General Principles Week 7 Flashcards
Topic 1: Basic Components of the Immune System
TLO 1.1: List the main characteristics of the innate and adaptive immune systems
- Innate Immunity:
o Speed of Response: Immediate (minutes to hours) upon infection.
o Specificity: Recognizes broad pathogen-associated molecular patterns (PAMPs); not highly specific to a single epitope.
o Memory: No immunologic memory; repeated exposures to the same pathogen do not generally enhance the response.
o Primary Components:
* Physical barriers: Skin, mucosal membranes.
* Cellular components: Neutrophils, macrophages, dendritic cells (DCs), natural killer (NK) cells, mast cells, eosinophils.
* Soluble factors: Complement proteins, cytokines, acute-phase proteins.
o Function: Provides an immediate line of defense; activates and shapes the adaptive immune system.
Topic 1: Basic Components of the Immune System
TLO 1.1: List the main characteristics of the innate and adaptive immune systems
- Adaptive Immunity:
o Speed of Response: Slower on first exposure (days to weeks), but quicker on subsequent exposures.
o Specificity: Highly specific to individual antigens and epitopes.
o Memory: Long-lasting immunologic memory ensures faster and more robust responses on re-exposure.
o Primary Components:
* Cellular components: B and T lymphocytes (Helper T cells, Cytotoxic T cells, Regulatory T cells).
* Humoral components: Antibodies (immunoglobulins).
o Function: Eliminates or neutralizes specific pathogens, provides long-term protection.
TLO 1.2: Contrast the differences between passive and active immunity, using examples
- Active Immunity:
o Definition: Immunity generated by the individual’s own immune system in response to exposure to an antigen.
o Mechanism: Involves B-cell and T-cell activation, clonal expansion, and formation of memory cells.
o Duration: Often long-lasting (years to lifelong).
o Examples:
* Natural: Infection with a pathogen (e.g., recovery from measles confers immunity).
* Artificial: Vaccination (e.g., administration of an inactivated or attenuated pathogen).
TLO 1.2: Contrast the differences between passive and active immunity, using examples
- Passive Immunity:
o Definition: Immunity conferred by transferring antibodies or immune cells from an immune individual to a non-immune individual.
o Mechanism: Does not require the recipient’s immune system to mount its own response; relies on exogenous antibodies/cells.
o Duration: Temporary; protection wanes as transferred antibodies degrade (weeks to a few months).
o Examples:
* Natural: Maternal IgG crossing the placenta or IgA in breast milk.
* Artificial: Administration of intravenous immunoglobulins (IVIG) or monoclonal antibodies.
TLO 1.3: Compare the primary and the secondary immune response to an antigen
- Primary Immune Response:
o Exposure: Occurs upon the first contact with a particular antigen.
o Lag Phase: Longer delay before a detectable immune response (often 5–7 days or more).
o Peak Response: Generally lower magnitude of antibody titer and effector cell function.
o Isotypes: Initial antibody is typically IgM, followed by class switching to other isotypes (IgG, IgA, etc.).
o Memory: Priming of memory B and T cells occurs.
TLO 1.3: Compare the primary and the secondary immune response to an antigen
- Secondary (or Anamnestic) Immune Response:
o Exposure: Occurs upon subsequent contacts with the same antigen.
o Lag Phase: Much shorter due to presence of memory cells.
o Peak Response: Higher and more rapid production of antibodies (often dominated by IgG, especially in serum).
o Higher Affinity: Antibodies have undergone affinity maturation, leading to stronger binding and greater efficacy.
o Clinical Relevance: Underpins the principle of booster vaccinations.
TLO 1.4: List several important morphologic features and functional activities of cells involved in the innate and adaptive immune response: B and T lymphocytes, natural killer cells, neutrophils, mast cells, eosinophils, monocytes, macrophages, and dendritic cells
- B Lymphocytes:
- B Lymphocytes:
o Morphology: Small lymphocytes with large nucleus, sparse cytoplasm; have surface immunoglobulin (B-cell receptor).
o Function: Produce antibodies, present antigen to helper T cells, differentiate into plasma cells (antibody-secreting) and memory B cells
TLO 1.4: List several important morphologic features and functional activities of cells involved in the innate and adaptive immune response: B and T lymphocytes, natural killer cells, neutrophils, mast cells, eosinophils, monocytes, macrophages, and dendritic cells
- T Lymphocytes (T cells):
- T Lymphocytes (T cells):
o Morphology: Similar to B cells in appearance but with T-cell receptors (TCRs).
o Subsets:
* Helper T Cells (CD4⁺): Coordinate immune response via cytokine secretion.
* Cytotoxic T Cells (CD8⁺): Kill virus-infected or tumor cells.
* Regulatory T Cells: Modulate and suppress excessive immune responses to maintain tolerance.
TLO 1.4: List several important morphologic features and functional activities of cells involved in the innate and adaptive immune response: B and T lymphocytes, natural killer cells, neutrophils, mast cells, eosinophils, monocytes, macrophages, and dendritic cells
- Natural Killer (NK) Cells:
- Natural Killer (NK) Cells:
o Morphology: Larger granular lymphocytes with cytotoxic granules.
o Function: Kill virus-infected cells and tumor cells without prior sensitization; recognize “missing-self” (lack of MHC I) or stressed cells.
TLO 1.4: List several important morphologic features and functional activities of cells involved in the innate and adaptive immune response: B and T lymphocytes, natural killer cells, neutrophils, mast cells, eosinophils, monocytes, macrophages, and dendritic cells
Neutrophils
- Neutrophils:
o Morphology: Granulocytes with multilobed nucleus and abundant cytoplasmic granules.
o Function: First responders to acute bacterial infection; phagocytic; release reactive oxygen species and granule enzymes to kill pathogens.
TLO 1.4: List several important morphologic features and functional activities of cells involved in the innate and adaptive immune response: B and T lymphocytes, natural killer cells, neutrophils, mast cells, eosinophils, monocytes, macrophages, and dendritic cells
- Mast Cells:
- Mast Cells:
o Morphology: Tissue-resident cells with abundant granules containing histamine and other mediators.
o Function: Crucial in allergic reactions (Type I hypersensitivity); degranulation triggered by cross-linking of surface-bound IgE.
TLO 1.4: List several important morphologic features and functional activities of cells involved in the innate and adaptive immune response: B and T lymphocytes, natural killer cells, neutrophils, mast cells, eosinophils, monocytes, macrophages, and dendritic cells
Monocytes
- Monocytes:
o Morphology: Large leukocytes in circulation with kidney-shaped nucleus.
o Function: Differentiate into macrophages or dendritic cells upon entering tissues; phagocytic and cytokine-producing.
TLO 1.4: List several important morphologic features and functional activities of cells involved in the innate and adaptive immune response: B and T lymphocytes, natural killer cells, neutrophils, mast cells, eosinophils, monocytes, macrophages, and dendritic cells
Macrophages
- Macrophages:
o Morphology: Tissue-resident phagocytes derived from monocytes; have pseudopods and large vacuoles.
o Function: Phagocytosis and digestion of pathogens, antigen presentation to T cells, release of inflammatory cytokines.
TLO 1.4: List several important morphologic features and functional activities of cells involved in the innate and adaptive immune response: B and T lymphocytes, natural killer cells, neutrophils, mast cells, eosinophils, monocytes, macrophages, and dendritic cells
- Dendritic Cells (DCs):
- Dendritic Cells (DCs):
o Morphology: “Stellate” cells with dendritic processes; found in tissues interfacing with the external environment.
o Function: Professional antigen-presenting cells (APCs); capture antigen in periphery and migrate to lymph nodes to activate T cells.
Topic 2: Antigen and Antibody
TLO 2.1: List the origins of antigens to which the immune system may respond
1. Exogenous Antigens
- Endogenous Antigens
- Autoantigens
- Alloantigens
- Xenoantigens
- Exogenous Antigens: Enter the body from outside (bacteria, viruses, fungi, allergens, toxins).
- Endogenous Antigens: Generated within cells due to infection (intracellular pathogens) or abnormal cellular proteins (tumor antigens).
- Autoantigens: The body’s own molecules that can trigger autoimmunity under certain conditions.
- Alloantigens: Antigens from other members of the same species (e.g., blood group antigens, transplanted organ antigens).
- Xenoantigens: Antigens from different species (e.g., pig heart valves in xenotransplantation).
TLO 2.2: Name the structural features and biologic properties of the different immunoglobulin classes
1. IgG:
2. IgA:
3. IgM:
4. IgE:
5. IgD:
- IgG:
o Structure: Monomer; four subclasses (IgG1–IgG4).
o Properties: Crosses the placenta (maternal-fetal immunity), opsonization, complement activation, neutralization of toxins/viruses. - IgM:
o Structure: Pentamer (5 monomers linked by J chain).
o Properties: First antibody produced during primary response; highly efficient in complement activation and agglutination. - IgA:
o Structure: Monomer in serum; dimer in secretions (linked by J chain and secretory component).
o Properties: Found in mucosal areas (GI tract, respiratory tract), breast milk; protects mucosal surfaces by neutralizing pathogens. - IgE:
o Structure: Monomer.
o Properties: Binds to mast cells and basophils; involved in Type I hypersensitivity and defense against parasites. - IgD:
o Structure: Monomer.
o Properties: Primarily membrane-bound on naive B cells; role in B-cell activation is less well-defined compared to other isotypes.
What cells produce IL-10 to induce peripheral tolerance of T and B cells? (Single choice)
Th1
Th2
CTLs
Treg
NK
I don’t know
Treg
TLO 2.3: Describe a range of diagnostic tests based on antigen-antibody interaction, indicating the general principle of each test
- ELISA (Enzyme-Linked Immunosorbent Assay):
- Western Blot:
- Immunofluorescence (Direct and Indirect):
- Flow Cytometry:
- Agglutination Tests (Latex Agglutination, Hemagglutination):
- ELISA (Enzyme-Linked Immunosorbent Assay):
o Principle: Detects antigen or antibody via enzyme-labeled secondary antibody and a colorimetric reaction.
o Applications: Quantification of hormones, antibodies (e.g., HIV test), detection of specific proteins in serum. - Western Blot:
o Principle: Proteins separated by electrophoresis, transferred to a membrane, and probed with specific antibodies; visualization by enzyme or chemiluminescence.
o Applications: Confirmatory test for HIV, detection of specific protein expression. - Immunofluorescence (Direct and Indirect):
o Principle: Fluorescently labeled antibodies bind to specific antigens in tissues or cells and are visualized under a fluorescence microscope.
o Applications: Autoantibody detection (e.g., in lupus), viral antigen detection, research staining. - Flow Cytometry:
o Principle: Cells are tagged with fluorescent antibodies to cell-surface or intracellular antigens, then passed through a laser beam for analysis of fluorescence.
o Applications: Immunophenotyping (CD4 counts in HIV), identification of abnormal cell populations in leukemia/lymphoma. - Agglutination Tests (Latex Agglutination, Hemagglutination):
o Principle: Visible clumping occurs when particulate antigen binds to specific antibodies.
Antibodies
Antibodies
Attach to antigens → Antibody-antigen complex
Attach to toxins (antigens) → Neutralise toxins
Attach to receptors → Disrupt the function
Attach to pathogens → Clump together → “Agglutination”
Act as opsonins → Present to phagocytes
Antibody-dependent cell-mediated cytotoxicityAttach to antigens → Antibody-antigen complex
Attach to toxins (antigens) → Neutralise toxins
Attach to receptors → Disrupt the function
Attach to pathogens → Clump together → “Agglutination”
Act as opsonins → Present to phagocytes
Antibody-dependent cell-mediated cytotoxicity
TLO 2.4: Explain the terms monoclonal antibodies (mAbs), hybridoma, fully human, humanized, and chimeric
Monoclonal Antibodies (mAbs) Antibodies produced by a single clone of cells, designed to target a specific antigen with high specificity and uniformity.
Hybridoma A cell line created by fusing an antibody-producing B cell with a myeloma (cancer) cell, allowing for the continuous production of monoclonal antibodies.
Fully Human Antibodies made entirely from human genetic material, reducing the risk of immune reactions when used in humans.
Humanized Antibodies that are mostly human, but contain small parts derived from non-human sources (e.g., mouse), engineered to reduce immune reactions.
Chimeric Antibodies that are part human and part non-human (e.g., mouse), with the variable regions from the non-human source and constant regions from humans.
1. Monoclonal Antibodies (mAbs): o Definition: Uniform antibodies derived from a single B-cell clone, each recognizing the same epitope. o Advantages: High specificity, consistent batch-to-batch reactivity. 2. Hybridoma: o Definition: A cell line produced by the fusion of an antibody-producing B lymphocyte with a myeloma cell, creating an immortalized cell line that secretes monoclonal antibodies. 3. Fully Human Antibodies: o Definition: Antibodies with both variable and constant regions derived entirely from human immunoglobulin sequences (generated via transgenic mice or phage display). 4. Humanized Antibodies: o Definition: Mostly human antibody framework with complementarity-determining regions (CDRs) from a non-human (e.g., mouse) source. 5. Chimeric Antibodies: o Definition: Antibodies where the variable regions (heavy and light) are from one species (often mouse) and the constant region from another (human).
TLO 2.5: List several examples of mAbs application in clinical medicine
- Cancer Therapy:
- Autoimmune Diseases:
- Transplant Rejection Prevention:
- Infectious Diseases:
- Cancer Therapy:
o Rituximab (anti-CD20) for certain B-cell malignancies (e.g., non-Hodgkin lymphoma).
o Trastuzumab (anti-HER2) for HER2-positive breast cancer. - Autoimmune Diseases:
o Infliximab (anti-TNF-α) for rheumatoid arthritis, Crohn’s disease.
o Natalizumab (anti-integrin) for multiple sclerosis. - Transplant Rejection Prevention:
o Basiliximab (anti-IL-2 receptor) used to prevent acute rejection. - Infectious Diseases:
o Palivizumab (anti-RSV F protein) for high-risk infants against respiratory syncytial virus.
Topic 3: Antigen Presentation and Recognition; Cytokines
TLO 3.1: Describe the main structural features of the class I and class II MHC gene products
- Class I MHC (HLA-A, -B, -C in humans):
- Class II MHC (HLA-DP, -DQ, -DR in humans):
Topic 3: Antigen Presentation and Recognition; Cytokines
TLO 3.1: Describe the main structural features of the class I and class II MHC gene products
1. Class I MHC (HLA-A, -B, -C in humans):
o Structure: Consists of a heavy α chain (three domains: α1, α2, α3) non-covalently associated with β2-microglobulin.
o Peptide-Binding Groove: Formed by α1 and α2 domains.
o Expression: All nucleated cells (and platelets).
o Presentation: Presents endogenous (intracellular) peptides to CD8⁺ T cells.
2. Class II MHC (HLA-DP, -DQ, -DR in humans):
o Structure: Composed of two chains (α and β), each with two domains (α1, α2 and β1, β2).
o Peptide-Binding Groove: Formed by α1 and β1 domains.
o Expression: Primarily on professional antigen-presenting cells (APCs) like dendritic cells, macrophages, B cells.
o Presentation: Presents exogenous (extracellular) peptides to CD4⁺ T cells.
TLO 3.2: Explain the genetic basis of MHC polymorphism and polygeny, and their significance for the functioning of the immune system
- Polymorphism:
pathogens.
2. Polygeny:
- Significance:
TLO 3.2: Explain the genetic basis of MHC polymorphism and polygeny, and their significance for the functioning of the immune system
1. Polymorphism:
o Definition: Multiple variants (alleles) of each MHC gene in a population.
o Result: Increases the range of peptides that can be presented by the population as a whole; enhances survival against diverse pathogens.
2. Polygeny:
o Definition: Multiple MHC genes encoding different class I and class II molecules in each individual (e.g., HLA-A, -B, -C for class I and HLA-DP, -DQ, -DR for class II).
o Result: Each individual co-expresses several MHC molecules, broadening peptide presentation.
3. Significance:
o Immune Defense: High MHC diversity makes it less likely that a single pathogen can evade the entire human population.
o Transplantation: MHC polymorphisms contribute to graft rejection.
TLO 3.3: Describe the concept of MHC restriction
The principle that T cells recognize antigens only when they are presented by the host’s own MHC molecules.
- Definition: T cells recognize antigenic peptides only when presented on self-MHC molecules.
- CD8⁺ T cells: Require peptide presented on class I MHC of the host.
- CD4⁺ T cells: Require peptide presented on class II MHC of the host.
- Clinical Implication: T cells generally do not respond to peptide antigens presented by non-self MHC, complicating allograft acceptance.
TLO 3.4: Compare peptide antigen binding to class I and class II molecules
1. Class I MHC:
- Class II MHC:
o Peptide Origin: Extracellular proteins taken up via endocytosis.
o Processing Pathway: Antigen is degraded in endosomal/lysosomal compartments; class II is assembled in ER with invariant chain → invariant chain is removed in endosome → peptide loaded.
o Peptide Length: Longer (usually 13–25 amino acids).
TLO 3.4: Compare peptide antigen binding to class I and class II molecules
1. Class I MHC:
o Peptide Origin: Intracellular proteins (viral, cytosolic).
o Processing Pathway: Proteasome degrades proteins → peptides transported into ER via TAP → loaded onto class I.
o Peptide Length: Typically 8–10 amino acids in length.
2. Class II MHC:
o Peptide Origin: Extracellular proteins taken up via endocytosis.
o Processing Pathway: Antigen is degraded in endosomal/lysosomal compartments; class II is assembled in ER with invariant chain → invariant chain is removed in endosome → peptide loaded.
o Peptide Length: Longer (usually 13–25 amino acids).
TLO 3.5: List the main categories of antigen recognition molecules, including coreceptor complexes
1. T-Cell Receptors (TCRs):
- Immunoglobulins (Surface B-cell Receptors):
- CD4 and CD8 Coreceptors:
- Pattern Recognition Receptors (PRRs) in Innate Immunity:
TLO 3.5: List the main categories of antigen recognition molecules, including coreceptor complexes
1. T-Cell Receptors (TCRs):
o Heterodimer of α and β chains (or γ and δ in fewer T cells).
o Recognize peptide bound to MHC.
2. Immunoglobulins (Surface B-cell Receptors):
o Membrane-bound form of antibodies on B cells.
3. CD4 and CD8 Coreceptors:
o CD4 binds MHC II, CD8 binds MHC I; stabilize TCR-MHC interaction and facilitate signaling.
4. Pattern Recognition Receptors (PRRs) in Innate Immunity:
o Toll-like receptors, NOD-like receptors, RIG-I-like receptors, etc.; recognize PAMPs.
TLO 3.6: Give two classifications of cytokines
1. By Function:
- By Structure/Family:
TLO 3.6: Give two classifications of cytokines
1. By Function:
o Pro-inflammatory: e.g., IL-1, IL-6, TNF-α.
o Anti-inflammatory: e.g., IL-10, TGF-β.
o Hematopoietic growth factors: e.g., GM-CSF.
o Antiviral: e.g., IFN-α, IFN-β.
2. By Structure/Family:
o Interleukins (IL-1, IL-2, etc.)
o Interferons (Type I: IFN-α/β; Type II: IFN-γ)
o Tumor Necrosis Factors (TNF family)
o Chemokines (CC, CXC families)
TLO 3.7: List main functions and properties of cytokines
1. Main Functions:
TLO 3.7: List main functions and properties of cytokines
1. Main Functions:
o Regulate immune cell activation, proliferation, and differentiation: IL-2 drives T-cell proliferation, IL-4 drives Th2 responses, etc.
o Mediate inflammation: TNF-α and IL-1 induce endothelial activation and recruit inflammatory cells.
o Influence hematopoiesis: Factors like G-CSF and M-CSF stimulate granulocyte or macrophage lineage expansion.
o Antiviral defense: Type I interferons (IFN-α, IFN-β) inhibit viral replication.
TLO 3.7: List main functions and properties of cytokines
- Properties:
o Pleiotropy: One cytokine can have different effects on different cell types.
o Redundancy: Different cytokines can exert similar biological effects.
o Synergy and Antagonism: Cytokines can work together or counteract each other.
o Local and Systemic Effects: Can act paracrine, autocrine, or endocrine.
- Properties:
o Pleiotropy: One cytokine can have different effects on different cell types.
o Redundancy: Different cytokines can exert similar biological effects.
o Synergy and Antagonism: Cytokines can work together or counteract each other.
o Local and Systemic Effects: Can act paracrine, autocrine, or endocrine.
Topic 4: T and B Lymphocytes
TLO 4.1: Name the major steps in the pathway of T-cell development; give definition to double-positive and single-positive thymocytes
- Location: T-cell precursors originate in the bone marrow and migrate to the thymus.
- Major Stages:
o Double-Negative (DN) Stage: T-cell progenitors do not express CD4 or CD8.
o Double-Positive (DP) Stage: Thymocytes express both CD4 and CD8 co-receptors (CD4⁺CD8⁺).
o Single-Positive (SP) Stage: Thymocytes differentiate into either CD4⁺ or CD8⁺ T cells, depending on TCR specificity for MHC II or MHC I, respectively.
TLO 4.2: Compare positive and negative selection of T lymphocytes in thymus
1. Positive Selection (occurs in the cortex):
- Negative Selection (occurs in the medulla):
TLO 4.2: Compare positive and negative selection of T lymphocytes in thymus
1. Positive Selection (occurs in the cortex):
o Mechanism: DP thymocytes that can weakly recognize self-MHC I or II survive.
o Outcome: Ensures T cells can interact with self-MHC (MHC restriction).
o Failure: Cells that do not recognize MHC at all undergo apoptosis.
2. Negative Selection (occurs in the medulla):
o Mechanism: T cells that strongly bind self-antigen presented on MHC undergo apoptosis.
o Outcome: Removal of autoreactive T cells; induces self-tolerance.
o Failure: Autoimmune pathology if highly self-reactive T cells escape deletion.
TLO 4.3: Draw the events involved in naive T-cell activation
(Conceptual description)
TLO 4.3: Draw the events involved in naive T-cell activation
(Conceptual description)
1. Antigen Recognition: Naive T cells bind specific peptide-MHC complexes on APCs via the TCR.
2. Co-stimulation: Additional signals needed, such as CD28 (on T cell) binding to B7-1/B7-2 (CD80/CD86 on APC).
3. Cytokine Environment: APC-derived cytokines (e.g., IL-12) influence T-cell differentiation.
4. Clonal Expansion: Activated T cells proliferate and differentiate into effector (e.g., Th1, Th2, Th17, CTLs) and memory cells.
TLO 4.4: Outline the differences between TH1, TH2, TH17, and CTL responses
TLO 4.4: Outline the differences between TH1, TH2, TH17, and CTL responses
1. TH1 Cells:
o Cytokines Produced: IFN-γ, IL-2, TNF-β.
o Function: Activate macrophages, support cell-mediated immunity against intracellular pathogens.
o Key Transcription Factor: T-bet.
2. TH2 Cells:
o Cytokines Produced: IL-4, IL-5, IL-13.
o Function: Help B cells produce antibodies (especially IgE), support eosinophil activation, involved in defense against parasites and allergic responses.
o Key Transcription Factor: GATA-3.
3. TH17 Cells:
o Cytokines Produced: IL-17, IL-22.
o Function: Recruit neutrophils, combat extracellular bacteria/fungi, involved in some autoimmune pathologies.
o Key Transcription Factor: RORγt.
4. Cytotoxic T Lymphocytes (CTLs, CD8⁺):
o Cytokines Produced: IFN-γ (some), also use perforin and granzymes.
o Function: Direct killing of virus-infected cells or tumor cells.
TLO 4.5: Recall changes in cell surface molecules during the B-cell development pathway
TLO 4.5: Recall changes in cell surface molecules during the B-cell development pathway
1. Pro-B Cell: Begins rearrangement of immunoglobulin heavy chain; no surface immunoglobulin.
2. Pre-B Cell: Expression of μ heavy chain with surrogate light chain on surface (Pre-BCR).
3. Immature B Cell: Expression of complete IgM on surface.
4. Mature (Naive) B Cell: Co-expression of IgM and IgD on surface.
5. Activated B Cell (After antigen encounter): Undergoes class switching (IgG, IgA, or IgE), affinity maturation, and differentiation into plasma or memory B cells.
TLO 4.6: Compare positive and negative selection of B lymphocytes in bone marrow
1. Positive Selection:
o Less pronounced in B cells than T cells.
o B cells that successfully rearrange and express functional BCR move to the next stage.
TLO 4.6: Compare positive and negative selection of B lymphocytes in bone marrow
- Negative Selection:
o Immature B cells that bind self-antigens strongly (in bone marrow) either undergo apoptosis or receptor editing (light chain gene rearrangement to reduce self-reactivity).
o Ensures central tolerance.
- Negative Selection:
o Immature B cells that bind self-antigens strongly (in bone marrow) either undergo apoptosis or receptor editing (light chain gene rearrangement to reduce self-reactivity).
o Ensures central tolerance.
TLO 4.7: Describe how naïve B and T cells are primed by cell-cell interactions with antigen-presenting cells
- Naive T Cells: Require APCs (e.g., dendritic cells) presenting antigen on MHC molecules along with co-stimulatory signals (CD80/CD86 → CD28).
- Naive B Cells: Can bind antigen via BCR directly, but often require T-cell help (for T-dependent antigens). Helper T cells recognize peptides from the same antigen presented on MHC II of the B cell, then provide signals (CD40L on T cell binds CD40 on B cell) plus cytokines that drive B-cell activation, class switching, and affinity maturation.
TLO 4.8: Compare T-dependent and T-independent B-cell activation
- T-Dependent Antigens:
o Composition: Typically proteins.
o Mechanism: B cell presents processed peptide on MHC II to helper T cell → receives help (CD40-CD40L interaction + cytokines).
o Outcome: Isotype switching, affinity maturation, robust memory response. - T-Independent Antigens:
o Composition: Often polysaccharides or repeating epitopes.
o Mechanism: Cross-linking of multiple BCRs → direct activation without T-cell help.
o Outcome: Mainly IgM response, limited immunologic memory, little or no class switching or affinity maturation.
Topic 5: Hypersensitivity
TLO 5.1: Explain the Gell and Coombs classification of hypersensitivity reactions
- Type I (Immediate):
o Mechanism: IgE-mediated mast cell degranulation.
o Examples: Allergic rhinitis, anaphylaxis, asthma. - Type II (Antibody-Mediated Cytotoxic):
o Mechanism: IgG or IgM antibodies directed against cell-surface or extracellular matrix antigens → complement activation or opsonization.
o Examples: Hemolytic anemia, Goodpasture’s syndrome, myasthenia gravis (some forms). - Type III (Immune Complex-Mediated):
o Mechanism: Antigen-antibody (IgG) complexes deposit in tissues → complement activation and inflammation.
o Examples: Serum sickness, Arthus reaction, certain forms of vasculitis. - Type IV (Delayed-Type or Cell-Mediated):
o Mechanism: T-cell mediated; either CD4⁺ T helper cells (Th1) activate macrophages or CD8⁺ cytotoxic T cells kill target cells.
o Examples: Contact dermatitis (e.g., poison ivy), tuberculin skin test, type 1 diabetes (β-cell destruction).
Hypersensitivity Reactions
Type Immune Response Immunoglobulin/Cells Response Time Mechanism Examples
Type I Antibody mediated immunity IgE Fast response (minutes) Allergic reactions Asthma, Allergic rhinitis
Type II Antibody mediated immunity IgG, IgM Intermediate Body cells directly attacked by antibodies Rheumatic heart disease, Autoimmune haemolytic anaemia
Type III Antibody mediated immunity IgG Intermediate Complex accumulation and destruction Rheumatoid arthritis, Poststreptococcal glomerulonephritis
Type IV Cell mediated immunity T helper cells (Th1) Late response (48-72 hours) Cell mediated cytotoxicity Transplant rejection, Contact dermatitis
If you need any more help or have further questions, feel free to ask!
TLO 5.2: Describe the immunologic factors that predispose to allergy and explain how these may be increasing allergy at a population level
- Genetic Factors:
o Atopic individuals have a predisposition (often multiple genes) leading to higher IgE production and increased Th2 responses.
o Polymorphisms in cytokines (IL-4, IL-13) or their receptors can enhance IgE class switching. - Environmental Factors:
o Hygiene Hypothesis: Reduced childhood infections may lead to an under-stimulated Th1 response, skewing toward Th2 and atopy.
o Exposure to pollutants, diet changes, antibiotic overuse can alter gut and skin microbiome, affecting immune tolerance. - Increasing Prevalence of Allergy:
o Urbanization, decreased exposure to farm animals or soil microbes, and other lifestyle changes may account for rising allergy rates.
TLO 5.3: Describe the techniques used to identify allergens involved in immediate hypersensitivity
- Skin Prick Test (SPT):
o Allergen extracts placed on skin → pricked → wheal-and-flare response indicates sensitization. - Serologic Tests:
o Specific IgE Measurement (e.g., RAST, ImmunoCAP): Detect allergen-specific IgE in patient serum. - Elimination/Challenge Testing:
o For food allergies, removing suspect foods from the diet and then reintroducing under controlled conditions.
TLO 5.4: Describe anaphylaxis and its immediate treatment
- Anaphylaxis:
o Definition: Severe, systemic allergic reaction triggered by widespread mast cell and basophil degranulation.
o Clinical Features: Hypotension (shock), bronchoconstriction (wheezing), laryngeal edema, urticaria, GI symptoms. - Immediate Treatment:
o Epinephrine (adrenaline) IM injection is the first-line therapy; stabilizes mast cells, reverses bronchospasm, and supports blood pressure.
o Additional treatments: Antihistamines, corticosteroids, IV fluids, and oxygen support as needed.
TLO 5.5: List the modes of action of drugs used to treat allergy
- Antihistamines (H1 blockers): Block histamine receptors (e.g., diphenhydramine, cetirizine).
- Mast Cell Stabilizers: Prevent degranulation (e.g., cromolyn sodium).
- Leukotriene Receptor Antagonists: (e.g., montelukast) reduce leukotriene-mediated inflammation.
- Corticosteroids: Suppress inflammatory gene expression (e.g., prednisone, fluticasone).
- Anti-IgE Antibodies (e.g., omalizumab): Binds circulating IgE, preventing its interaction with mast cells/basophils.
Topic 6: Autoimmune Diseases
TLO 6.1: List what evidence there is for autoimmunity in normal, healthy individuals
- Natural Autoantibodies: Low affinity, polyreactive antibodies often present at low levels.
- Autoreactive T Cells: Low-level autoreactive T cells can exist but are kept in check by regulatory mechanisms.
- Fas-Fas Mechanisms: Continuous peripheral deletion of self-reactive lymphocytes.
TLO 6.2: Describe how the immune system tolerates most autoantigens and how tolerance can break down
- Central Tolerance:
- Central Tolerance:
o T cells in the thymus (negative selection) and B cells in bone marrow (clonal deletion or receptor editing).
TLO 6.2: Describe how the immune system tolerates most autoantigens and how tolerance can break down
- Peripheral Tolerance:
- Peripheral Tolerance:
o Anergy: Lack of co-stimulatory signals leads to non-responsiveness.
o Regulatory T Cells: Secrete immunosuppressive cytokines (IL-10, TGF-β) to maintain tolerance.
o Ignorance: Self-antigens may be sequestered in immune-privileged sites (brain, eye, testes).
TLO 6.2: Describe how the immune system tolerates most autoantigens and how tolerance can break down
- Breakdown of Tolerance:
- Breakdown of Tolerance:
o Molecular Mimicry: Infectious agents share epitopes with self-antigens → cross-reactivity.
o Epitope Spreading: Tissue damage exposes hidden self-epitopes.
o Genetic Susceptibility: Certain MHC alleles predispose to autoimmunity.
TLO 6.3: Using the examples of type 1 diabetes, celiac disease, and systemic lupus erythematosus, describe how genes and environmental factors work together to cause autoimmune disease
- Type 1 Diabetes (T1D):
o Genetic Factors: Strong association with certain HLA class II alleles (e.g., HLA-DR3, DR4).
o Environmental Triggers: Viral infections (coxsackie virus), gut microbiome factors.
o Mechanism: Autoreactive T cells attack pancreatic β-cells → insulin deficiency.
TLO 6.3: Using the examples of type 1 diabetes, celiac disease, and systemic lupus erythematosus, describe how genes and environmental factors work together to cause autoimmune disease
- Celiac Disease:
o Genetic Factors: Predominantly HLA-DQ2 or DQ8 haplotypes.
o Environmental Trigger: Dietary gluten (gliadin component).
o Mechanism: Immune-mediated damage to small intestinal villi.
TLO 6.3: Using the examples of type 1 diabetes, celiac disease, and systemic lupus erythematosus, describe how genes and environmental factors work together to cause autoimmune disease
- Systemic Lupus Erythematosus (SLE):
o Genetic Factors: Multiple genes (HLA-DR2/DR3); complement deficiencies (C1q, C2, C4).
o Environmental Factors: UV light, sex hormones (estrogen), infections can exacerbate.
o Mechanism: Loss of tolerance leads to autoantibody production (especially anti-nuclear antibodies) and immune complex deposition.
TLO 6.4: Describe how immunofluorescence tests and ELISAs are used to detect autoantibodies
- Immunofluorescence Tests (Indirect):
o Patient serum applied to substrate tissue (e.g., HEp-2 cells), autoantibodies bind, then detected by fluorescently labeled anti-human Ig. - ELISA:
o Antigens (specific autoantigens, e.g., dsDNA, tissue transglutaminase) coated on a plate → patient serum added → enzyme-labeled anti-human IgG → colorimetric readout.
Topic 7: Immunodeficiencies
TLO 7.1: Explain differences between primary and secondary immunodeficiencies
- Primary (Congenital):
o Definition: Genetic or developmental defects resulting in defective immune function (e.g., SCID, DiGeorge syndrome, Bruton’s agammaglobulinemia).
o Onset: Often in early childhood with recurrent, severe infections. - Secondary (Acquired):
o Definition: Result from external factors (e.g., HIV infection, chemotherapy, malnutrition).
o Onset: Can occur at any age depending on exposure or underlying disease.
TLO 7.2: Construct lists of the types of infections that affect patients with T- and B-cell disorders
- T-Cell Disorders:
o More susceptible to intracellular pathogens (viruses, fungi, opportunistic organisms like Pneumocystis jirovecii), and certain intracellular bacteria (mycobacteria). - B-Cell (Humoral) Disorders:
o Recurrent pyogenic bacterial infections (e.g., Streptococcus pneumoniae, Haemophilus influenzae), especially encapsulated organisms; can also struggle with some viruses that rely on neutralizing antibodies (e.g., enteroviruses).
TLO 7.3: List the cells affected by HIV infection and briefly describe their functions and roles in HIV infection
- CD4⁺ T Cells (Helper T cells):
o Function: Orchestrate immune responses via cytokine secretion; essential for B-cell antibody production and macrophage activation.
o Role in HIV: Main target for HIV binding via gp120 → progressive depletion leads to immunodeficiency (AIDS). - Macrophages and Dendritic Cells:
o Function: Antigen presentation, phagocytosis, and immunoregulation.
o Role in HIV: Act as reservoirs; HIV can infect these cells (via CCR5 co-receptor), allowing for persistent infection and spread.
TLO 7.4: Describe how you would monitor a patient with HIV infection
- CD4⁺ T-Cell Count:
o Critical for determining degree of immunosuppression and opportunistic infection risk. - Viral Load (HIV RNA PCR):
o Indicates level of active viral replication; used to monitor response to antiretroviral therapy (ART). - Clinical Monitoring:
o Track opportunistic infections, overall health, and medication side effects. - Other Laboratory Tests:
o Complete blood counts, liver and renal function tests to monitor ART toxicity or comorbidities.
TLO 7.5: List host factors that affect the course of HIV infection
- Genetic Factors:
o CCR5∆32 mutation confers resistance or slower disease progression.
o HLA types can influence immune response effectiveness. - Co-infections and Comorbidities:
o Certain infections (e.g., TB, hepatitis) can exacerbate or accelerate progression. - Immune Status and Nutrition:
o Malnutrition or other immunocompromising conditions worsen outcomes. - Adherence to ART:
o Poor adherence → higher viral loads → more rapid disease progression.
Topic 8: Immunity in Malignancy
TLO 8.1: Describe the different types of tumor antigen and explain how tumors evade the immune response
- Types of Tumor Antigens:
o Tumor-Specific Antigens (TSAs): Unique to tumor cells (e.g., mutated oncogenes or viral antigens).
o Tumor-Associated Antigens (TAAs): Overexpressed or re-expressed normal proteins (e.g., prostate-specific antigen). - Evasion Strategies:
o Reduced MHC Expression: Tumor cells downregulate MHC I to avoid CTL recognition.
o Immunosuppressive Molecules: Secretion of TGF-β, IL-10 to inhibit T-cell function.
o Immune Checkpoints: Upregulation of PD-L1 or CTLA-4 pathways to dampen T-cell activity.
TLO 8.2: Explain how host and viral oncogenes interact to cause cancer
- Host Oncogenes (Proto-oncogenes):
o Mutations or overexpression convert them into oncogenes → uncontrolled cell proliferation. - Viral Oncogenes:
o Some viruses (e.g., HPV, EBV, HTLV-1) introduce or activate oncogenes or inactivate tumor suppressor genes (e.g., p53, Rb). - Interaction:
o Viral infection can initiate or promote oncogenic processes in a genetically susceptible host, leading to malignant transformation.
TLO 8.3: List several approaches to cancer immunotherapy
- Checkpoint Inhibitors
- CAR T-Cell Therapy:
- Cancer Vaccines:
- Monoclonal Antibodies:
- Adoptive Cell Transfer (ACT):
- Checkpoint Inhibitors:
o Antibodies blocking PD-1/PD-L1 or CTLA-4, reactivating T cells against tumors (e.g., nivolumab, pembrolizumab). - CAR T-Cell Therapy:
o Engineering patient T cells with chimeric antigen receptors targeting tumor-specific antigens (e.g., CD19 in B-cell malignancies). - Cancer Vaccines:
o Prophylactic (e.g., HPV vaccine) or therapeutic vaccines to elicit antitumor immunity. - Monoclonal Antibodies:
o Direct tumor targeting (e.g., rituximab, trastuzumab) or immune modulation (e.g., anti-CD40). - Adoptive Cell Transfer (ACT):
o Expansion of tumor-infiltrating lymphocytes (TILs) ex vivo and re-infusion to the patient.
Topic 9: Transplantation
TLO 9.1: List the different types of transplants and the organs transplanted
- Autograft: Transplant from one site to another on the same individual (e.g., skin graft).
- Isograft (Syngeneic Graft): Between genetically identical individuals (e.g., identical twins).
- Allograft: Between different individuals of the same species.
- Xenograft: Between different species (e.g., pig to human).
* Commonly Transplanted Organs: Kidney, liver, heart, lung, pancreas, cornea, bone marrow/stem cells.
TLO 9.2: Describe the three phases of rejection of solid organs
TLO 9.2: Describe the three phases of rejection of solid organs
1. Hyperacute Rejection:
o Timing: Minutes to hours after transplant.
o Mechanism: Pre-formed antibodies against donor ABO blood group or HLA antigens → complement activation → rapid thrombosis and necrosis.
2. Acute Rejection:
o Timing: Days to weeks (or months) post-transplant.
o Mechanism: T-cell mediated (cellular) or antibody-mediated (humoral) attack on donor tissue.
3. Chronic Rejection:
o Timing: Months to years post-transplant.
o Mechanism: Low-level immune response leading to vascular damage (intimal thickening, fibrosis), gradual organ failure.
TLO 9.3: Explain how stem cell transplantation differs from solid organ transplant
- Stem Cell (Bone Marrow) Transplant:
o Replacing Hematopoietic and Immune System: Infusion of donor stem cells repopulates recipient’s bone marrow.
o Graft-versus-Host Disease (GVHD): Donor T cells can attack recipient’s tissues (skin, liver, gut); a major complication unique to stem cell transplants.
o Immunologic Reconstitution: Takes months to fully recover an immune system; prophylaxis against infections is critical. - Solid Organ Transplant:
o Replacing a Specific Organ: Donor organ must be matched for ABO compatibility and partially for HLA.
o Host-versus-Graft Reactions: Predominant concern. The recipient’s immune system can reject the donor organ.
TLO 9.4: List the problems that need to be overcome to make xenotransplantation safe
- Hyperacute Rejection: Pre-existing natural antibodies to animal epitopes (e.g., alpha-gal).
- Zoonotic Infections: Potential cross-species transmission of viruses (porcine endogenous retroviruses).
- Physiological and Size Mismatch: Ensuring transplanted organ functions adequately in a human environment.
- Ethical/Regulatory Concerns: Pathogen control, public health risk, and acceptance.
Topic 10: Vaccination
TLO 10.1: Explain the mechanism of action of vaccines
- Mechanism:
o Vaccines introduce antigens (live attenuated, killed, subunit, etc.) that mimic infection, prompting the immune system to generate a protective adaptive response (antibody production, memory B/T cells) without causing the full-blown disease. - Immunologic Memory:
o Upon real exposure to the pathogen, the immune response is rapid and prevents clinical disease.
TLO 10.2: Give classification of vaccines
- Live Attenuated:
o Weakened form of the pathogen (e.g., measles, mumps, rubella, varicella).
o Induce robust immunity; can be contraindicated in immunocompromised individuals. - Inactivated (Killed):
o Pathogen killed by chemicals/heat (e.g., inactivated polio, hepatitis A).
o Generally safer; often require boosters. - Subunit/Conjugate:
o Contain only essential antigens (e.g., hepatitis B surface antigen, pneumococcal conjugate).
o Reduced risk of adverse effects; may need adjuvants. - Toxoid:
o Inactivated bacterial toxins (e.g., tetanus, diphtheria).
o Elicit neutralizing antibodies against the toxin. - mRNA Vaccines:
o Encode antigenic proteins (e.g., COVID-19 vaccines).
o Stimulate robust B- and T-cell responses.
TLO 10.3: Describe three different types of vaccine currently in use and how these vary in their safety and efficacy
- Live Attenuated Vaccine (e.g., MMR):
o Safety: Risk of reversion to virulence is extremely low but possible; contraindicated in immunosuppression or pregnancy.
o Efficacy: Induces strong, long-lasting immunity, often with a single dose. - Inactivated Vaccine (e.g., Inactivated Poliovirus Vaccine, IPV):
o Safety: Cannot replicate; minimal risk even in immunocompromised.
o Efficacy: Often requires multiple doses and boosters; immunity may be less robust compared to live vaccines. - Subunit/Conjugate Vaccines (e.g., Hepatitis B, Pneumococcal Conjugate):
o Safety: Extremely safe due to containing only specific antigens.
o Efficacy: Generally good; immunogenicity can be enhanced by conjugating the antigen to a carrier protein and/or adding adjuvants. Often require booster doses.
What type of vaccine is CONTRAindicated for patients with severe immunodeficient states?” is:
- Live attenuated
Contraindicated means that a specific procedure or treatment is advised against due to potential harm or adverse effects. It is a medical term used to indicate that certain actions should be avoided because they could be dangerous or inappropriate for a particular patient.
Type of Immunity
Innate Immunity Physical barriers (skin, mucous membranes), chemical barriers (stomach acid, enzymes), cellular components (phagocytes, NK cells)
Humoral Immunity B cells, antibodies, memory B cells
Cellular Immunity T cells (helper, cytotoxic, regulatory)
different types of vaccines:
Type of Vaccine Description
Live Attenuated Contains weakened form of the pathogen.
Inactivated (Killed) Contains killed pathogen that cannot cause disease.
Subunit, Recombinant, Conjugate Contains pieces of the pathogen (like protein or sugar), not the whole microbe.
In which of the following is GVHR (graft vs host reaction) seen?” The options are:
* Stem cell transplantation
* Kidney transplantation
* Heart transplantation
* Liver transplantation
* Skin transplantation
* I don’t know
Stem cell transplantation.
Graft-versus-host reaction (GVHR) typically occurs in stem cell or bone marrow transplants. In this condition, the donated cells (graft) recognize the recipient’s body (host) as foreign and attack it.
“HIV infection belongs to which type of immunodeficient state according to the classification of immunodeficiencies?”
The options are:
* Stimulated
* Primary
* Spontaneous
* Induced
* Acquired
* I don’t know
Acquired
The question asks: “What cells produce IL-10 to induce peripheral tolerance of T and B cells?”
The options are:
* Th1
* Th2
* CTLs
* Treg
* NK
* I don’t know
Treg
What are interleukins
Interleukins are essential for the proper functioning of the immune system and play critical roles in both normal immune responses and various immune-related diseases.
- IL-1: Promotes inflammation and fever; activates T cells and macrophages.
- IL-2: Stimulates the growth and activity of T cells and natural killer (NK) cells.
- IL-6: Promotes inflammation and immune responses; stimulates antibody production.
- IL-10: Suppresses inflammation and promotes immune tolerance; produced by regulatory T cells (Treg).
- IL-17: Involved in inflammatory responses and autoimmune diseases.
The image you uploaded shows a question related to immunology. It asks about the term used to describe the binding strength of an antigen molecule and an immunoglobulin molecule. The options provided are:
1. Specificity
2. Valency
3. Affinity
4. Avidity
5. Currency
6. I don’t know
- Affinity
Affinity refers to the strength of the interaction between a single antigen-binding site on an antibody and a single epitope on an antigen.
- Specificity: This refers to the ability of an antibody to recognize and bind to a specific antigen. It’s about how precisely the antibody targets a particular antigen.
- Valency: This indicates the number of antigen-binding sites on an antibody molecule. For example, IgG antibodies have two binding sites, making them bivalent.
- Avidity: This is the overall strength of binding between an antibody and a multivalent antigen. It considers multiple interactions, so it’s a cumulative measure of binding strength.
The question asks: “Which type of hypersensitivity is involved in anaphylaxis?”
- I type
- II type
- III type
- IV type
- V type
- I don’t know
Type I hypersensitivity (I type).
which of the listed cytokines are used in cytokine therapy for tumor processes. The options provided are:
A. IL-10 B. IL-2 C. IFN D. IL-5 E. TGF-beta
B. IL-2 and C. IFN.
The answer is B. IL-2 and C. IFN because these cytokines are specifically known for their roles in enhancing the immune response against cancer cells.
1. IL-2 (Interleukin-2): This cytokine plays a crucial role in the activation and proliferation of T cells and NK (Natural Killer) cells. It promotes the growth and differentiation of these immune cells, which are essential for targeting and destroying cancer cells. IL-2 has been used in the treatment of certain cancers, such as metastatic melanoma and renal cell carcinoma, to boost the patient’s immune response.
2. IFN (Interferon): Interferons are a group of signaling proteins that have antiviral, antiproliferative, and immunomodulatory effects. There are different types of interferons, such as IFN-alpha, IFN-beta, and IFN-gamma. In the context of cancer therapy, interferons 2. IFN (Interferon): Interferons are a group of signaling proteins that have antiviral, antiproliferative, and immunomodulatory effects. There are different types of interferons, such as IFN-alpha, IFN-beta, and IFN-gamma. In the context of cancer therapy, interferons can enhance the immune response by increasing the expression of MHC (Major Histocompatibility Complex) molecules on the surface of cancer cells, making them more recognizable and targetable by immune cells. They can also inhibit tumor cell proliferation and promote apoptosis (programmed cell death) of cancer cells.
A 22-year-old female has a history of recurrent herpes simplex rash on her lips over the last three years.She had treatment with antiviral medicines with minimal success. The doctor decided to addimmunostimulatory medicine to increase internal antiviral immune factors.
Which cytokines play the main role in antiviral immunity?
a.
Type I IFNs
b.
TNF
c.
Type II IFNs
d.
G-CSF
a.
Type I IFNs
Certain components of our immune system are characterized by two attributes: being able (1) torespond specifically to microbes and (2) to exhibit memory of having responded to a particular microbepreviously. Which one of the following has BOTH specificity and memory?
a.
Neutrophils
b.
B cells
c.
Basophils
d.
Dendritic cells
B cells
A 34-year-old female complains of fatigue, tiredness, increased sensitivity to cold and most recently,hair loss. During examination the Doctor notices she has a pale skin and puffy face. The Doctor alsonoticed an enlarged thyroid gland and suspects Hashimoto’s thyroiditis (autoimmune disease)complicated with hypothyroidism.
What cells of the immune system prevent the development of autoimmune pathologies in a healthyperson?
a.
T cytotoxic
b.
T double-positive
c.
T helper
d.
T reg
T reg
the year) and frequent respiratory viral infections. Doctor suspects acquired T cellimmunodeficiency, which was confirmed by low level of T lymphocytes in the immunogram.
What subtype of T lymphocytes is most likely to be decreased in this patient?
a.
T reg
b.
T cytotoxic
c.
T helper
d.
T double-positive
T cytotoxic
A 20-year-old patient complains of recurrent respiratory infections and pustular rash. Doctor suggestsimmunogram test.
What is the marker for B lymphocytes in immunogram?
a.
CD 4+
b.
CD 22+
c.
CD 95+
d.
CD 8+
b.
CD 22+
A 32-year-old female was diagnosed with genital condylomas. The Doctor explained to the patient thatthis is infectious disease, induced by HPV (human papilloma virus) and can indicate a predisposal tocervical cancer.
What HPV types are most oncogenic?
a.
44 and 54
b.
16 and 18
c.
43 and 71
d.
6 and 11
b.
16 and 18
Which one of the following sets of cells can present antigen to helper T cells?
a.
Neutrophils and cytotoxic T cells
b.
Macrophages and eosinophils
c.
B cells and dendritic cells
d.
B cells and cytotoxic T cells
B cells and dendritic cells
A 32-year-old female presents to the ER complaining of pain and swelling in her lower extremities fortwo days, more severe in her right knee. The patient denies any history of recent or past trauma to thatregion. She further added that she had previously experienced similar pain in her elbows and ankles.Laboratory tests revealed leukocytosis and elevated ESR (erythrocyte sedimentation rate). Furthertesting revealed a positive throat culture for group A streptococcus and elevated titers ofantistreptolysin O (ASO).
What is the most probable trigger for development of the pathology in this patient?
a.
Molecular mimicry
b.
Genetic factors
c.
Breakdown of central tolerance
d.
Hyperproduction of Treg
Molecular mimicry
samplewas sent to the laboratory for histological tests. Microscopy revealed infiltration of multilobed cells withsegmented nuclei (see picture).
What cells first react and migrate to the tissues during Antigen invasion?
a.
Mast cells
b.
Eosinophiles
c.
Neutrophiles
d.
Basophiles
Neutrophiles
Historically, Murine monoclonal antibodies (MAB) were successfully used in patients but over time theireffectiveness was observed to decrease or even to be blocked.
What is the mechanism which leads to the decreased/blocked activity of murine MAB in patients?
a.
Production of HAMA
b.
Production of TNF
c.
Production of HAHA
d.
Production of HACA
Production of HAMA
An Immunoglobulin that is the first class of antibody to appear, so its presence indicates an activeinfection rather than an infection that occurred in the past. It can fix complement, which is an importantdefense against many bacterial infections. It’s found in plasma as a pentamer.
a.
IgD
b.
IgE
c.
IgM
d.
IgG
e.
IgA
IgM
Opsonization is the process by which:
a.
Chemokines attract neutrophils to the site of infection
b.
The alternate pathway of complement is activated
c.
Bacteria are made more easily phagocytized
d.
Neutrophils migrate from the blood through the endothelium to reach the site of infection
Bacteria are made more easily phagocytized
A healthy person has been protected from the tumor formation process by his/her cytotoxic Tlymphocytes (CTLs) which recognize potential tumor cells and destroy them via two killing mechanisms,one of which is induction of apoptosis (programmed cell death).
What receptors are used by CTLs for apoptosis induction?
a.
TCR/CD4+
b.
CD8+/CD3+
c.
MHC/TCR
d.
Fas ligand/Fas
Fas ligand/Fas
A 16-year-old patient presents with complaints of recurrent viral infections and herpes rash on the lips(15 times during a year). Doctor suggests immunogram test.
What is the marker for T lymphocytes in immunogram?
a.
CD 22+
b.
CD 3+
c.
CD 95+
d.
CD 19+
CD 3+
A 71-year-old male noticed a painless lump on his forearm, which grew steadily over the next 8 months.After MRI and biopsy a diagnosis of soft tissue sarcoma was made. No metastases were detected. Thepatient was offered chemotherapy in combination with immunotherapy with LAK-cells.
LAK cells are:
a.
Treg cells activated by IL-6
b.
Macrophages activated by IFN-gamma
c.
T cells and NK cells activated by IL-2
d.
B cells activated by IL-4
T cells and NK cells activated by IL-2
Which type of immunity is specific and has high diversity?
Adaptive
Innate
Adaptive
Which cells participate in adaptive immunity? Select all that apply
Mast cells
T lymphocytes
B lymphocytes
Dendritic cells
Eosinophils
T lymphocytes
B lymphocytes
Which cells participate in innate immunity? Select all that apply
Eosinophils (selected)
B lymphocytes
T lymphocytes
Mast cells (selected)
Dendritic cells (selected)
Mast cells
Dendritic cells
Eosinophils
Which immunoglobulin protects mucosa from infections?
Ig A
Ig M
Ig E
Ig D
Ig G
Ig A
Which laboratory test uses fluorescent compounds to aid in the detection of antibodies?
Enzyme linked immunosorbent assay
Immunofluorescence
Lateral flow test
Immunofluorescence
Which class of antigen is expressed only by immune cells capable of phagocytosis?
MHC Class II
MHC Class III
MHC Class I
MHC Class II
Which differentiated effector T cells will remain in the lymphoid organs and help B cells produce antibodies?
Th2
Th1
Th17
Tfh
Tfh
Match the effector T cell with its principle target cell
Th1: Macrophages
Th2: Eosinophils
Th17: Neutrophils
Tfh: B cells
Th1: Macrophages
Th2: Eosinophils
Th17: Neutrophils
Tfh: B cells
The autoimmune condition Graves’ disease can be classified as which type of hypersensitivity?
Type IV
Type II
Type III
Type I
Type II
Which type of hypersensitivities have inflammatory reactions mediated by cytokines? Select all that apply.
Type II
Type IV
Type I
Type III
Type IV (selected)
Type I (selected)
Which of the following will lead to immune tolerance through negative selection?
Strong recognition of self antigens
Weak recognition of self antigens
No recognition of self antigens
Strong recognition of self antigens (selected)
Tumors can use different mechanisms to evade the immune system. Which mechanism results in reduced immunogenicity of tumor cells over time?
Immune editing
Immune checkpoint
Secretion of suppressive products
Down regulation of Class I MHC
Immune editing (selected)
Which one of the following immune cells does HIV induce death in?
CD4+ T cells
Neutrophils
B cells
CD8+ T cells
CD4+ T cells (selected)
Match the type of vaccine to the correct description of its active component
Live vaccine: Whole weak virus that does not cause disease
Inactivated vaccine: Whole virus that has been killed
Nucleic acid vaccines: DNA or RNA from a virus
Viral vector vaccines: Harmless virus is used to carry viral DNA/RNA
Subunit vaccines: Part of a virus (e.g., antigen or epitope)
Live vaccine: Whole weak virus that does not cause disease
Inactivated vaccine: Whole virus that has been killed
Nucleic acid vaccines: DNA or RNA from a virus
Viral vector vaccines: Harmless virus is used to carry viral DNA/RNA
Subunit vaccines: Part of a virus (e.g., antigen or epitope)
Which type of allograft rejection occurs due to the presence of preformed antibodies against the transplant tissue?
Hyperacute rejection
Chronic rejection
Acute rejection
Graft vs host reaction
Hyperacute rejection (selected)
A 21-year-old female complains of joint pain, skin rash on her cheeks and bridge of nose and enlarged lymph nodes. After examination and laboratory tests she was diagnosed with Systemic Lupus Erythematosus (SLE, lupus).
What selection do T and B cells undergo to eliminate potential autoreactive cells?
a.
Positive selection
b.
Overlap selection
c.
Negative selection
d.
Neutral selection
Negative selection
A 48-year-old female complains of difficulty swallowing, loss of appetite, weight loss (12 kg over the last three months), irritability and progressive fatigue. On examination: exophthalmia (see the picture) though the thyroid gland is not enlarged. The Doctor suspects Graves’ disease.
What antibodies can be tested to confirm the diagnosis?
Question 2
a.
Ab to acetylcholine receptors
b.
Ab to gluten and gliadin
c.
Ab to ds-DNA
d.
Ab thyroid-stimulation hormone receptor
Ab thyroid-stimulation hormone receptor
Regarding IgG, which one of the following is the most accurate?
Question 3
a.
The ability of IgG to fix complement resides on the constant region of the light chain
b.
It is the most important antigen receptor on the surface of neutrophils
c.
It is the only one of the five immunoglobulins that is transferred from mother to fetus in utero
d.
During the primary response, it is made in larger amounts than is IgM
It is the only one of the five immunoglobulins that is transferred from mother to fetus in utero
A 31-year-old female with asthma was undergoing allergic skin testing. 15 minutes after exposure to the allergens, her skin was seen to blister at the site of contact with allergen of birch.
What cells are responsible for histamine release and induction of a positive reaction in this patient?
Question 4
a.
Mast cells
b.
Macrophages
c.
Dendritic cells
d.
Neutrophiles
Mast cells
Which one of the following host defence processes is the MOST important in preventing the action of exotoxins?
Question 5
a.
Lysis of exotoxins by perforins produced by cytotoxic T cells
b.
Degradation of exotoxins by the membrane attack complex of complement
c.
Neutralization of exotoxins by antibody prevents binding to target cell membrane
d.
Binding of cytokines to exotoxin-specific receptors inhibits the attachment of exotoxins
Neutralization of exotoxins by antibody prevents binding to target cell membrane
Certain components of our immune system are characterized by two attributes: being able (1) to respond specifically to microbes and (2) to exhibit memory of having responded to a particular microbe previously. Which one of the following has BOTH specificity and memory?
Question 6
a.
Neutrophils
b.
Basophils
c.
Dendritic cells
d.
B cells
B cells
A 22-year-old female has a history of recurrent herpes simplex rash on her lips over the last three years. She had treatment with antiviral medicines with minimal success. The doctor decided to add immunostimulatory medicine to increase internal antiviral immune factors.
Which cytokines play the main role in antiviral immunity?
a.
TNF
b.
Type II IFNs
c.
G-CSF
d.
Type I IFNs
Type I IFNs
Which one of the following sets of cells can present antigen to helper T cells?
Question 13Answer
a.
B cells and cytotoxic T cells
b.
B cells and dendritic cells
c.
Neutrophils and cytotoxic T cells
d.
Macrophages and eosinophils
B cells and dendritic cells
