immunology CU dental micro exam 3

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Name four classes of pathogens: 1. extracellular 2. Intracellular 3. viruses 4. parasitic worms.
3 perio pathogens: 1. P. gingivalis 2. A. a. 3. B forsythus
P. gingivalis: G-, anaerobe, non motile, rods
A. a.: G-, anaerobe, non-motile, cocco
B forsythus: G-, anaerobe, fusiform
3 Cariogenic pathogens: 1. Strep mutans 2. S. sobrinus 3. Lactobacilus
Strep mutans S. sobrinus: G+, cocci chains, enamel caries
Lactobacilus: G+, rod chains, dentinal caries
Host response to extracellular pathogens (bacteria, parasites): Innate (antimicrobial, complement, phags) Adaptive (B cells = ab's)
Host response to intracellular pathogens (bacteria, parasites,mycobacteria, spirochetes): Innate (NK) Adaptive (T-cell, Th1 macrophage activation)
Host response to viruses: IFN-alpha/beter stimulates NK cells, T-cells (Th2 ab response), fever = viral destabilization
IFN-alpha/beter key roles: 1. turns on viral interfering genes 2. Increase MHC C1 = inc susceptibility to T-cell 3. activates NK's
Innnate response to virus, list cytokines released by macrophages: macrophages release TNF-alpha, IL-1,6 = inflam. IL-12 = NK stimulation. IL-8 chemotactic
Adaptive humoral response to virus key roles (4): Neutralization, comp fixation, opsonization, ADCC (antibody-dependent cell mediated cytotoxicity
Adaptive cell-mediated response to virus: most important after virus infects cell. T-Cells: CD8+(CTL), CD4+ (Th2 --> Bcell, Th1 --> macrophage)
Host response to multicellular parasites (extracellular worms): Th2 ab response, Ig-Fc eosinophilic degranulation(humoral) + mast cells = inflam + inc mucous secretion in GI promoting expulsion
Host respnse to fungi: Th1 macrophage activation, Th2 opsonization/neutralization, resistant to complement
Stages of perio lesioins: Initial - early - established - advanced
Initial perio: >2-4 days, few neutro, macro or lympho
early perio: >4-14 days, inc neutros, *microabscess, T-cell
established perio: >14 days, intense neutro, B-cell differentiation, macrophages
advanced perio: > 14 days, bone dest, plasmacytes, epithelial ulceration
Virulence factors: Encapsulation, ag variation, intracellular survival, suppress immune system, Biofilm
Encapsulation: polysach coat = resist phagocytosis, usually pyogenic
ag variation: impaired recognition
intracellular survival: evades humoral response
suppress immune system: impairs immune fuction and response
Biofilm: bacterial cells form "sheltered" communities --> phagocytosis is frustrated --> host tissue damage
Virulence factors P gingivalis: encapsulation, ag variation, toxins: tissue destruction, inhibit cell fxn, impair opsonins, amplify inflam response, invades host to evade complement and antibody
Virulence factors A a: encapsulation, toxins: tissue destruction (collagenase), Ig protease, endo/leuko-toxins, suppression of T cell cytokines (IL-2,4,5)
Virulence factors Strep mutans: Degrades, sheds IgA
Systemic effects of perio: pathogens in crevice --> degrade host --> bacterial invasion --> inflam response --> bacteria into circ --> lymph nodes --> systemic
Aquired pellicle def.: host salivary proteins which coat surface teeth = binding site for cariogenic bacteria via glucans (glucosyltransferases)
cariogenic bacteria accumulation and metabolism: sucrose-dependent, sucrose --> lactic acid
colonization on enamel by S mutans list 4: 1. initial (directily to pellicle) 2. interbacterial (adehere to early colonizer) 3. glucan mediated 4. sucrose dependant
_______ inhibits biofilm formation.: Lactoferrin
2 type of immunization: 1. Passive (natural = mom, or artificial = ab injection.) 2. Active (natural = exposed to pathogen, or artificial = injection of vaccine)
Passive imm. Disadvantages (3): short term, dosen't activate immune system, repeated use = dec response or hypersensitivity
Passive imm. Advantage: immediate protection
Active imm advantage: long term protection
Active imm disadvantages (1 natural, 3 artificial): subject to infection (natural) or side effects, not life long, difficult to develop effective immunity (artificial)
Live vaccine: live pathogen attenuated to be avirulent = longer lasting, more complete immunity
Inactivated vaccine 3 types: inactivated whole pathogen (polio), toxoid = toxin proteins ( DPT) or components (flu)
List two methods used to improve response to immunization: 1. Adjuvant 2. Conjugation
Adjuvant: given w/ immunogen --> potent immune response
Conjugation: immunogen (covalent linkage) to protein carrier = hapten carrier effect
hapten carrier effect: B cell recognizes hapten = internalizes it --> T cell help = humoral cell mediated ab production.
Routes of vaccine administration (2): 1. Parenteral 2. Mucosal
Parenteral vaccine pros and cons: IM, ID, IV - pros = systemic immunity, avoids tolerance and ag degradation, cons = lack mucosal immunity
Mucosal vaccine pros and cons: oral/nasal - pros = systemic + mucosal immunity, cons = ag degredation and tolerance *needs adjuvant
Antibodies used for immunization and serologic testing (2): 1. Polyclonal 2. Monoclonal
Polyclonal sources - 2: animal (antivenin), human serum pool (intravenous gamma globulin = IVGG) *derived from many different B cell clones
Monoclonal: single B cell clone fused to tumor cell line then engineered "humanized" eg. anti-HER2 mAb
Polyclonal ab's: multiple isotypes and affinities
Monoclonal ab's: single isotype, selective binding properties
Dental vaccines (3 possibilities): 1. Hyperimmunization S mutans --> crossreactive ab's to heart and IgG 2. Subunit vaccine (fibrillar proteins (AgI/II) or glucosyltransferase conjuguated to cholera (adjuvant) 3. Passive S mutan ab mouthwash
List three immunodiagnostic tests: 1. Agglutination 2. Immunochem 3. Immunofluorescence
Agglutination test: Coombs test = ag:ab crosslink. Eg. Hemolytic, rheumatoid, pregnancy.
Universal donor type: O+ Rh-
Univeral acceptor type: AB+ Rh+
Immunochemistry test: ab-enzyme = substrate --> chromophore. 3 types
3 types of immunochemistry tests: 1. ELISA 2. Immunoblotting 3. Immunohistochemistry
ELISA: enzyme linked immunosorbant assay. Determines presence and/or concentration of ag's or ab's eg. Detect proteins in GCF
Immunoblotting: Western blot test = SDS-polyacrylamide gel + electrophoresis (PAGE) to separate proteins (break disulfide bonds) prior to ab detection. Eg. Oral prion testing
Immunohistochemistry: like ELISA but used to detect tissue ag's like immunofluorescence
Immunofluorescence: ab-fluorophone + laser = light. Used for detecting cell surface ag's in tissue. Eg. Dx plasminogen deficiency -->gingival hyperplasia
Serology: detection and measurement of antibodies to a given antigen
Serotyping: identifies ab's to particular ag
Seroconversion: first detection of ag specific ab's in = 4 x increase in titer between acute and convalescent. Primary infection IgM>>IgG, Anamnestic IgG>>IgM
Titer: inverse of greatest dilution = detectible activity
Type I hypersensitivity is: immediate or atopic allergy (anaphylaxis)
What is type I hypersensitivity mediated by?: IgE
What is the pathology triggered by in type I hypersensitivity: IgE-FcR of mast and basophils -> degranulation
What are the three phases of Type I hypersens.?: sensitization, activation, and effector
What occurs during sensitization in type I?: first exposure (protein ag only) --> production of IgE (IL-4 --> TH2 response), mechanism = genetic, downregulation of TNF
What occurs during activation of type I?: sencond exposure, ag:IgE-FcR cross linking --> mast cell/basophil degranulation (also caused by non-specific = lectins, chemicals, cold heat, pressure)
What stages occur during the effector phase?: Early stage and late stage
Early stage occurs when?: less than 4-6 hours after exposure
What mediates this early stage during effector phase?: Products of mast cells and basophils
What preformed granules are stored in the mast cells?: histamines/serotonin, chemotactic factors, heparin
What granules are made by the mast cells upon activiation?: leukotrienes, thromboxanes/prostoglandins, PAF (platelet activating factor)
Late stage of the effector phase occurs when?: greater than 4-8 hours post-exposure
What is the late stage of effector phase mediated by?: recruited neutrophils and eosinophils; cytokines (esp. IL-4) also promotes TH2-type response
Eosinophils degranulation damages what?: parasites, may also cause tissue damage
Neutrophils activation causes?: release of lysosomal contents, inflamatory mediators and chemotactic factors
What is the route of exposure with anaphylactic shock?: IV (drugs, serum, venom), sytemic = most dangerous
Type 1 hypersnsitivity is characterized by: edema, erythema and smooth muscle contraction
What is the route of exposure with wheal and flare (atopic dermatitis): Subcutaneous (Insect bites, allergy testing)
What is the route of exposure with allergic rhinitis?: Inhaled (pollen, dust mite feces)
What is the route of exposure with Bronchial asthma?: Inhaled (pollen, dust mite feces)
What is the route of exposure with food allergies?: Oral (shellfish, milk, eggs, fish, wheat)
Response to anaphylactic shock?: edema, vasodilation, tracheal occlusion, circulatory collapse,
Response to wheal and flare?: local vasoldilation, local edema
Response to allergic rhinitis (hay fever)?: edema and irritation or nasal mucosa
Response to bronchial asthma?: bronchial constriction, increased mucosa, airway inflammation
Response to food allergy?: vomiting, diarrhea, itching, and hives
How do you treat early phase of type I hyper.?: anti-histamines
How do you treat late phase of type I hyper?: corticosteroids (anti-inflammatory and immunosuppressive agents repress recruited cells)
type II hypersensitivity is?: cytolytic/cytotoxic response
What is type II hypersensitivity mediated by?: IgG/IgM
What is the pathology triggered by in type II hypersensitivity?: antibody binding to cell surface molecules leads to target cell (1. complement -mediated 2. ADCC or 3. altered receptor signaling)
Most dangerous route of exposure for type I hypersensitivity?: via stream
Types of altered signaling in type II hypersensitiviy?: antagonist (inhibiting its function); agonist (mimcks the receptor's normal ligand)
Key example of type II hyper.?: blood transfusion rxns, induced rxns (hapten), autoimmune syndromes
2 Autoimmune examples of type II hyper.: Myesthenia gravis and Grave's disease
Autoimmune disease that is antagonist?: Myesthenia gravis
Autoimmune disease that is agonist?: Grave's disease (hyperthyroidism)
Autoantibodies to acetocholine receptor impairs neuromuscular trans.?: Myesthenia gravis
Autoantibodies to thyroid hormone receptor cause stimulate cells, hyper thyroidism: Grave's disease
Type III hypersensitivity is: an immune complex disease
What is type III hyper. Mediated by?: IgG and IgM
What is the pathology of Type III triggered by?: tissue deposition of immune complexes
What are the three phases of Type III hyper.?: 1. immune complex formation (IgG), immune complex deposition, complex mediated inflamm.
Immune complex formation involves?: small/medium size immune complex
Immune complex deposition involves?: deposit locally(e.g. subcutaneous) or systemically (e.g. intravenously)
Complex mediated inflammtion involves?: initiation of complement cascade (C3a, C5a), recruitment/activation of PMNs lead to inflam. And tissue damage
Example of Systemic immune complex diseases?: serum sickness; IV of animal serum, subsequent IV, anti-serum complex form, pathology
Example of localized immune complex disease?: Arthus rxn; subcutaneous injection or antigen into pt. sensitized to antigen leads to formation of immun complexes that deposit into tissue, leading to localized tissue necrosis
What is infection-induced immune complex disease?: antibodies produced in response to an infectious microorg. Cross-react against normal tissue
Example of infection induced immune complex disease?: rheumatic fever- antibodies against group A strep
What are occupational diseases?: Intrpulmonary arthus-type rxn, due to inhalation of lg. amts. Of antigenic material over time
Examples of occupational disease?: farmer's lung a.k.a. allergic alveolitis, pneumonitis
Type IV hypersensitivity is?: delayed type hypersensitivitiy
Type IV hypersensitivity is mediated by?: T cells
What is the pathology of Type IV hyper. Triggered by?: activation of sensitized TH1 cells
What are the two phases of Type IV hyper.?: Sensitization and Elicitation
Sensitization involves: primary exposure to protein or hapten-conjugates primes responding naive T cells, causing differentiation into TH1 type
Elicitation involves: subsequent exposure activated TH1 cell; resulting in cytokine/chemokine production leads to macrophage activation, inflamm. And tissue damage
Damage of Type IV hyper. Is characterized by: erythema, skin induration, cell infiltrates
Treatment of Type IV hyper.?: usually resolves once antigen is removed (â‰¤1 week)vtopical coritcosteroids for more severe
Type IV hyper. Syndromes are?: Jones-mote, contact, TB test, and Granulomatous
Rxn time, clinical appearance of jone-mote (cutaneous basophil hypers.: 24 hours, skin swelling
Histological appearance and antigen of Jones-mote: basophils. Lymphocytes and mononuclear cells; intradermal
Rxn time, clinical appearance of contact (epidermal): 48 hours; eczema (dermatitis)
Histological appearance and antigen of contact: mononuclear cells, edema, and raised epidermis; haptens: (poison ivy) Metals
Rxn time and clinical appearance of TB test: 48 hours; local induration and swelling +/- fever
Histological appearance and antigen of TB test: mononuclear cells, lymphocytes, and macrophages; Tuberculin mycobacterial leishmanial
Rxn time and clinical appearance of Granulomatous: 4 weeks; skin induration
Histological appearance and antigen of granulomatous: granulomous, giant cells, macs, fibrosis +/- necrosis; persistant Ag or Ab:Ag complexin macrophages
Type IV dental reactions are elicited by what substances: metals, composite resins
Sx of type IV dental reactions include swollen lips, rashes of the head and neck and_____________ in the oral cavity.: lesions
Auto-reactive B cells usually do not pose a problem as long as auto reactive __ _____ are removed by the ________: t cells, thymus
Auto reactive B cells are as dangerous as auto-reactive T cells. T/F: False, auto-reactive B cells won't have T-cell help for activation
T cells may cross react to B cell presented ag, or with a novel ______.: epitope
Can mitogens activate T and B cells?: Yes, both
modes of activation of auto reactive b cells are:: (A)T cell reacts with novel or modified self antigen and stimulates b cell activity (B) mitogens may trigger T or B cells against self antigens
Acute rheumatic fever: Type II Hypersensitivity/ anti- strep ab. vs. cardiac muscle --> Myocarditis &valve scarring
Autoimmune hemolytic anemia: Type II Hypersensitivity/ Rh antigen --> RBC destruction
Goodpastureâ€™s syndrome: Type II Hypersensitivity/ab vs. basement membrane type IV collagen --> lung hemorrhage, renal failure, vasculitis
Hemolytic anemia, Goodpasture's and RF are all type II reactions causing cell _______.: destruction (Type II)
Grave's disease, Myasthenia gravis, insulin-resistant diabetes and hypoglycemia are Type II hypersensitivity reactions involving ______ ______: surface receptors
Graveâ€™s disease: Type II Hypersensitivity/ ab. Stimulate thyroid --> hyperthyroidism
Hashimoto's thyroiditis: Type IV / Thyroglobulin --> Destruction of Thyroid
Hypoglycemia: Type II Hypersensitivity/ ab. Have insulin-like effect (agonist) --> hypoglycemia
Insulin dependent diabetes mellitus: Type IV Hypersensitivity / pancreatic B cell ag --> Beta cells of pancreas destroyed
insulin-resistant (receptor) diabetes: Type II Hypersensitivity/ ab blocks effect of insulin by binding receptor (antagonist) --> hyperglycemia
Mixed essential cryoglobulinemia: Type III Hypersensitivity IgG --> vasculitis
Multiple sclerosis: Type IV Hypersensitivity / myelin basic protein -->brain invasion by CD4+ T cells, paralysis
Myasthenia gravis: Type II / Ab binds acetylcholine receptors --> impaired neuromuscular transmission
Subacute bacterial endocarditis: Type III Hypersensitivity / bacterial ag --> glomerulonephritis
Systemic lupus erythematosus (SLE): Type III Hypersensitivity /Arthritis glomerulonephritis, vasculitis
SBE, mixed essential cryoglobulinemia and SLE are all type ___ reactions: III
Insulin-dependent diabetes, Rheumatoid arthritis, EAE, MS and Hashimoto's thyroditis are all reactions of what type?: IV
Rheumatoid arthritis: Type IV Hypersensitivity / joint inflammation and destruction
In _________ ________, auto antibodies disrupt the desmosomes of epithelial cells (struatum spinosum) causing sloughing of tissue, bullae and ulceration: Pemphigus vulgaris
Pemphigus vulgaris is usually treated with:: Corticosteroids and immunosuppressive
In benign mucous membrane pemphigoid, auto-antibodies are produced against the ______ _______ of the oral mucosa and ______.: basement membrane, eyes (gingiva peels off)
benign mucous membrane pemphigoid is usually treated with:: Corticosteroids and immunosuppressive
Auto antibodies mediate destruction of secretory acini of salivary glands in ________ syndrome: Sjogren's
Clinical symptoms of Sjogren's are ________ (dry mouth), ________ (dry eyes) cobblestone/fissured tongue and _____ filiform papillae.: Xerostomia; xerophthalmia' atrophied
This fungus often infects the oral cavity as a result of xerostomia.: Candida albicans (thrush)
With lupus, auto antibodies are produced against what type of antigens?: antinuclear antigens (ANA)
Lupus affects what parts of the body?: skin, joints, lungs, kidneys, heart, brain, just about any other organ or system of the body (70% systemic)
Oral Lichen planus is also known as _____ ________.: Wickhams striae
Oral Lichen planus is presumed to be caused by an autoimmune reaction to ______ cells of the oral mucosa and skin.: Basal
T/F Oral Lichen planus can lead to squamous cell carcinoma: TRUE
B cell deficiencies generally lead to an increase in ___________ infections: Bacterial
T cell deficiencies generally lead to an increase in ______, _______, and ________ infections.: viral, fungal, protozoal(mostly opportunistic)
What general immune cell deficiency leads to increased infections with pyogenic bacteria and bacteria of usually low virulence,: Phagocytic cell deficiency
NK cell deficiency leads to increased _________ infections.: Viral
SCID patients are most susceptible to CMV, Pneumocystis carnii and _____ ______: Candida albicans (thrush)
SCID is a reduction in the number of which lymphocytic cells?: B and T
X linked SCID (40-50%): T cells reduced most, variable B
Both T and B cells reduced in (30%): ADA, defective VDJ, RAG proteins
Bare lymphocytes (no MHC 2) Ataxia Telangectasia and WASP are all forms of: SCID both T and B cells variable (20%)
DiGeorge syndrome is a T cell deficiency syndrome that is cause by:: Thymic aplasia (no thymus)
T cell deficiency diseases include __ _______, T cell mutations and chronic mucocutaneous ________: DiGeorge's, candidiasis
chronic mucocutaneous candidiasis is a defect in what?: cell-mediated immunity to fungi
X-linked gamma globulinemia results in no B cellls T or F: False --> no mature B cells --> repeated bacterial infection
Common variable immunodeficiency is a __ cell deficiency disease that has a specific decrease of these two antibody classes.: B : IgG, IgA = susceptible to pyogenic bacteria
selective immunoglobulin deficiency involve which antibodies and lead to what: IgM, IgA mostly A --> respiratory infection
XLA, common variable immunodef., and selective immunoglobulin def. are all _ ___ immunodeficiency diseases: B Cell
Lack of IgA will lead to susceptibility to __________ infections.: Respiratory(mucosal)
Lack of IgM leads to susceptibility of these types of organisms.: Encapsulated bacteria
Name three specific phagocyte immunodeficiency diseases:: LAD (leukocyte adhesion deficiency)/ CHS (Chediak-Higashi syndrome)/ CGD (Chromic granulomatous disease)
Main result of LAD (leukocyte adhesion deficiency): impaired migration of phagocytes to site of infection (neutropenia)
Main result of CHS (Chediak-Higashi syndrome): Impaired phagosome-lysosome fusion and poor intracellular ----giant lysosomes
Main result of CGD (Chromic granulomatous disease): Poor of organisms due to defective NADPH oxidase that forms hydrogen peroxide and superoxide
Complement deficiencies generally lead to increased _____________ infections: Bacterial
Deficiency of early complement components (C1-C4) leads to:: infections with Encapsulated bacteria(G -)/ poor clearance of immune complexes
Deficiency of late complement components (C5-C9) leads to:: Deficient membrane attack complex (MAC) / impaired defense against G- bacteria
Complement regulatory factor deficiency causes Hereditary angiodema (uncontrolled release of vasoactive peptides) and _______ ______ causing uncontrolled host bystander cell: Paroxysmal Nocturnal Hemoglobulinemia
Certain staph infections can cause secondary immunodeficiency by producing ____________ which activate 2 - ___ % of T cells and cause massive cytokine production: Superantigens; 20
HIV infects these two types of immune cells.: macrophages and CD4+ T cells
T/F HIV is a retrovirus?: TRUE
Why does treatment of transplant recipients or cancer patients cause secondary immunodeficiency?: Chemotherapy or irradiation kills rapidly dividing cells, including lymphocytes. Cell signaling pathways are also effected.
oral conditions common in HIV patients that are listed in the lecture notes include:(3): candidiasis, Oral hairy leukoplakia, Kaposi's sarcoma
What conditions: are associated with the following viruses? Epstein-Barr virus, Human Herpes virus: Epstein-Barr: Oral Hairy Leukoplakia / Human Herpes virus: Kaposi's Sarcoma
Name five general treatments of immunodeficiency:: Antibiotics, gamma globulins, bone marrow transplants, gene therapy, antiviral
T/F A Xenograph is between individuals of the same species.: False--- between different species.
An __________ comes from a different site of the same individual.: autograph
T/F An allograph is from a genetically related individual?: False
What is another name for an isograph?: syngenic or syngraph
What is the time frame of each of the 4 types of graph rejection?: hyperacute : minutes to hours/ Accelerated : 2-5 days/ Acute : 7-21 days/ chronic : months to years
Which two of the four types of rejection occur because of prior exposure to transplanted antigens?: Hyperacute, accelerated
T/F acute graft rejection occurs because of prior exposure to transplanted antigens?: FALSE
What immune components are responsible for hyperacute, acute, and accelerated graft rejection?: hyperacute : antibodies, acute : T cells, accelerated : T cells
T/F Rejection of transfusions is mainly cell mediated.: False :(humoral-- antibodies destroy rbcs with non matching A,B,or RH antigens)
T/F Graft verses host disease seen with bone marrow transplants occurs when immature T cells attack host tissues.: False, (mature T cells)
How can Graft verses host (GVH) disease be avoided in bone marrow transplants?: deplete donor bone marrow of mature T cells before transplant good matching
Six characteristics of GVH disease:: enlarged liver, spleen, and lymph nodes; diarrhea; anemia; and weight loss
Two methods used to decrease likelihood of graft/transplant rejection:: A: find closest match of minor and major histocompatibility antigens B: immunosuppression after grafting
Three factors influencing cancer:: genetic predisposition, lifestyle, immune status
Four listed cause of cancer:: Chemical carcinogens, irradiation, stochastic DNA events, viruses
A carcinoma is of _________ origin.: Epithelial
Leukemia is generally found in ______ or _____ _______ and lymphoma is generally found in _______ tissue: blood, bone marrow/ lymphoid
multiple myeloma displays effected _______ cells and is found where?: plasmacyte, in bone marrow
B cell acute lymphoblastic leukemia (B-ALL) is cancer of B cells and normally found where?: blood, bone marrow
Follicular and Burkitt's lymphoma are found in peripheral lymphoid organs effecting mature __ cells.: B
Chronic lymphocytic leukemia (B-CLL) is a cancer of CD5+ B cells and is found in bone marrow, and ____.: organs
Acute lymphoblastic luekemia/lymphoma (T-ALL) affect _____: thymocytes
Adult T cell leukemia occurs in the and ______: periphery
Where do lymphoid cancers often exhibit chromosomal translocations?: Ig or TCR loci
Intra-oral lymphomas may be found on the gingiva or hard palate T/F: True - they may be misdiagnosed for Kaposi's sarcoma
Acute leukemia oral manifestation: gingival swelling and bleeding
Hepatitis B virus is associated with which type of cancer?: Hepatocellular carcinoma
Epstein-Barr virus is associated with which type of cancer?: B cell lymphoma
HHV8 (+HIV) is associated with which type of cancer?: Kaposi's sarcoma
Human T cell lymphotrophic virus (HTLV-1) is associated with which type of cancer?: T cell leukemia
Human papillomaviruses 16 and 18 are associated with which type of cancer?: Cervical carcinoma
Mutations, abnormal gene activation and viral encoded genes refered to as _____ antigens are often expressed and detected by the immune system.: novel
3 key cellular responses to cancer: novel ag's, cell mediated immunity (most important), ab's
TH1 T cells activate __________: macrophages
CD8+ cytotoxic T cells detect _____ ______ on MHC: altered peptides
Which cell is cytotoxic to cells with loss of MHC and ADCC: NK cells
Lymphokine activated killer cells (LAK) are activated by____?: IL-2
Humoral immunity against tumor cells includes ________ _________, inhibition of _____ and __________.: Complement fixation; adesion; opsonization
Inhibition of adhesion is a defense against _______: metastasis
3 types of cancer Tx: Radiation, chem and immunotherapy

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