Summer Immuno Lecture 16 Flashcards

A hybridoma is formed by combining an antibody-producing B cell with what other cell?

A. Cancerous B cell

B. Stem cell

C. Plasma cell

D. Tfh cell

In hybridoma production, the cancerous B-cell parent contributes which key property?

A. Antigen specificity

B. Indefinite growth

C. Cytokine secretion

D. Class switching

In hybridoma production, the normal B-cell parent contributes which key property?

A. Antibody production

B. Tumor invasion

C. Infinite replication

D. Phagocyte targeting

A hybridoma is useful because it functions as what?

Antibody ______

Hybridomas generate a clone of cells with what survival property?

A. Short-lived

B. Immortal

C. Anergic

D. Exhausted

A hybridoma-derived clone produces how many antibody specificities?

A. Two specificities

B. Many specificities

C. No specificity

D. One specificity

Antibodies made by one immortal hybridoma clone are called what?

_____ antibodies

The common term for a therapeutic monoclonal antibody is what?

A. Biologic

B. Probiotic

C. Toxoid

D. Adjuvant

Adalimumab is the generic name for which biologic?

A. Cosentyx

B. Herceptin

C. Humira

D. Rituximab

Humira decreases ______ ______ symptoms by blocking ______.

Blocking TNF with Humira increases susceptibility to what?

A. Yeast infections

B. Malignancy

C. Infections

D. Autoantibodies

Secukinumab is the generic name for which biologic?

A. Humira

B. Herceptin

C. Rituximab

D. Cosentyx

Cosentyx treats plaque psoriasis by blocking which cytokine?

Cosentyx blocks IL-17 interaction with receptors on which cell type?

A. Chondrocytes

B. Keratinocytes

C. Oligodendrocytes

D. Monocytes

Blocking IL-17 with Cosentyx increases susceptibility to which infection type?

A. Mycobacterial

B. Yeast

C. Viral

D. Helminthic

Alemtuzumab is also known as which monoclonal antibody?

A. Herceptin

B. Rituximab

C. Campath-1H

D. Humira

Campath-1H binds which surface molecule?

A. CD20

B. CD28

C. CD40

D. CD52

CD52 is found on _____ cells, _____ cells, and _____

Campath-1H targets CD52-positive cells for removal by which cells?

_______

Campath-1H is a modern treatment for which autoimmune disease?

______ ______

Multiple sclerosis is mediated by which pathogenic lymphocyte type?

A. Self-reactive T cells

B. IgE-producing B cells

C. Hyperactive basophils

D. Defective neutrophils

Campath-1H spares which cell population?

_____ stem cells

Sparing lymphocyte stem cells allows what after initial lymphocyte destruction?

A. Continued lymphocyte proliferation

B. Permanent T-cell absence

C. Immediate antibody blockade

D. Complete marrow failure

Which was the first humanized antibody approved by the FDA?

A. Humira

B. Rituximab

C. Herceptin

D. Campath-1H

Rituximab is used to treat which malignancy?

Non-Hodgkin lymphoma can arise when which cells acquire maturation-blocking mutations?

_____ cells

Rituximab targets which B-cell surface molecule?

A. CD52

B. HER2

C. CD20

D. TNF

CD20 is present specifically on which target cells?

_____ B cells

CD20 is absent from which antibody-producing stage?

A. Plasma-cell stage

B. Immature B-cell stage

C. Naive B-cell stage

D. Memory B-cell stage

CD20 is also absent from which precursor population?

A. Monocytes

B. Tregs

C. Blood stem cells

D. Keratinocytes

About what fraction of metastatic breast cancers overproduce HER2?

A. 5%

B. 10%

C. 50%

D. 25%

HER2 acts as what type of signal on breast cancer cells?

A. Death receptor

B. Growth factor receptor

C. MHC molecule

D. Cytokine sink

Trastuzumab is the generic name for which biologic?

A. Herceptin

B. Humira

C. Cosentyx

D. Rituximab

Herceptin binds which receptor on breast cancer cells?

A. CD20

B. CD52

C. HER2

D. TNF

Herceptin treats metastatic breast cancer by blocking HER2’s function as what?

A. Costimulatory ligand

B. Checkpoint receptor

C. Complement receptor

D. Growth factor receptor

Which biologic is paired correctly with TNF blockade?

A. Cosentyx

B. Humira

C. Herceptin

D. Campath-1H

Which biologic is paired correctly with IL-17 blockade?

A. Herceptin

B. Rituximab

C. Campath-1H

D. Cosentyx

Which biologic is paired correctly with CD20 targeting?

A. Rituximab

B. Humira

C. Cosentyx

D. Herceptin

Which monoclonal antibody blocks CTLA-4 on T cells?

A. Nivolumab

B. Ipilimumab

C. Rituximab

D. Trastuzumab

CTLA-4 is found on the surface of which cells?

A. T cells

B. B cells

C. Neutrophils

D. Keratinocytes

Ipilimumab has been effective in treating which cancer?

A. Hodgkin lymphoma

B. Lung cancer

C. Metastatic melanoma

D. Cervical cancer

CTLA-4 normally helps protect against which problem?

A. Viral latency

B. Tumor mutation

C. Toxin release

D. Autoimmunity

CTLA-4 blockade can cause which autoimmune-like GI toxicity?

______

CTLA-4 blockade can also cause inflammation of which organ?

______

CTLA-4 normally competes with CD28 for which APC ligand?

A. PD-L1

B. CD40

C. Fas ligand

D. B7

Blocking CTLA-4 allows B7 to better support which T-cell signal?

A. Costimulation

B. Anergy

C. Opsonization

D. Degranulation

Which checkpoint blockade has successfully treated Hodgkin lymphoma?

A. CTLA-4 blockade

B. CD20 blockade

C. PD-1 blockade

D. TNF blockade

PD-1 blockade has shown success in advanced ____ and ____ cancer.

Which cancer is strongly associated with response to PD-1/PD-L1 blockade?

A. Hodgkin lymphoma

B. Colon adenoma

C. T-cell leukemia

D. Osteosarcoma

Checkpoint blockade requires that the patient already has which cells?

A. Naive B cells

B. Anti-tumor T cells

C. Resting mast cells

D. Immature neutrophils

_____ _____ works when anti-tumor T cells are limited by poor function or low numbers

Tumor-specific T cells are absent from what fraction of human tumors?

A. Few tumors

B. Half tumors

C. All tumors

D. Most tumors

Tumor-specific T cells often recognize which antigen type?

A. Neoantigens

B. Toxoids

C. Adjuvants

D. Autoantibodies

Neoantigens arise from mutations in DNA encoding which proteins?

A. Viral proteins

B. Normal proteins

C. Bacterial toxins

D. MHC molecules

Neoantigens are recognized by CTLs because they appear what?

A. Self

B. Tolerogenic

C. Foreign

D. Hidden

CTLs are not tolerant to neoantigens because they result from what?

A. Germline inheritance

B. Thymic deletion

C. IgE switching

D. Tumor mutations

PD-L1 on tumor cells binds which T-cell checkpoint?

A. CTLA-4

B. PD-1

C. CD28

D. B7

High PD-L1 expression is generally seen in which cancer?

A. Cervical cancer

B. Osteosarcoma

C. Hodgkin lymphoma

D. Hepatocellular cancer

Genetic mutations can create neoantigens but also generate which tumor variant?

A. Attenuated variants

B. Toxoid variants

C. Anergic variants

D. Escape variants

Escape variants evade immunity by losing detectable or presentable _____.

Checkpoint inhibitor responses may last years but eventually tumors may do what?

A. Sterilize fully

B. Grow again

C. Lose all cells

D. Become toxoids

TILs found in resected tumors showed the immune system was doing what?

A. Ignoring cancer entirely

B. Producing IgE only

C. Destroying all tumors

D. Recognizing tumor antigens

Tumor-infiltrating lymphocytes (TILs) possess receptors that specifically recognize antigens expressed by ____ cells.

TIL findings suggested tumors persisted partly because there were too few what?

A. Mast cells

B. Tumor-specific T cells

C. Bacterial antigens

D. MHC molecules

Tumor-specific T-cell receptors bind antigens generated by what process?

A. Class switching

B. IgE crosslinking

C. DNA mutation

D. Complement lysis

A tumor with many neoantigens may initially respond to checkpoint blockade but later escape due to what?

A. High mutation rate

B. Low proliferation

C. Absent mutations

D. Strong tolerance

A cancer therapy expands tumor-reactive lymphocytes recovered from a patient’s tumor. What is this procedure called?

A. Checkpoint blockade

B. Hybridoma fusion

C. Adoptive cell transfer

D. Passive immunization

ACT begins by culturing which cells recovered from tumors?

A. Tumor-infiltrating lymphocytes

B. Follicular dendritic cells

C. Immature blood stem cells

D. Regulatory B cells

During ACT, recovered tumor lymphocytes are cultured with which cytokine?

IL-2 is added during ACT primarily to drive TILs to do what?

A. Become anergic

B. Proliferate

C. Lose receptors

D. Secrete antibodies

After initial ACT cultures grow, they are tested for highest what against tumor cells?

A. Affinity

B. Anergy

C. Tolerance

D. Exhaustion

The selected ACT culture is expanded to approximately how many cells?

A. One million

B. Ten million

C. One billion

D. One hundred billion

ACT has been most successful against which cancer?

______

CAR T-cell therapy modifies a patient’s T cells to express what?

A. Natural BCR

B. Native CD20

C. Artificial TCR

D. Soluble antibody

The “CAR” in CAR T-cell therapy stands for what?

A. Cancer antigen receptor

B. Chimeric antigen receptor

C. Cytokine activating receptor

D. Complement attachment receptor

The surface portion of a CAR T receptor is mainly responsible for what?

A. Antigen recognition

B. IL-2 secretion

C. MHC loading

D. Thymic deletion

The CAR recognition domain binds antigens located where?

A. Inside lysosomes

B. On MHC

C. Cell surface

D. Inside nucleus

The CAR recognition domain is linked intracellularly to which signaling protein?

A. CD28

B. CD3-zeta

C. CTLA-4

D. PD-1

CD3-zeta in CAR T cells signals that what has occurred?

A. Target receptor engagement

B. Antibody class switching

C. MHC II recognition

D. Fc receptor binding

In CAR T cells, CD3-zeta is additionally linked to what component?

A. Cytokine receptor

B. IgE receptor

C. Complement receptor

D. Costimulatory molecule

The most successful CAR T-cell target so far has been which marker?

A. CD20

B. CD19

C. CD52

D. HER2

CD19 is expressed on many cancers from which categories?

_____ and _____

CAR T-cell therapy has successfully treated which leukemia?

A. Chronic myeloid leukemia

B. Acute myeloid leukemia

C. Chronic lymphocytic leukemia

D. Acute lymphoblastic leukemia

CAR T-cell therapy has also successfully treated which lymphoma type?

A. Non-Hodgkin lymphoma

B. Hodgkin lymphoma

C. Burkitt-like sarcoma

D. Cutaneous T lymphoma

Why do CAR T cells not require MHC presentation?

A. They bind soluble cytokines

B. They only kill APCs

C. They recognize surface antigens

D. They lack CD3 chains

A major safety issue with CAR T cells is that they have not matured where?

A. Thymus

B. Bone marrow

C. Lymph node

D. Spleen

Because CAR T cells skip thymic maturation, they may lack training for what?

A. Antigen spreading

B. Class switching

C. Somatic hypermutation

D. Self-tolerance

Neurologic toxicity after CAR T therapy is related to failure of what protective process?

A. IgG neutralization

B. Self-tolerance testing

C. Complement fixation

D. Toxoid formation

Which therapy selects the tumor-reactive culture before reinfusion?

A. ACT

B. Rituximab

C. Omalizumab

D. Humira

Which therapy uses genetically engineered T cells rather than naturally recovered TILs?

A. ACT

B. BCG therapy

C. CAR T-cell therapy

D. Toxoid vaccination

In ACT, the final expanded TIL population is returned to whom?

A. Healthy donor

B. Same patient

C. Universal recipient

D. Unrelated host

Which statement best distinguishes CAR T cells from ordinary CTLs?

They bypass ______ restriction

Rituximab-coated CD20+ B cells are marked for destruction mainly by which mechanism?

A. Complement tolerance

B. Thymic deletion

C. T-cell anergy

D. ADCC

Antibody-dependent cellular cytotoxicity depends on antibodies marking target cells for what outcome?

A. Cell killing

B. Class switching

C. Treg induction

D. Antigen editing

CTLA-4 mainly prevents T-cell activation in which location?

_____ _____ organs

PD-1 normally suppresses which T-cell property?

A. MHC expression

B. Effector function

C. Antibody secretion

D. Antigen uptake

PD-1 signaling limits T cells by reducing which process?

_____

The main goal of adoptive cell transfer is to increase which cells?

A. Tumor-specific lymphocytes

B. Tolerant B cells

C. Resting macrophages

D. Naive eosinophils

Adoptive Cell Transfer (ACT) expands tumor-reactive cells that originally came from which source?

A. Bone marrow

B. Donor thymus

C. Patient tumor

D. Lymph node

In CAR T therapy, which signaling domain can provide costimulation?

A. CD3-zeta

B. CD28

C. CTLA-4

D. PD-1

In a CAR receptor, CD28 signaling helps provide which T-cell signal?

A. Anergy

B. Tolerance

C. Apoptosis

D. Costimulation

CD19 is best described as a surface marker of which cells?

CD19 CAR T therapy is designed to kill which broad cell group?

A. Mature plasma cells

B. CD52+ monocytes

C. CD19+ B cells

D. HER2+ epithelial cells

CD19 CAR T therapy can kill cancerous and noncancerous cells sharing what feature?

A. CD20 expression

B. CD19 expression

C. HER2 expression

D. TNF expression

CD19 CAR T therapy kills B cells that are not yet doing what?

A. Presenting antigen

B. Entering follicles

C. Expressing MHC

D. Producing antibodies

CAR T targets should ideally be found on cells that are what?

A. Nonessential

B. Highly essential

C. Universally expressed

D. MHC-negative

Why should CAR T targets be chosen carefully?

A. They block all IL-2

B. They prevent MHC loading

C. Normal cells may die

D. Tumors stop mutating

Which of the following cancer immunotherapies carries a significant risk of "on-target, off-tumor" toxicity, where the treatment inadvertently destroys healthy, normal cells that express the same target antigen as the tumor?

A. ACT

B. CAR T therapy

C. BCG therapy

D. Checkpoint blockade