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Summer Immuno Lecture 12

front 1

A pregnant patient’s placenta produces a cytokine that shifts maternal helper T cells away from a Th1 profile to improve fetal survival. Which cytokine is responsible?

back 1

IL-4

front 2

Because of placental immune biasing during pregnancy, most humans are born with helper T cells skewed toward which cytokine profile?

Th___ cytokines

back 2

Th2 cytokines

front 3

A child raised with limited microbial exposure later develops multiple environmental allergies. Which concept best explains this association?

A. Molecular mimicry

B. Hygiene hypothesis

C. Epitope spreading

D. Anergy escape

back 3

B. Hygiene hypothesis

front 4

According to the hygiene hypothesis, early childhood microbial infections tend to bias immune responses toward which helper T-cell subset?

A. Th17 cells

B. Tfh cells

C. Th2 cells

D. Th1 cells

back 4

D. Th1 cells

front 5

In populations with improved hygiene and fewer childhood infections, which disease pattern is expected to increase?

A. Allergic disease

B. Severe neutropenia

C. Complement deficiency

D. Chronic granulomas

back 5

A. Allergic disease

front 6

Early exposure to certain allergens is thought to reduce later allergy risk by promoting which immune bias?

A. Th2 polarization

B. Th1 polarization

C. IgE fixation

D. Mast-cell priming

back 6

B. Th1 polarization

front 7

Which T-cell population helps prevent IgE production against common environmental allergens?

____ ____ cells

back 7

Regulatory T cells

front 8

A tissue helper T cell is induced to suppress allergic antibody production. What cell type has it most likely become?

____ cell

back 8

iTreg cell

front 9

An iTreg suppresses allergic sensitization by producing cytokines that redirect antibody class switching. Which cytokine pair is involved?

A. IL-4 and IL-5

B. IL-2 and IL-12

C. IFN-gamma and TNF

D. IL-10 and TGF-beta

back 9

D. IL-10 and TGF-beta

front 10

In non-atopic individuals, most CD4+ T cells specific for common allergens belong to which population?

A. Th17 cells

B. Regulatory T cells

C. Cytotoxic T cells

D. Follicular T cells

back 10

B. Regulatory T cells

front 11

A patient has mutant IgE receptors that signal excessively after crosslinking. Which mast-cell cytokine is abnormally increased?

back 11

IL-4

front 12

Excessive IL-4 secretion from mast cells in an atopic patient would most directly increase production of which antibody class?

back 12

IgE

front 13

Omalizumab prevents allergic activation by binding which region of IgE?

___ region

back 13

Fc region

front 14

Omalizumab blocks IgE from binding most directly to which allergy-effector cell?

A. Eosinophils

B. Mast cells

C. Th1 cells

D. Tregs

back 14

B. Mast cells

front 15

What defines autoimmune disease?

A. Loss of self-tolerance

B. Excessive IgA switching

C. Persistent eosinophilia

D. Failed antigen uptake

back 15

A. Loss of self-tolerance

front 16

Chronically stimulated self-reactive T cells are normally eliminated after ligation of which surface molecule?

____

back 16

Fas

front 17

Which tolerance mechanism eliminates chronically stimulated T cells through Fas-mediated signaling?

A. Somatic hypermutation

B. Molecular mimicry

C. Class switching

D. Activation-induced cell death

back 17

D. Activation-induced cell death

front 18

Molecular mimicry is when a microbe expresses an _____ that resembles a _____ _____ , activating self-reactive _____ .

back 18

antigen

host antigen

lymphocytes

front 19

Molecular mimicry can activate lymphocytes that had previously failed to respond to which antigen type?

____-____

back 19

Self-antigens

front 20

A patient develops seasonal allergic rhinitis after exposure to outdoor aeroallergens. Which source most likely triggered hay fever?

A. Mold spores or pollens

B. Animal venoms

C. Indoor endotoxins

D. Bacterial capsules

back 20

A. Mold spores or pollens

front 21

Compared with hay fever allergens, asthma-triggering allergens are most commonly found in which location?

back 21

Indoors

front 22

A non-allergic person and an atopic person encounter the same environmental antigen. Which antibody pattern is most likely?

A. IgE versus IgG

B. IgG versus IgE

C. IgA versus IgM

D. IgM versus IgA

back 22

B. IgG versus IgE

front 23

During initial allergen sensitization, mast cells bind which region of newly produced IgE?

A. Fab region

B. Variable region

C. Hinge region

D. Fc region

back 23

D. Fc region

front 24

An atopic patient is re-exposed to an allergen after prior sensitization. What event directly initiates mast-cell degranulation?

A. IgE crosslinking

B. IgG opsonization

C. Fas ligation

D. Treg induction

back 24

A. IgE crosslinking

front 25

Free IgE in blood has approximately what half-life?

A. Two months

B. Two weeks

C. Two days

D. Two hours

back 25

C. Two days

front 26

When IgE is attached to mast cells, it can persist for approximately how long?

A. Hours

B. Days

C. Weeks

D. Months

back 26

D. Months

front 27

Which cells mediate the immediate phase of allergic reactions?

_____ cells and _____

back 27

Mast cells and basophils

front 28

Which allergic effector cell is primarily stationed in tissues?

back 28

Mast cell

front 29

Which allergic effector cell is primarily found circulating in blood?

back 29

Basophil

front 30

Which cell type mainly mediates the delayed phase of allergic reactions?

_____

back 30

Eosinophils

front 31

In chronic allergic reactions, T-cell production of which cytokine recruits eosinophils from bone marrow?

back 31

IL-5

front 32

A germinal center dominated by Th1 cells is most likely to generate B cells producing which antibody class?

back 32

IgG

front 33

Th1-dominated germinal centers promote IgG class switching through secretion of which cytokine?

back 33

IFN-gamma

front 34

A germinal center dominated by Th2 cells is most likely to generate B cells producing which antibody class?

back 34

IgE

front 35

Th2-dominated germinal centers promote allergic antibody production through which cytokines?

A. IL-2 and IL-12

B. IL-10 and TGF-beta

C. IL-4 and IL-5

D. IFN-gamma and TNF

back 35

C. IL-4 and IL-5

front 36

An atopic patient has recurrent allergic rhinitis and asthma after common environmental exposures. Which helper T-cell subset would be increased?

A. Th1 cells

B. Th2 cells

C. Th17 cells

D. Tfh cells

back 36

B. Th2 cells

front 37

A Th1 cell secretes TNF during a cellular immune response. Which innate immune cell is most directly activated?

___ ___ cell

back 37

NK cell

front 38

A Th1 response produces IL-2 during intracellular infection. Which cell populations proliferate in response?

____ cells and ____

back 38

NK cells and CTLs

front 39

At the maternal-fetal interface, placental cytokines shift helper T cells away from Th1 immunity. Which helper T-cell fate is promoted?

A. Th17 cell

B. Tfh cell

C. Th1 cell

D. Th2 cell

back 39

D. Th2 cell

front 40

An infant’s early microbial infection biases later immune responses toward which helper T-cell subset?

A. Th1 cells

B. Th2 cells

C. Tfh cells

D. Treg cells

back 40

A. Th1 cells

front 41

The composition of the intestinal microbiota is mainly established during which period?

A. First few years

B. Early adolescence

C. Late adulthood

D. Fetal development

back 41

A. First few years

front 42

A patient has inherited allergy susceptibility involving antigen presentation to CD4 cells. Which gene group is implicated?

A. Class I MHC

B. Class II MHC

C. TCR alpha

D. CD8 coreceptor

back 42

B. Class II MHC

front 43

An atopic patient has inherited IgE receptor variants that amplify mast-cell signaling. Which cytokine becomes elevated?

A. IL-10

B. IFN-gamma

C. IL-4

D. IL-12

back 43

C. IL-4

front 44

A patient receives glucocorticoids for severe allergic disease. Which immune effect explains symptom improvement?

Block ____ ____

back 44

Block helper cytokines

front 45

Glucocorticoids reduce allergic responses partly by lowering helper T-cell cytokines. What downstream B-cell effect follows?

Fewer activated ____ cells

back 45

Fewer activated B cells

front 46

A patient on chronic glucocorticoids has improved allergies but develops recurrent infections. What adverse immune effect explains this?

A. Weakened immune system

B. Enhanced Th1 immunity

C. Increased complement lysis

D. Excessive IgA secretion

back 46

A. Weakened immune system

front 47

Which allergy treatment is described as the only approach capable of curing allergies?

A. Omalizumab therapy

B. Glucocorticoid therapy

C. Specific immunotherapy

D. Antihistamine therapy

back 47

C. Specific immunotherapy

front 48

Specific immunotherapy treats allergy by repeatedly giving which type of exposure?

A. Decreasing allergen doses

B. Increasing allergen doses

C. Single allergen bolus

D. Continuous steroid pulses

back 48

B. Increasing allergen doses

front 49

Current theory suggests allergen immunotherapy induces regulatory T cells to produce which cytokines?

A. IL-4 and IL-5

B. IFN-gamma and TNF

C. IL-2 and IL-12

D. IL-10 and TGF-beta

back 49

D. IL-10 and TGF-beta

front 50

An allergy patient develops increased IL-10 after therapy. What outcome would this cytokine most likely promote?

A. Prevent allergic reaction

B. Increase IgE secretion

C. Activate mast cells

D. Recruit eosinophils

back 50

A. Prevent allergic reaction

front 51

A child has autoimmune lymphoproliferative syndrome with enlarged lymph nodes. What mechanism best explains the disorder?

____ signaling defect

back 51

Fas signaling defect

front 52

In autoimmune lymphoproliferative syndrome, defective Fas signaling causes which cellular abnormality?

A. B cells die early

B. T cells survive too long

C. NK cells lose cytotoxicity

D. Eosinophils leave marrow

back 52

B. T cells survive too long

front 53

A patient with Canale-Smith syndrome develops lymphadenopathy and autoantibodies. Which cell type accumulates abnormally?

A. T cells

B. Mast cells

C. Neutrophils

D. Basophils

back 53

A. T cells

front 54

Which finding is characteristic of autoimmune lymphoproliferative syndrome?

A. Self-reactive antibodies

B. Absent class II MHC

C. Low lymphocyte counts

D. Failed IgE binding

back 54

A. Self-reactive antibodies

front 55

For autoimmune disease to occur, MHC molecules must be able to present which antigen type?

____ antigen

back 55

Self antigen

front 56

Which lymphocyte feature is required for autoimmune disease development?

Self-____ ____

back 56

Self-reactive receptors

front 57

Besides genetic susceptibility and self-reactive lymphocytes, which factor often contributes to autoimmunity?

____ trigger

back 57

Environmental trigger

front 58

A patient develops autoimmune disease after infection because lymphocyte receptors cross-react with host tissue. Which hypothesis explains this?

back 58

Molecular mimicry

front 59

Rheumatic heart disease after streptococcal infection is classically an example of which mechanism?

back 59

Molecular mimicry

front 60

A self-reactive T cell encounters a microbial mimic of self antigen. What additional condition is needed for activation?

A. Simultaneous local inflammation

B. Absent antigen presentation

C. Complete cytokine silence

D. Immediate eosinophil depletion

back 60

A. Simultaneous local inflammation

front 61

For molecular mimicry to activate self-reactive T cells, inflammation must occur in tissue that also expresses what?

A. IgE receptor

B. Self antigen

C. Fc fragment

D. Complement receptor

back 61

B. Self antigen

front 62

In insulin-dependent diabetes mellitus, which pancreatic cell type is initially targeted by autoimmune injury?

A. Alpha cells

B. Beta cells

C. Delta cells

D. Acinar cells

back 62

B. Beta cells

front 63

In insulin-dependent diabetes mellitus, beta cells are located in which organ?

A. Pancreas

B. Thyroid

C. Adrenal gland

D. Pituitary

back 63

A. Pancreas

front 64

Which immune cell initially attacks beta cells in insulin-dependent diabetes mellitus?

____ ____ cells

back 64

Killer T cells

front 65

Reduced CTLA-4 RNA increases diabetes susceptibility by impairing control of which cells?

_____-____ T cells

back 65

Self-reactive T cells

front 66

Which molecule normally helps restrain self-reactive T cells in diabetes susceptibility?

A. CTLA-4

B. CD40L

C. IL-17

D. IgM

back 66

A. CTLA-4

front 67

Plaque psoriasis most characteristically produces which skin finding?

____ and ____

back 67

Thickening and scaling

front 68

Plaque psoriasis is driven mainly by which immune cell type?

A. Th2 cells

B. B cells

C. CD8 cells

D. Neutrophils

back 68

C. CD8 cells

front 69

In plaque psoriasis, CD8 cells produce which cytokine that promotes keratinocyte proliferation?

back 69

IL-17

front 70

In plaque psoriasis, IL-17 causes proliferation of which cell type?

A. Keratinocytes

B. Fibroblasts

C. Chondrocytes

D. Oligodendrocytes

back 70

A. Keratinocytes

front 71

The proposed self-reaction in psoriasis involves class I MHC recognition of streptococcal antigens and what self-cell target?

A. Cartilage

B. Keratinocytes

C. Myelin

D. Beta cells

back 71

B. Keratinocytes

front 72

The proposed infectious trigger in plaque psoriasis involves which organism group?

A. Mycobacteria

B. Epstein-Barr virus

C. Streptococcal bacteria

D. Candida species

back 72

C. Streptococcal bacteria

front 73

Rheumatoid arthritis is primarily characterized by autoimmune inflammation of which structure?

A. Pancreatic islets

B. Central myelin

C. Hair follicles

D. Joints

back 73

D. Joints

front 74

In rheumatoid arthritis, autoimmune cells react against cartilage and a protein from which infection?

A. Tuberculosis

B. Epstein-Barr virus

C. Streptococci

D. Influenza

back 74

A. Tuberculosis

front 75

Which tissue antigen is targeted in rheumatoid arthritis?

A. Myelin

B. Cartilage

C. Keratin

D. Insulin

back 75

B. Cartilage

front 76

In rheumatoid arthritis, abundant IgM antibodies bind which region of IgG?

A. Fab region

B. Hinge region

C. Fc region

D. Variable region

back 76

C. Fc region

front 77

The IgM antibody that binds IgG Fc in rheumatoid arthritis forms which pathogenic structure?

A. Cytotoxic synapse

B. IgE tetramer

C. MHC complex

D. Immune complex

back 77

D. Immune complex

front 78

In rheumatoid arthritis, IgM-IgG immune complexes activate which inflammatory cell?

A. Macrophage

B. Mast cell

C. Basophil

D. Keratinocyte

back 78

A. Macrophage

front 79

Activated macrophages in rheumatoid arthritis produce which cytokine causing inflammation?

back 79

TNF

front 80

Multiple sclerosis involves immune-mediated destruction of which structure?

A. Cartilage

B. Keratin

C. Myelin

D. Beta cells

back 80

C. Myelin

front 81

Myelin is required primarily for which nervous-system function?

A. Cytokine production

B. Antibody secretion

C. Cartilage repair

D. Electrical signaling

back 81

D. Electrical signaling

front 82

Multiple sclerosis occurs almost exclusively in people previously infected with which virus?

back 82

Epstein-Barr virus

front 83

Epstein-Barr virus establishes chronic infection in which cell type?

____ cells

back 83

B cells

front 84

The classic facial rash of lupus involves which areas?

____ and ____

back 84

Forehead and cheeks

front 85

The “red wolf” appearance in lupus refers most directly to which manifestation?

A. Kidney damage

B. Hair loss

C. Arthritis

D. Facial red rash

back 85

D. Facial red rash

front 86

Systemic lupus erythematosus results from breakdown of tolerance in which lymphocyte groups?

A. B and T cells

B. NK and mast cells

C. CD8 and basophils

D. Neutrophils and monocytes

back 86

A. B and T cells

front 87

In lupus, loss of B- and T-cell tolerance results in production of which self-reactive antibody class?

back 87

IgG

front 88

One proposed lupus mechanism involves defective interaction between Fas and which partner molecule?

back 88

Fas ligand

front 89

Another proposed lupus mechanism involves mutation in which innate immune receptor family?

A. IgE receptors

B. TNF receptors

C. IL-2 receptors

D. Toll-like receptors

back 89

D. Toll-like receptors