and ther is litle or no inflammation ofthe muscle in ryasthenia gravis. Delayed-type hypersensitivity reactions are more likely in parasitic infestations of muscles. Immune complex-mediated injury is a feature of dermatomyositis “Muscle lysis by CD8+ cells occurs in polymyositis 7009 205-206 115,000 PADEOD BPE 26 1H13.B When antibody is dicted at parasitic infection, there is Fe receptor-medited inflammation and phagocyto- sis, characteristic for ADC. IgG and IgE antibodies beating Fe receptors cout the parte: Mecrophages, natura kilt calls and neutrophil can then recognize the Fe receptor and destroy the antibody-coated target cells Acute inflammatory reactions with absces formation have ile effect against tis sue parasites. Complement-medisted lysis is most typical of immune destruction of RECs with hemolysis. Langhans ian cells are seen in granulomatous inflammation, a form ff type V hypersensitivity. Leukotriene Cs a potent agent that promotes vascular permeability and bronchial smooth muscle contraction in type T hypersensitivity reactions PRD? 205206 PPIIS FRDE 195-196. BPR 124-125 AEB in the localized immune complex reaction (Arthus re ction) at thei ofijecton, thre car be acvation ae Sep tion of complement C3. The reaction descrbed heres serum sickaess in response to the nected foreign protein and pro ced mare widespread antigen anivody complex deposition, artery inthe Edneys. CDt+ lymphocytes eat verous Tintody-tedioted end colt medisted tmnane reactions bat their numbers in peripheral blood donot change appreciably IgE concentration is increased in individuals with stopy and the potential for typeI hypersensitivity. Although neutrophils are being reeratedlcaly to he infantry rescton fx tis tase they are not depleted systemically, and they may bei creased in the eelation, Thromborytopeia could Be seen wth thrombotic microangiopathy such as thrombotic thom ochispene purpura) bat et pial ven Aroha ears 809208 BPP 117. PBS 97.208 oe 07-18 [IBA cis calls of the Ty2 type are essential to the recite Apel Nip recee rey AbecrieeT oerhea secrete cytokines such av interleukin (L)3, TL 1, and granulocyte-macrophage colony-stimulating factor, which are required for the growth, recruitment, and activation of ‘mast cells and eosinophils. Dendritic cells trap antigen and, ‘id in antigen presentation. Macrophages are also antigen- presenting cells, and they can secrete various cytokines, but they are not essential to type I hypersensitivity. Natural killer cells can lyse other cell, such as virus-infected cells, without prior sensitization. Neutrophils are recruited by cytokines to participate in acute inflammatory reactions, PBDI 198,202 BPP 118-120 PEDB 95. BPE 120-122 HHGIE The T,7 subse of CD4 cells plays a role in delayed- {ype hypersensitivity reactions. Many persons react o nick: cl particularly with body piercing jewelry. L-17 may als be ‘ef in recruiting neutrophils to fight bacterial as well a5 Fargal indectione ech as ssperploos ane candidiasis IL-2 acts as an autocrine growth factor promoting T ell prolif eration, ILS activates eosinophils as part of a Ty2 response 1-10 is an immunosuppressive cytokine that. diminishes Iymphocyte activation, NK cells may secrete interferoney in ‘eaponse to stimulation by IL-12. RDS 198,208-209 BPP 19-120 PROB INS.206 BPE 128-10 HHT. Perivascular accumulation of T cells, particularly CD4+ cells is typical of delayed hypersensitivity skin reac- tions, driven by a Ty response mediated largely by release of the cytokine interleukin-2. The tuberculin skin test also ‘works through this pathway. Anaphylaxis (type I hyper- sensitivity) typically occurs within minutes to hours after fan encounter with an antigen to which sensitization has oc- curred; the localized form may occur following ingestion of the foreign protein antigen. Systemic and localized immune complex diseases (Arthis reactions and serum sickness) are type Ill hypersensitivity reactions; they often exhibit vaseu- Iii, Graft-versus host disease is characterized by epidermal apoptosis and rash in persons receiving an allogeneic hema- topoietic stem cell transplant. P89 20%-211 9119-120 PBR 205-207 BPe 128-130 [148 € Streptococeal M proteins cross-react with eardiae glycoproteins, resulting in rheumatic heart disease, a form of autoimmunity. The other listed options are not major immune responses to streptococcal infection. Breakdown of T cell anergy usually occurs when localized tissue dazn- age and inflammation cause up-regulation of co-stimu latory molecules on the target tissues. This is a possible mechanism of autoimmunity in the brain and in pancreatic islet cells. Failure of T cell-mediated suppression has not yet been shown to cause any autoimmune disease; it re- rains a potential mechanism. Microbial products such as endotoxin or bacterial superantigens may ease polyclonal lymphocyte activation. Release of sequestered antigens can cause autoimmunity; this mechanism is likely in at toimmune uveitis (sympathetic ophthalmia) following eye trauma P809207,216 BP9 124 PBDB2I2 BPB 119,24 CHAPTER 6 | Immune System Diseases 19 B This young woman has a classic picture of systemic lupus erythematosus (SLE) — the erythematous malar facial, skin rash shown in the figure, and renal failure with pro- teinuria and hematuria from immune complex deposition in the glomeruli. Defective clearance and hence increased, burden of nuclear apoptotic bodies in thymie lymphocyte development is considered a fundamental mechanism, that underlies SLE, This along with loss of self-tolerance to nuclear antigens gives rise to the pathogenic DNA-anti DNA immune complexes, as measured by the antinuclear antibody test, Antiphospholipid antibodies may be present with SLE, but lead to coagulopathy. IFN-y is a product of (CD4+ T cells and NK cells, There is no evidence of delayed hypersensitivity or NK cell dysfunction in SLE. Molecular ‘mimicry oceurs when a microbial antigen cross-reacts with, ‘anormal tissue as in rheumatic fever, Widespread and non- specifi activation of T cells by superantigens occurs in toxic shock syndrome. PDS 216-226 BPP 125-130 PBDEIS-218 BPE 139-144 [2O.E ‘The serologic featres of systemic lupus enytherna- tomus (SLE) include the more sensitive ANA test and the tore specific antidsDNA test. The abnormal coagulation tests suggest the presence of anticardiolipin antibodies. ‘These antibodies against phospholipid-protein complexes {antiphospholipid antibodies) also are called Taps antio- gules because they interfere with in vitro clotting test In vivo, they are thrombogenic. Hence these patients can have recurrent thrombosis Lupus anticoagulants also can ‘occur in the absence of SLE. The other listed options are lily to be common at associat complications of SLE abo 218221 BPP 125-120 POBI7-21 BFE 19-144 IBID Many patients with systemic lupus erythematosus (GLE) have. lemerulorephalty as efldencad by protine tra with hematuria, and eventually develop renal failure Blindness is uncominon in SLE. Raynaud phenomenon is associated with many autoimmune diseases, bu its most eeuasece lacie era AltigegtVeyen el amen tions common in SLE ist defor le rare. Libman Sack endocarditis associated with SLE tends to be nondelorming and limite, so there is inimal valve damage It is now une common because of the use of corticosteroid therapy in the treatment of SLE D9 222-224 BPP 125-130 PBDEI7-219 BPE 139-144 [22°C Patients with systemic Inpus erythematosus (SLE) can develop ant RBC antibodies, which can cause hemolytic anemia. Cytopenias, including leukopenia, thrombocytope- nia, and anemia, also are common, Bronchoconstiction is a feature of bronchial asthma and can occur in allergies as a predominantly type I hypersensitivity reaction. Cerebral lymphomas are rare, but may occur in immunodeficient pax tients, particularly patients with AIDS, Keratoconjunctvitis can be seen in Sjogren syndrome asa result of decreased tear production from lacrimal gland inflammation. Sacroilitis is 4 feature of many ofthe spondyloarthropathies, such as an- keylosing spondylitis, Sclerodactyly is seen in scleroderma UNIT | General Pathology ‘When extensive, its usually part ofthe spectrum of findings, associated with diffuse scleroderma; when it involves only a few areas ofthe skin (e.g, just the hands), itis more likely to indicate limited scleroderma (CREST syndrome). PDS 218 BPs 125-120 PBDR 2I7 BE 139-144 [128°D The figure shows the so-called wire loop glome lar capillary lesions of laps nephritis. Ant-Smith nd an double-stranded DNA are more specie fr systemic lupus crytheratosus, but sensitivity is low: anti-Smith is present in only 25% of SLE cases, Anticentromere antibody i seen most often with limited scleroderma, whereas anti-DNA topoisomerase I is found with diffuse scleroderma, Cycle citrullinated polypeptide and rheumatoid factor are found ‘most often with rheumatoid arthritis. Anti-UL-RNP can be found with mixed connective iste disease PeD9 223-224 BPP 128-129 PEDE2IT-219 BPE 142-149 AIG A drug induced systemic pus erythematosus (SLE) like condition may be caused by drugs such assoniazi,pro- csinamide, and hydralazine, Test results for ANA are often positive, but tet results for anti-double-stranded DNA are hegative, Anihistone antibodies are present in many eases. Characteristic signs and symptoms of SLE may be lacking, and renal involvement is incommon, Remission occite ‘wt the patent stops taking the drug. AntiSin antibody shoves specificity for SLE. Anti-Jo- antibody has spect for polymyositis/dermatomyosits. Ant-UT ribonucleotide protein has specificity for mixed connective tssue disease. Anticentromeri antibody’ i most Iikely to be present with limited scleroderma (CREST syndrome). Ant-SS-A an body is most characteristic of Sjogren syndrome. PRD 26 BPP 126. PBDB221. 878 M0 HHRIEE The igure shes extensive elector der deposiia Within glomerular basement membrane characteristic of ime tune complex-mediated glomerulonephrits. The immune complexes activate complement and result in act inflam {raton, Granalomatoustidlammation and all cytotoxicity are features of type V hypersensitivity Antibody-dependent cellzmediated cytotoxicity is initiated when IgG or IgE coats ‘target o attrac cells that affect ss immune complexes do not form, Localized anaphylaxis isa type I hypersensitivity Teaction that is mediated by IgE antibody RD9 207-206,222 8P9 128-129 PRORTIT-AIP. BPR E-127 IBBIE she has discoid Iupus erythematosus, with skin lo sions similar to thove of eyteic lupus erxythematoeus GLE), tht with steric involvement mh les Hkly to occur: Self nucleic cts mimic her ncrobial counterparts, an in con fanction with TLRs, they incite type Interferon proton folactivals dendiibe cote and B cals they ao promote a Ty responee which contrates to astlmenunity. Mast cell degranulation with type I hypersensitivity may produce an turtcarial rash, but without autoimmune entgerrantbody arte copes Clee my alent tion and lea to polyclonal Beal sctvation, but automate diseases involve self antigens, not exogenous antigens. Re- lease of sequestered antigens is the mechanism for sympa thetic ophthalmia, A Ty:17 response may be present in chron- ic inflammatory conditions such as inflammatory bowel diseases with macrophage and neutrophilic infiltrates, PRD9 225-226 PP 126 PBDB 214,221 BPE LAO 127 B Sjogren syndrome is characterized by immunologically tnediaied detrcton of elivary and lacrimal glands and other ‘xccrine glands ining the respiratory and gustrintestna tracts. Dryness and crusting ofthe nose cn lead to perforation ofthe natal septum, In 25% of cases, extraglandular tissues, such 35 Tere ok, Kidney, and anaclen enay bn feed The asin dlysrgulation that accompanies autimenune diseases increas 6 the risk for B ell Imphoid malignancies, such as MALT Iymphoma, Libman-Sacks endocarditis i mort often a featire of apeinni: ayia ybnecatoers LE). Reval bahare is mere Iikely to ocur with SLE frm glomerulonephrits, Esophageal

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