Immunology Flashcards
(173 cards)
1
Q
Lecture 1:
Who is considered the pioneer of vaccination, and what disease did he target?
A
Edward Jenner is considered the pioneer of vaccination; he targeted smallpox using cowpox pus.
2
Q
What major concept in immunology did Elie Metchnikoff describe and name?
A
Elie Metchnikoff described and named phagocytosis, the ingestion of foreign matter by white blood cells.
3
Q
What are the two primary arms of adaptive immunity?
A
Humoral immunity (antibody production by B cells) and cell-mediated immunity (T cells killing infected cells and aiding other immune cells).
4
Q
What are the main cells involved in natural immunity?
A
Granulocytes (Neutrophils, Eosinophils, Basophils), Monocytes, and Natural Killer (NK) cells.
5
Q
Define ‘antigen’ and list its key characteristics.
A
An antigen is a substance recognized as foreign by the immune system, provoking a response. Key characteristics include immunogenicity (ability to provoke an immune response) and reactivity (ability to react with antibodies or T cells).
6
Q
What is the primary function of the complement system in immunity?
A
The complement system aids in pathogen elimination and links innate and adaptive immunity through a cascade of protein reactions.
7
Q
What are the four properties of specific immunity, often referred to as the 4 Rs?
A
Recognition (identifying foreign antigens), Response (eliminating the antigen), Remember (memory of the antigen for quicker future response), and Regulate (reducing the immune response once the threat is diminished).
8
Q
What are the phases of immune response to infection, and their time frames?
A
Innate Immunity: Immediate response (0-4 hours)
Early Induced Response: Activation of innate effectors (4-96 hours)
Adaptive Response: Activation of T and B cells, pathogen removal, and memory formation (>96 hours)
9
Q
What is the significance of immunological memory in vaccination?
A
Immunological memory allows for long-term protection against diseases by leveraging the memory response developed after vaccination.
10
Q
Describe Paul Ehrlich’s Side Chain Theory.
A
Paul Ehrlich’s Side Chain Theory, blood cells- bind and inactivate pathogens= antibody production.
11
Q
Name the primary and secondary organs involved in the immune system.
A
Primary Organs: Bone marrow and thymus (formation and maturation of immune cells).
Secondary Organs: Lymphatic system and spleen (immune cells’ activity).
12
Q
Differentiate between active and passive immunity.
A
Active immunity develops after exposure to a disease or vaccine, while passive immunity is transferred from another individual, such as from mother to fetus.
13
Q
What were some of the major infectious diseases and their mortality rates? (Name at least 1)
A
AIDS: 2.6 million deaths per year
Infantile respiratory infections: 3.5 million
Infantile diarrhea: 2.2 million
Tuberculosis: 1.5 million
Malaria: 1.1 million
14
Q
Lecture 2:
Name the main types of phagocytic cells involved in innate immunity.
A
Monocytes/macrophages and neutrophils.
15
Q
What are the three types of epithelial barriers involved in innate protection?
A
Mechanical barriers (flow of air or fluid, movements of mucus), chemical barriers (fatty acids in skin, lysozyme in saliva and tears, pepsin in the gut), and microbiological barriers (commensal bacteria).
16
Q
What is the importance of Mucosal-Associated Lymphoid Tissue (MALT)?
A
It is the principal site for infections and allergic reactions, serves as an absorptive surface for food and oxygen, acts as a barrier against antigen penetration, and responds to antigens.
17
Q
What role do commensal bacteria play in innate immunity?
A
They prevent adherence and penetration into the mucosa and are the main immune stimuli for neonates from microbial signals.
18
Q
Define opsonization and name two types of opsonins.
A
Opsonization is the process by which pathogens are marked for ingestion and destruction by phagocytes. Two types of opsonins are immunoglobulins and complement protein fragments.
19
Q
What are Pattern Recognition Receptors (PRRs) and what do they recognize?
A
PRRs are receptors that recognize pathogen-associated molecular patterns (PAMPs).
20
Q
Name the types of PRRs and give one example of each.
A
Cellular: Scavenger receptors
Humoral: Collectins
Intracellular/Cytosolic: NOD-like receptors
Surface: Toll-like receptors (TLRs)
21
Q
What are the functions of Toll-like Receptors (TLRs)?
A
TLRs bind to PAMPs, triggering immune responses such as cytokine production and inflammation.
22
Q
List four examples of antimicrobial factors and their functions.
A
Salivary Peroxidase: Bactericidal effects
Lysozyme: Digests bacterial cell walls
Lactoferrin: Iron-binding to block bacterial growth
Histatins: Anti-fungal agents
23
Q
What are antimicrobial peptides, and what is their mechanism of action?
A
Antimicrobial peptides are amphipathic cationic molecules that interact with membrane phospholipids to form pores in pathogens’ membranes.
24
Q
What are the key functions of Natural Killer (NK) cells in innate immunity?
A
NK cells defend against viruses and tumors, produce interferon-gamma (IFN-γ), and contain perforin and granzymes for cell-mediated cytotoxicity.
25
Summarize the main characteristics of innate immunity.
Innate immunity is the first line of defense, versatile despite limited diversity, does not react against host cells, is activated only on microbial surfaces, and lacks immunological memory.
26
What are the main components of innate immunity?
Barriers (prevent microbial entry), circulating cells (neutrophils, macrophages, NK cells), and soluble factors (complement, mannose-binding lectin, C-reactive protein, cytokines).
27
Lecture 3:
What are the primary lymphoid tissues and their functions?
Bone Marrow: Produces all blood cell lineages including B cells.
Thymus: Site for T cell maturation.
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What are the secondary lymphoid tissues and their functions?
Spleen and lymph nodes; sites for immune responses.
29
Describe the typical structure of immunoglobulin molecules.
Immunoglobulin molecules have two heavy chains and two light chains joined by disulphide bonds, with variable and constant regions.
30
What are the functions of IgM?
IgM is the first antibody produced, activates complement, and is too large to cross the placenta.
31
What role does IgG play in the immune system?
IgG is the most abundant immunoglobulin, can cross the placenta, and is involved in opsonization and complement activation.
32
What are the primary and secondary immune responses?
Primary Response: Slow, brief initial production of IgM followed by IgG.
Secondary Response: Rapid, longer-lasting, mainly IgG, with higher affinity due to affinity maturation.
33
What are the two types of B cell activation?
T-Independent Activation: Bacterial endotoxins trigger IgM production.
T-Dependent Activation: Requires help from T-helper cells for B cell proliferation and antibody secretion leading to memory formation.
34
How do B lymphocytes differ from T lymphocytes?
B Lymphocytes: Produce antibodies, mainly effective against extracellular infections.
T Lymphocytes: Recognize antigens via T-cell receptors, involved in intracellular infection response.
35
What is class switching in immunoglobulins?
Class switching is the change of heavy chains in immunoglobulins while retaining antigen specificity.
36
What is somatic hypermutation and its significance?
Somatic hypermutation alters variable regions of immunoglobulins to improve antigen binding affinity.
37
Name and describe the specific functions of IgE.
IgE is involved in allergic responses and defense against parasites.
38
Where is IgA primarily found and what is its function?
IgA is found in mucosal areas and is involved in mucosal immunity.
39
What are the roles of immunoglobulins in the immune system?
Immunoglobulins act as adapter molecules that can activate complement, mediate phagocytosis, and trigger allergic reactions.
40
Lecture 4:
What are the three main types of T cells?
Cytotoxic T Cells (CD8+)
Helper T Cells (CD4+)
Regulatory T Cells
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How do Helper T Cells (CD4+) assist in the immune response?
Helper T Cells assist in activating immune cells by recognizing antigens presented by MHC Class II molecules and producing cytokines.
41
What is the primary function of Cytotoxic T Cells (CD8+)?
Cytotoxic T Cells kill virus-infected and abnormal cells by inducing apoptosis.
42
What is the role of Regulatory T Cells?
Regulatory T Cells inhibit immune responses to prevent autoimmunity by producing cytokines like IL-10 and TGF-beta.
43
Where are T cells activated?
T cells are activated in secondary lymphoid tissues, such as lymph nodes and the spleen.
44
Describe the structure of T-cell receptors (TCR).
T-cell receptors have a similar structure to immunoglobulins but remain membrane-bound, consisting of constant and variable regions. They come in two forms: αβ (common) and γδ (less common).
45
What is antigen presentation?
Antigen presentation is the process by which protein fragments from pathogens or other foreign substances are displayed on the surface of cells by MHC molecules, allowing T cells to recognize and respond to the antigens.
46
Differentiate between MHC Class I and MHC Class II molecules.
MHC Class I: Present on all nucleated cells, present intracellular antigens to CD8+ T cells.
MHC Class II: Present on antigen-presenting cells (APCs) like dendritic cells, macrophages, and B cells, present extracellular antigens to CD4+ T cells.
47
How are antigens processed in the MHC Class I pathway?
Intracellular antigens are processed in the endoplasmic reticulum and presented on the cell surface by MHC Class I molecules.
48
How are antigens processed in the MHC Class II pathway?
Extracellular antigens are processed in acidified endosomes and presented on the cell surface by MHC Class II molecules.
49
What mechanisms do Cytotoxic T Cells use to kill infected cells?
Cytotoxic T Cells induce apoptosis in infected cells using perforin, granzymes, and granulysin.
50
What is the role of Helper T Cells in activating macrophages and assisting B cells?
Th1 cells activate macrophages, while Th2 cells assist B cells in antibody production.
51
Explain the concept of MHC polymorphism and its significance.
MHC polymorphism refers to the high variability in MHC genes, allowing for a broad range of antigen presentation, which is essential for effective immune responses and complicates organ transplantation.
52
What is apoptosis, and why is it important in the immune response?
Apoptosis is programmed cell death used by cytotoxic T cells to eliminate infected cells without releasing pathogens, ensuring controlled cell death to prevent the spread of infections.
53
Define cytokines and their primary functions.
Cytokines are low molecular weight proteins secreted by immune cells to regulate immune responses, acting in autocrine, paracrine, and endocrine manners.
54
What are the properties of cytokines?
Cytokines are pleotropic, synergistic, and can have a cascade effect, meaning they have different effects depending on the target cell, work together to enhance effects, and one cytokine can stimulate the production of others.
55
Name and describe the cytokine families
Haematopoietin Family: IL-2, IL-4
Interferon Family: IFN-alpha, beta, gamma
Chemokine Family: Attracts cells to sites of infection
Tumor Necrosis Family: Involved in inflammation and cell death
56
What is the function of IL-2 and IL-4 cytokines?
IL-2: T cell growth factor.
IL-4: B cell growth factor.
57
What is the role of Interferon-gamma (IFN-γ)?
Interferon-gamma (IFN-γ) activates macrophages and has antiviral properties.
58
What are the effects of TNF-alpha cytokine?
TNF-alpha promotes inflammation and can kill cancer cells.
59
What can result from a cytokine imbalance?
Cytokine imbalance can lead to diseases such as cytokine storm, which involves excessive cytokine release causing multi-organ failure.
60
How do inflammatory cytokines contribute to sepsis?
Inflammatory cytokines like TNF-alpha, IL-1, and IL-6 contribute to the symptoms and severity of sepsis, leading to septic shock with poor blood perfusion, abnormal clotting, and organ dysfunction.
61
Summarize the primary functions of MHC-I and MHC-II molecules.
MHC-I: Presents intracellular antigens to CD8+ T cells.
MHC-II: Presents extracellular antigens to CD4+ T cells.
62
What is a cytokine storm, and what are its consequences?
A cytokine storm is an excessive cytokine release causing multi-organ failure and is often associated with severe infections and immune responses.
63
Name the three pathways that activate the complement system.
Classical Pathway
Lectin Pathway
Alternative Pathway
64
How is the Classical Pathway triggered?
The Classical Pathway is triggered by C1q binding to immune complexes (antigen-bound IgM or IgG).
65
What does the Classical Pathway produce that is crucial for its function?
It produces C3 convertase (C4b2a) which cleaves C3 into C3a and C3b, leading to the formation of C5 convertase (C4b2aC3b) and ultimately the Membrane Attack Complex (MAC) (C5b C6 C7 C8 C9).
66
What activates the Lectin Pathway?
The Lectin Pathway is activated by mannose-binding lectin (MBL) binding to pathogens.
67
What is the role of the alternative pathway in complement activation?
The Alternative Pathway is continuously active at a low level ("tick-over" mechanism) and is activated by pathogen surfaces.
68
What are the primary roles of the complement system?
Opsonization: C3b binds to pathogens marking them for phagocytosis.
Inflammation: C3a and C5a act as anaphylatoxins promoting inflammation.
Pathogen Lysis: MAC creates pores in pathogen membranes causing cell lysis.
69
What are the main regulatory proteins of the complement system?
C1 Inhibitor
C4-binding Protein (C4BP)
Membrane Cofactor Protein (MCP/CD46)
Factor H and Factor I
Decay-Accelerating Factor (DAF)
CD59
70
What disease is associated with C1 Inhibitor Deficiency?
C1 Inhibitor Deficiency leads to hereditary angioedema characterized by episodic swelling due to increased bradykinin.
71
What conditions arise from Factor H or Factor I Deficiency?
Factor H or Factor I Deficiency causes uncontrolled activation of the alternative pathway leading to rapid consumption of complement proteins and increased susceptibility to infections.
72
What is the result of Decay-Accelerating Factor (DAF) Deficiency?
DAF Deficiency results in paroxysmal nocturnal hemoglobinuria, a condition with recurrent red blood cell lysis.
73
What is the consequence of Complement Receptor 1 (CR1) Deficiency?
CR1 Deficiency impairs the clearance of immune complexes associated with conditions like systemic lupus erythematosus.
74
Summarize the importance and function of the complement system.
The complement system is a critical part of the immune response bridging innate and adaptive immunity. It is activated through three pathways that converge to form C3 convertase leading to opsonization, inflammation, and pathogen lysis. Proper regulation is essential to prevent damage to host cells and deficiencies in complement proteins can lead to various diseases.
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Lecture 6:
What is the mechanism of Type I Hypersensitivity (Allergy or Atopy)?
Mediated by IgE antibodies; upon exposure to an allergen, IgE binds to mast cells causing degranulation and release of histamine and other mediators.
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Give examples of conditions caused by Type I Hypersensitivity.
Allergic rhinitis, asthma, anaphylaxis.
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What are the symptoms of Type I Hypersensitivity?
Immediate reaction, vasodilation, smooth muscle contraction, and increased vascular permeability leading to edema.
78
Describe the mechanism of Type II Hypersensitivity (Antibody-Mediated).
Mediated by IgM and IgG antibodies that bind to cell surface antigens leading to cell destruction, inflammation, and cellular dysfunction.
79
Provide examples of conditions associated with Type II Hypersensitivity.
Hemolytic disease of the newborn (Rh incompatibility), transfusion reactions.
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What are the symptoms of Type II Hypersensitivity?
Symptoms depend on the specific cells or tissues targeted, often involving destruction of red blood cells or other cellular components.
81
Explain the mechanism of Type III Hypersensitivity (Immune Complex-Mediated).
Formation of immune complexes (antigen-antibody) that deposit in tissues and cause inflammation and tissue damage.
82
Give examples of diseases caused by Type III Hypersensitivity.
Systemic lupus erythematosus, rheumatoid arthritis, Arthus reaction.
83
What are the symptoms of Type III Hypersensitivity?
Localized inflammation, thrombosis, and tissue necrosis.
84
Describe the mechanism of Type IV Hypersensitivity (Delayed-Type T-Cell Mediated).
Mediated by T cells rather than antibodies, involving the release of cytokines that recruit and activate macrophages and other immune cells.
85
Provide examples of conditions associated with Type IV Hypersensitivity.
Contact dermatitis (e.g., poison ivy), tuberculosis, chronic transplant rejection.
86
What are the symptoms of Type IV Hypersensitivity?
Delayed reaction (24-48 hours), local tissue damage, and inflammation.
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What are the pathological consequences of Type I, Hypersensitivity?
Rapid onset with symptoms like swelling, itching, and anaphylaxis in severe cases.
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What are the pathological consequences of Type II Hypersensitivity?
Destruction of target cells leading to conditions like hemolytic anemia or organ-specific autoimmune diseases.
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What are the pathological consequences of Type III Hypersensitivity?
Immune complexes deposit in tissues causing inflammation and damage, as seen in diseases like lupus.
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What are the pathological consequences of Type IV Hypersensitivity?
Delayed reaction causing chronic inflammation and granuloma formation, significant in infections like tuberculosis.
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How is Type I Hypersensitivity regulated?
Involves identifying allergens and using treatments like antihistamines, mast cell stabilizers, and desensitization therapy.
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How is Type II Hypersensitivity regulated?
Requires careful blood matching and use of medications like corticosteroids to reduce immune response.
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How is Type III Hypersensitivity regulated?
Involves managing underlying autoimmune conditions and using immunosuppressive drugs.
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How is Type IV Hypersensitivity regulated?
Involves avoiding known contact allergens and using anti-inflammatory drugs to control reactions.
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Lecture 7:
What is central tolerance and where does it occur?
Central tolerance occurs in primary lymphoid organs (thymus and bone marrow), where self-reactive T and B cells are deleted or rendered anergic.
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What is peripheral tolerance and where does it occur?
Peripheral tolerance occurs outside primary lymphoid organs and involves mechanisms like anergy, deletion, and regulatory T cell (T-reg) induction.
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Describe the process of central tolerance in the thymus.
In the thymus, T cells undergo positive selection (interaction with MHC) and negative selection (elimination of self-reactive T cells).
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How are self-reactive B cells handled in the bone marrow?
In the bone marrow, B cells encountering self-antigens become anergic.
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What are the mechanisms of peripheral tolerance?
Mechanisms of peripheral tolerance include anergy (self-reactive T and B cells become inactive without co-stimulatory signals), deletion (apoptosis of self-reactive cells), and regulatory T cells (T-reg) suppression of immune responses to self-antigens.
100
What role do CD4+CD25+ T-reg cells play in immune tolerance?
CD4+CD25+ T-reg cells prevent other T cells from attacking self-antigens, maintaining tolerance.
101
What is FOXP3 and its significance in autoimmunity?
FOXP3 is a transcription factor crucial for T-reg function. Its deficiency leads to autoimmunity.
102
Name an autoimmune disorder associated with hyperthyroidism.
Graves' Disease is an autoimmune disorder associated with hyperthyroidism caused by autoantibodies to TSH receptors.
103
What causes Hashimoto's Thyroiditis?
Hashimoto's Thyroiditis is caused by antibodies and T cells attacking thyroid tissues, leading to hypothyroidism.
104
Which cells are targeted in Type 1 Diabetes Mellitus?
In Type 1 Diabetes Mellitus, T cells attack insulin-producing cells in the pancreas.
105
What is the immunological target in Multiple Sclerosis?
In Multiple Sclerosis, T cells target CNS neurons leading to demyelination.
106
What causes inflammation and joint damage in Rheumatoid Arthritis?
In Rheumatoid Arthritis, autoantibodies against joint antigens cause inflammation and joint damage.
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What autoantibodies are involved in Systemic Lupus Erythematosus (SLE)?
Autoantibodies against DNA and other nuclear components are involved in Systemic Lupus Erythematosus (SLE), leading to systemic inflammation.
108
How do genetics influence autoimmunity?
Genetics influence autoimmunity, with HLA associations with diseases (e.g., HLA-B27 with ankylosing spondylitis).
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Why are females generally more susceptible to autoimmune disorders?
Females are generally more susceptible due to hormonal influences.
110
What environmental triggers can lead to autoimmune responses?
Infections, such as Epstein-Barr virus, can trigger autoimmune responses.
111
Explain molecular mimicry in the context of autoimmunity.
Molecular mimicry occurs when pathogens have antigens similar to self-antigens, triggering an autoimmune response.
112
What is the consequence of defective clearance of apoptotic cells?
Defective clearance of apoptotic cells can lead to autoantibody production.
113
What are the pathophysiological manifestations of chronic inflammation in autoimmune diseases?
Continuous immune response causes chronic inflammation and organ damage.
114
What is the aim of treatment for autoimmune diseases?
The aim of treatment is to suppress the immune response and manage symptoms.
115
Lecture 8:
Define immunodeficiencies and their types.
Immunodeficiencies are defects in the immune system's functional capacity. Types include congenital (inherited) immunodeficiencies and acquired immunodeficiencies.
116
What are congenital immunodeficiencies?
Congenital immunodeficiencies are genetic defects impairing the immune system, affecting about 1 in 500 people in Europe and the US.
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What genetic factors contribute to congenital immunodeficiencies?
They are often X-linked, making males more susceptible, with autosomal recessive disorders also common in cultures with consanguinity.
118
Name key defects associated with phagocyte deficiencies.
Leukocyte Adhesion Deficiencies: Impaired leukocyte recruitment.
Lazy Leukocyte Syndrome: Faulty chemotaxis in neutrophils.
Chronic Granulomatous Disease (CGD): Defective NADPH oxidase; recurrent infections and granuloma formation.
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What are the key defects associated with lymphocyte deficiencies?
Severe Combined Immunodeficiency (SCID): Absence of T and B lymphocytes; commonly due to adenosine deaminase (ADA) deficiency.
DiGeorge Syndrome: Chromosome 22q11 deletion affecting thymic development and T-cell responses.
Bruton’s Agammaglobulinemia: Failure of B-cell maturation; requires frequent immunoglobulin infusions.
120
What are the primary causes of acquired immunodeficiencies?
Infections: HIV leading to AIDS.
Therapeutics: Chemotherapy, radiotherapy, immunosuppressive drugs.
Nutritional Deficiencies: Lack of essential micronutrients like zinc and vitamin C.
Other Factors: Stress, substance misuse, malnutrition, and surgical interventions.
121
How does HIV/AIDS affect the immune system?
HIV targets CD4+ cells, impairing both innate and adaptive immunity, leading to progressive immune function decline, increased susceptibility to infections and cancers.
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How is HIV transmitted?
HIV is transmitted via body fluids including blood, sexual contact, and shared needles.
123
What is the progression and treatment of HIV/AIDS?
HIV leads to AIDS, characterized by a progressive decline in immune function. Treatment includes antiretroviral therapies (ART), which slow disease progression but do not eradicate the virus.
124
What is the management approach for immunodeficiencies?
Effective management involves identifying underlying causes and providing appropriate treatments such as bone marrow transplants for inherited immunodeficiencies or ART for HIV/AIDS.
125
Lecture 9:
What is transplantation?
Transplantation is the process of taking cells, tissue, or organs (graft) from one individual and placing them into another (recipient).
126
Differentiate between orthotopic and heterotopic transplants.
Orthotopic: Transplant placed in the same anatomical location (e.g., heart).
Heterotopic: Transplant placed in a different anatomical location (e.g., kidney).
127
What are the two main immune recognition mechanisms in transplantation?
Direct Allorecognition: Host T cells recognize intact MHC molecules on donor APCs within the graft.
Indirect Allorecognition: Donor MHC molecules are processed by recipient APCs, and host T cells recognize these processed donor peptides.
128
Name the four types of graft rejection.
Hyperacute Rejection
Accelerated Rejection
Acute Rejection
Chronic Rejection
129
Describe hyperacute rejection.
Hyperacute rejection occurs minutes to hours post-transplant and is mediated by preexisting antibodies.
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What is the typical timeframe for acute rejection?
Acute rejection occurs around 10-30 days post-transplant and is mediated by CD4, CD8, NK cells, and macrophages.
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What factors influence transplant success?
Matching MHC types and ABO blood groups, and the use of immunosuppressive therapy to prevent rejection while avoiding infections and cancer.
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What is the purpose of bone marrow transplantation (BMT)?
BMT replaces diseased or damaged bone marrow with healthy cells.
133
What is graft-versus-host disease (GVHD)?
GVHD is a condition where donor immune cells attack recipient tissues after a bone marrow transplant.
134
Name an immunosuppressive therapy that inhibits calcineurin to reduce T cell activation.
Cyclosporine A and Tacrolimus.
135
What is the function of Mycophenolate Mofetil (MMF) in immunosuppression?
MMF inhibits lymphocyte proliferation by blocking guanine nucleotide synthesis.
136
How does Azathioprine work as an immunosuppressive drug?
Azathioprine inhibits DNA synthesis, blocking lymphocyte proliferation.
137
What are some side effects of corticosteroids like Prednisone?
Side effects include fluid retention and bone mineral loss.
138
Lecture 10:
What is carcinoma?
Carcinoma is cancer of epithelial cells.
139
What is sarcoma?
Sarcoma is cancer of connective tissues.
140
What is lymphoma?
Lymphoma is cancer of the lymphoid system.
141
What is leukemia?
Leukemia is cancer of blood cells.
142
Name some common types of carcinomas.
Basal-cell carcinoma, breast carcinoma, prostate carcinoma, lung carcinoma, colorectal carcinoma, melanoma.
143
What are tumor-specific antigens?
Tumor-specific antigens are unique to tumors and result from DNA mutations, such as the CDK-4 gene in melanoma.
144
What are tumor-associated antigens?
Tumor-associated antigens are normal proteins with abnormal expression, such as PSA in prostate cancer and HER-2/NEU in breast cancer.
145
How does the immune system eliminate virus-transformed cells?
Immune cells target viruses that can cause cancer and eliminate the virus-transformed cells.
146
What role does the immune system play in regulating inflammation related to cancer?
Immune cells control pathogens and inflammation that can lead to cancer.
147
How do tumors evade immune surveillance through low immunogenicity?
Tumors may not display enough antigens to be recognized by the immune system.
148
What is one way tumors present as normal cells?
Tumors may present as normal cells through self-recognition mechanisms.
149
How do tumors use immune suppression to evade detection?
Tumors may secrete factors that inhibit the immune response.
150
What is mutation escape in the context of tumor evasion?
Tumor cells mutate to evade detection by the immune system.
151
How do tumors create physical barriers to shield themselves?
Tumors create barriers to shield themselves from immune cells
152
What is the role of monoclonal antibodies in cancer immunotherapy?
Monoclonal antibodies target specific tumor antigens to mediate cytotoxicity.
153
What are immunotoxins?
Immunotoxins are antibodies conjugated with toxic drugs to kill cancer cells.
154
What is adoptive cell transfer in cancer immunotherapy?
Adoptive cell transfer involves transferring immune cells with anti-tumor activity back into the patient.
155
What is CAR T-Cell Therapy?
CAR T-Cell Therapy involves genetically engineered T cells with receptors specific to tumor antigens.
156
How does checkpoint blockade enhance T cell activity against tumors?
Checkpoint blockade uses monoclonal antibodies to block inhibitory signals, enhancing T cell activity against tumors.
157
What is the role of IL-12 in cancer immunity?
IL-12 protects against chemically induced tumors.
158
How does Tumor Necrosis Factor-alpha (TNF-alpha) contribute to cancer treatment?
TNF-alpha induces tumor necrosis.
159
What is the function of Interferon-gamma in cancer immunity?
Interferon-gamma enhances antigen presentation, inhibits angiogenesis, and activates macrophages.
160
Why is understanding tumor evasion mechanisms important in cancer immunotherapy?
Understanding how tumors evade immune responses is crucial for developing effective cancer immunotherapies.
161
Lec 11:
What is the primary purpose of vaccines?
To prevent infectious diseases and protect public health.
162
What impact have vaccines historically had on public health?
Vaccines have dramatically reduced or eradicated diseases such as smallpox.
163
Name the key features of an effective vaccine.
Safety, protection, longevity, and practicality.
164
What are live attenuated organisms in vaccines?
Live attenuated organisms are weakened forms of the pathogen used in vaccines to elicit a strong immune response. Examples include measles, mumps, and rubella.
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What are the advantages and disadvantages of live attenuated vaccines?
Advantages: Strong immune response, fewer doses needed.
Disadvantages: Requires special storage, risk of reverting to virulent form.
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What are inactivated/killed organism vaccines?
Vaccines that use pathogens that have been killed or inactivated, such as the polio (Salk) and rabies vaccines.
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What are the advantages and disadvantages of inactivated/killed vaccines?
Advantages: Stable product, safer than live vaccines.
Disadvantages: Weaker immune response, requires boosters.
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What are toxoid vaccines?
Vaccines that use inactivated bacterial toxins, such as diphtheria and tetanus toxoids.
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What are subunit vaccines?
Vaccines that use specific parts of the pathogen, such as hepatitis B and pertussis vaccines.
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What are recombinant protein vaccines?
Vaccines that use genetically engineered proteins from the pathogen, such as the hepatitis B vaccine.
171
What are DNA vaccines?
Vaccines that use plasmid DNA encoding the antigen to promote both humoral and cellular immunity, examples include HPV and Zika (in clinical testing).
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