Formative Questions EXAM 1 Flashcards
1
Q
How does innate immunity differ from adaptive immunity?
A
Innate immunity is an immediate, nonspecific defense with no memory response, while adaptive immunity is a delayed, highly specific response involving B and T lymphocytes with memory formation.
2
Q
What are the principal classes of cells in the innate immune system?
A
Neutrophils, macrophages, dendritic cells, natural killer (NK) cells, and innate lymphoid cells (ILCs).
3
Q
What are the distinguishing characteristics of neutrophils?
A
Neutrophils are first responders and phagocytic.
4
Q
What are the distinguishing characteristics of macrophages?
A
Macrophages are long-lived phagocytes and antigen-presenting cells.
5
Q
What are the distinguishing characteristics of dendritic cells?
A
Dendritic cells are professional antigen-presenting cells (APCs) that link innate and adaptive immunity.
6
Q
What are the distinguishing characteristics of NK cells?
A
NK cells kill infected or tumor cells without MHC recognition.
7
Q
What do phagocytes react to when activated in an innate response?
A
Phagocytes recognize pathogen-associated molecular patterns (PAMPs) using pattern recognition receptors (PRRs) such as Toll-like receptors (TLRs).
8
Q
What are Innate Lymphoid Cells (ILCs)?
A
ILCs are innate counterparts to T cells that help regulate inflammation and immune defense. At mucosal surfaces, they maintain barrier integrity and secrete cytokines.
9
Q
What are the functions of NK cells?
A
NK cells kill virus-infected or cancer cells by releasing perforin and granzymes, inducing apoptosis.
10
Q
How do NK cells recognize targets?
A
NK cells detect cells lacking MHC I molecules or those expressing stress signals.
11
Q
How are NK cells activated?
A
NK cells are activated through activating receptors (e.g., NKG2D) and inhibited by MHC I.
12
Q
How do innate cells relay signals to activate adaptive immunity?
A
Dendritic cells capture antigens and migrate to lymph nodes to present antigens to naïve T cells, initiating the adaptive immune response.
13
Q
What is the basic principle of operation for the immune defense?
A
To recognize, respond to, and eliminate pathogens while avoiding self-reactivity.
14
Q
What are the principal classes of cells in the immune system?
A
Innate cells: Neutrophils, macrophages, dendritic cells, NK cells. Adaptive cells: B cells, T cells, plasma cells.
15
Q
How do immune cells develop (hematopoiesis)?
A
Immune cells originate from hematopoietic stem cells (HSCs) in the bone marrow, differentiating into common lymphoid or myeloid progenitors.
16
Q
Which immune cells operate in innate and specific immunity?
A
Innate immunity: Macrophages, dendritic cells, NK cells, granulocytes. Specific immunity: B cells (humoral response) and T cells (cell-mediated response).
17
Q
What are the lymphoid organs?
A
Primary lymphoid organs: Bone marrow (B cell maturation) and thymus (T cell maturation). Secondary lymphoid organs: Lymph nodes, spleen, and mucosa-associated lymphoid tissues (MALT) where antigen presentation occurs.
18
Q
How does germline DNA in fetal cells differ from recombined DNA in mature B/T cells?
A
Germline DNA contains unaltered V, D, and J gene segments, while mature B/T cells undergo VDJ recombination to form unique antigen receptor sequences.
19
Q
Do T/B lymphocytes know what they want to bind to when they produce their receptors?
A
No, receptor generation is random. Specificity is determined by random recombination of gene segments and selection processes in the bone marrow (for B cells) and thymus (for T cells).
20
Q
What is the advantage of assembling receptors with small parts?
A
It increases diversity, allowing the immune system to generate billions of unique antigen receptors.
21
Q
What can cause a change in specificity during VDJ recombination?
A
Somatic recombination errors, insertion or deletion of nucleotides by TdT, or faulty junctional processing.
22
Q
When and where does somatic hypermutation occur?
A
Somatic hypermutation occurs in the germinal centers of lymph nodes after B cell activation, increasing antibody affinity for antigens.
23
Q
Can antibodies with the same specificity have different biological functions?
A
Yes, the Fc region of antibodies determines the effector function, and class switching allows different classes (IgG, IgA, etc.) to be produced.
24
Q
What events occur in the bone marrow during B cell development?
A
VDJ recombination and selection against self-reactive B cells (central tolerance).
25
What events occur in the spleen and lymph nodes during B cell development?
Activation by antigens, class switching, and somatic hypermutation.
26
What are plasmablasts?
Plasmablasts are short-lived, antibody-secreting cells that develop shortly after B cell activation during an immune response.
27
How are plasma cells different from B cells?
Plasma cells are terminally differentiated B cells that secrete large amounts of antibodies but lack surface B cell receptors.
28
Where and how is self-reactivity prevented?
In the bone marrow (B cells) and thymus (T cells) during development through negative selection.
29
What is BAFF?
BAFF (B-cell activating factor) is a cytokine that promotes B cell survival and maturation.
30
What are the differences between B1 and B2 cells?
B1 cells are innate-like, produce natural antibodies, and are mainly found in peritoneal and pleural cavities. B2 cells are conventional adaptive B cells that undergo class switching and somatic hypermutation.
31
What does T-dependent and T-independent mean?
T-dependent (TD) means B cell activation requires help from T cells, leading to class switching and memory cell formation. T-independent (TI) means B cell activation occurs without T cell help, usually triggered by repetitive antigens.
32
During what stage of T cell development do you find CD4 and CD8 molecules?
CD4 and CD8 are expressed during the double-positive stage in the thymus.
33
Do TCRαβ or TCRγδ T cells express CD4 or CD8?
TCRαβ T cells undergo MHC restriction and become either CD4+ or CD8+ single-positive, while TCRγδ T cells do not express CD4 or CD8.
34
What events happen during the MHC selection process?
Positive selection ensures T cells can recognize self-MHC, while negative selection eliminates T cells that bind too strongly to self-peptides.
35
Where are T cells reactive against self-molecules identified and deleted?
In the thymus medulla during negative selection via interaction with medullary thymic epithelial cells (mTECs).
36
Where do Treg cells develop?
Treg cells develop in the thymus (natural Tregs) and periphery (induced Tregs).
37
Do TCRγδ T cells go through MHC selection?
Only TCRαβ T cells go through MHC selection; TCRγδ T cells do not require MHC.
38
How many pathways for the presentation of protein antigens are known?
Two main pathways: endogenous pathway (MHC I) for internal antigens and exogenous pathway (MHC II) for external antigens.
39
What molecules are used for antigen presentation?
MHC I molecules present endogenous antigens to CD8+ T cells, while MHC II molecules present exogenous antigens to CD4+ T cells.
40
Which molecules present external and internal antigens?
External antigens are presented by MHC II, while internal antigens are presented by MHC I.
41
Can you give examples of internal and external antigens?
Internal antigens: Viral proteins, intracellular bacteria, or tumor antigens. External antigens: Bacterial toxins, fungi, and parasites taken up by phagocytosis.
42
Why do we need MHC I molecules on every nucleated cell?
To detect and present intracellular infections (especially viruses) to CD8+ cytotoxic T cells.
43
Which cells can present antigens by MHC II?
Professional antigen-presenting cells (APCs) such as dendritic cells, macrophages, and B cells.
44
How are internal protein antigens processed for presentation?
Proteins are degraded in the proteasome, transported into the ER by TAP, and loaded onto MHC I.
45
How are external protein antigens processed for presentation?
Antigens are taken up by endocytosis or phagocytosis, degraded into peptides, and MHC II molecules bind peptides in the endosome.
46
Which presentation pathways activate functional classes of T lymphocytes?
MHC I pathway activates CD8+ cytotoxic T cells, while MHC II pathway activates CD4+ helper T cells.
47
What are the co-stimulatory molecules?
Molecules such as CD80 (B7-1) and CD86 (B7-2) bind to CD28 on T cells to provide essential second signals for activation.
48
What molecule presents lipid antigens?
CD1 molecules present lipid and glycolipid antigens.
49
Which part of the MHC molecules is polymorphic?
The peptide-binding groove (α1 and α2 domains of MHC I, α1 and β1 of MHC II) is highly polymorphic.
50
Why does having polymorphism in peptide-binding help protect a species from extinction?
Polymorphism increases the diversity of peptides that can be presented, ensuring that the population can mount immune responses against a wide range of pathogens.
51
How do immune cells meet antigens and circulate in the body?
Antigens are carried by APCs to secondary lymphoid organs where naïve T and B cells encounter them. Immune cells circulate via the lymphatic system and bloodstream.
52
How do T lymphocytes get activated?
By receiving three signals:
• Signal 1: TCR binds to antigen presented by MHC.
• Signal 2: Co-stimulation via CD28 binding to B7 (CD80/CD86).
• Signal 3: Cytokines direct T cell proliferation and differentiation.
53
What type of MHC do CD4+ T cells recognize?
MHC II.
54
What type of MHC do CD8+ T cells recognize?
MHC I.
55
What induces the development of Th1 cells?
IL-12 and IFN-γ.
56
What cytokines do Th1 cells produce?
IFN-γ.
57
What is the main function of Th1 cells?
Activate macrophages to kill intracellular pathogens.
58
What induces the development of Th2 cells?
IL-4.
59
What cytokines do Th2 cells produce?
IL-4, IL-5, IL-13.
60
What is the main function of Th2 cells?
Activate eosinophils and promote B cell class switching to IgE for defense against parasites.
61
What induces the development of Th17 cells?
IL-6, 23
62
What cytokines do Th17 cells produce?
IL-17 and IL-22.
63
What is the main function of Th17 cells?
Recruit neutrophils to fight extracellular pathogens like fungi and bacteria.
64
What induces the development of Tfh cells?
IL-6.
65
What cytokine do Tfh cells produce?
IL-21.
66
What is the main function of Tfh cells?
Help B cells in germinal center formation and class switching.
67
What induces the development of Treg cells?
TGF-β.
68
What cytokines do Treg cells produce?
IL-10 and TGF-β.
69
What is the main function of Treg cells?
Suppress immune responses and maintain self-tolerance.
70
What induces the development of M1 macrophages?
IFN-γ.
71
What cytokines do M1 macrophages produce?
IL-1, IL-6, TNF-α.
72
What is the main function of M1 macrophages?
Inflammation, microbial killing, and tissue destruction.
73
What induces the development of M2 macrophages?
IL-4 and IL-13.
74
What cytokines do M2 macrophages produce?
IL-10 and TGF-β.
75
What is the main function of M2 macrophages?
Tissue repair, anti-inflammatory effects, and fibrosis.
76
What cytokines facilitate the development of Treg cells?
TGF-β.
77
What cytokines do Treg cells secrete?
IL-10 and TGF-β.
78
What is the main function of Treg cells?
Suppress immune responses and maintain tolerance to self-antigens.
79
How are CTLs (CD8+ T cells) activated?
By three signals:
• Signal 1: TCR binds to antigen presented by MHC I.
• Signal 2: Co-stimulatory signal via CD28 binding to B7.
• Signal 3: IL-2 from helper T cells.
80
What do CTLs release to kill infected cells?
Perforin (creates pores) and granzymes (induce apoptosis).
81
What cytokines support the survival of T memory cells?
IL-7 and IL-15.
82
What is the function of T memory cells?
Rapidly respond to subsequent exposures of the same antigen.
83
What is the role of IL-2?
Promotes T cell proliferation.
84
What is the role of IL-4?
Induces Th2 differentiation and promotes B cell class switching to IgE.
85
What is the role of IL-10?
Suppresses immune responses (anti-inflammatory).
86
What is the role of IL-12?
Induces Th1 differentiation.
87
What is the role of IFN-γ?
Activates macrophages to enhance microbial killing.
88
What is the role of TGF-β?
Promotes Treg development and anti-inflammatory effects.
89
How are T cells activated and deactivated? What are the 3 signals?
Activation Signals:
• Signal 1: TCR binds to MHC-peptide complex.
• Signal 2: Co-stimulation via CD28 binding to B7 (CD80/CD86).
• Signal 3: Cytokines direct proliferation and differentiation.
Deactivation:
• Involves inhibitory receptors (e.g., CTLA-4 binding to B7 instead of CD28) or production of suppressive cytokines like IL-10 and TGF-β.
90
Which signals are involved in T cell up-regulation and down-regulation?
• Up-regulation: IL-2 (T cell proliferation), co-stimulatory molecules (e.g., CD28-B7).
• Down-regulation: CTLA-4 and PD-1 inhibitory receptors, IL-10, and TGF-β.
91
What does the term “T cell exhaustion” mean?
T cell exhaustion occurs when T cells become dysfunctional due to chronic antigen exposure (e.g., in cancer or chronic infection). It is characterized by reduced cytokine production and expression of inhibitory receptors like PD-1.
92
What are the biological properties of cytokines?
• Pleiotropy: A single cytokine can have multiple effects on different cells.
• Redundancy: Different cytokines can have the same effect.
• Synergy: Cytokines can work together to enhance an effect.
• Antagonism: Cytokines can inhibit the effects of other cytokines.
93
How do cytokines activate cells?
Cytokines bind to specific receptors on target cells, triggering intracellular signaling pathways (e.g., JAK-STAT pathway) that lead to changes in gene expression.
94
What happens when cytokine receptors bind ligands?
Binding of cytokines to their receptors leads to receptor dimerization or multimerization, activation of signaling cascades (e.g., JAK-STAT), and transcription of target genes.
95
What makes a cytokine redundant and pleiotropic?
• Redundant: When multiple cytokines have similar functions (e.g., IL-2, IL-7, and IL-15 promoting T cell survival).
• Pleiotropic: When one cytokine affects different types of cells (e.g., IL-4 promotes B cell antibody switching and Th2 differentiation).
96
What are some therapeutic applications of cytokines, cytokine receptors, and antibodies against cytokines and cytokine receptors?
• Cytokine therapy: IL-2 for boosting T cell activity in cancer.
• Cytokine receptor blockers: Anti-TNF-α (e.g., infliximab) for autoimmune diseases like rheumatoid arthritis.
• Antibodies against cytokine receptors: Anti-IL-6 receptor (tocilizumab) for inflammation.
97
What are the three pathways for complement activation?
Classical, lectin, and alternative pathways.
98
What triggers the classical pathway?
Antigen-antibody complexes (IgG or IgM).
99
What triggers the lectin pathway?
Mannose-binding lectin (MBL) binding to microbial carbohydrates.
100
What triggers the alternative pathway?
Spontaneous hydrolysis of C3 or direct interaction with microbial surfaces.
101
What enzyme is central to complement amplification?
C3 convertase.
102
What does C3 convertase do?
Cleaves C3 into C3a and C3b, amplifying the complement response.
103
What is the function of C3b?
Acts as an opsonin, tagging microbes for phagocytosis.
104
What components make up the membrane attack complex (MAC)?
C5b, C6, C7, C8, and multiple C9 molecules.
105
What is the function of the MAC?
Forms pores in the target cell membrane, causing cell lysis.
106
What are the main outcomes of complement activation?
Opsonization, inflammation, cytolysis, and clearance of immune complexes.
107
What role does C3b play in opsonization?
Binds to the pathogen surface and enhances phagocytosis by interacting with complement receptors.
108
What is the role of C3a and C5a in inflammation?
They act as anaphylatoxins, causing mast cell degranulation and recruitment of immune cells.
109
What is the result of complement-mediated cytolysis?
Cell lysis via the MAC.
110
How does the complement system assist phagocytosis?
C3b binds microbes, allowing phagocytes to recognize and engulf them via complement receptors.
111
How does the complement system contribute to anaphylaxis?
C3a and C5a cause the release of histamine, promoting vasodilation and increased permeability.
112
How is the complement system down-regulated?
By regulatory proteins like CD59 (MAC inhibitor) and Factor H (prevents C3 convertase formation).
113
What happens if complement regulation fails?
Uncontrolled activation can cause autoimmune diseases like angioedema
114
What are the three pathways for activation of the complement cascade?
The three pathways are the Classical Pathway, the Alternative Pathway, and the Lectin Pathway.
115
What will trigger the activation of each of these pathways?
Classical Pathway: Triggered by antibodies (IgG or IgM) bound to antigens.
Alternative Pathway: Triggered by pathogen surfaces without the need for antibodies.
Lectin Pathway: Triggered by mannose-binding lectin (MBL) binding to carbohydrate residues on pathogens.
116
How does amplification occur?
Amplification occurs via the formation of C3 convertase, which cleaves C3 into C3a and C3b. C3b acts as an opsonin and helps generate more convertases, creating a positive feedback loop.
117
How are the pathways similar?
All three pathways converge at the cleavage of C3 to C3a and C3b and share the same terminal pathway, leading to the formation of the membrane attack complex (MAC).
118
What comprises the membrane attack complex (MAC)?
The MAC is composed of complement proteins C5b, C6, C7, C8, and multiple C9 molecules. It forms a pore in the target cell membrane, causing cell lysis.
C5bC6C7C8 acts as receptor for C9 molecules
119
What are the results of the activation of these pathways?
Opsonization (enhanced phagocytosis by C3b)
Recruitment of inflammatory cells (via C3a and C5a)
Direct lysis of pathogens through MAC.
120
How does the complement system assist in the elimination of microbes by phagocytosis?
Complement proteins like C3b and C4b coat pathogens, (complements receptors CR1,3,4 bind to these) making them recognizable and easier to engulf by phagocytic cells like NK cells and macrophages(opsonization).
121
How does it contribute to the cause of inflammation and anaphylaxis?
C3a , C4a, and C5a act as anaphylatoxins, promoting inflammation by recruiting immune cells (chemotaxis doe neutrophils and granulocytes), increasing vascular permeability (inducing expression of adhesion molecules), and triggering degranulation of mast cells.
122
How is the system down-regulated, and what would happen if this fails?
The complement system is down-regulated by regulatory proteins like Factor H, Factor I, and CD59, which prevent overactivation. Failure of regulation can result in excessive inflammation, tissue damage, or autoimmune diseases.
123
How many types of hypersensitivities are there?
Four types (Type I, II, III, and IV).
124
How are hypersensitivities classified?
Based on the immune mechanism involved:
- Type I: IgE-mediated (immediate)
- Type II: Antibody-mediated (IgG or IgM)
- Type III: Immune complex-mediated
- Type IV: T-cell-mediated (delayed)
125
What is the underlying cause of each type of hypersensitivity?
- Type I: Mast cell degranulation due to allergen-specific IgE binding.
- Type II: Antibodies bind to cell surface antigens, leading to complement activation or cytotoxicity.
- Type III: Immune complexes deposit in tissues, causing inflammation.
- Type IV: Delayed T-cell response, leading to cytokine release and tissue damage.
126
Which type is due to IgE? Why does it manifest so fast?
Type I hypersensitivity. It is fast because pre-formed IgE on mast cells and basophils trigger rapid degranulation upon allergen exposure.
127
Which type is cell-mediated? Why does it take longer to manifest?
Type IV. It requires T-cell activation and cytokine release, which takes hours to days.
128
IgG mediates which types of hypersensitivity?
Type II (cytotoxic) and Type III (immune complex-mediated).
129
What happens when immune complexes fail to clear?
They deposit in tissues, causing inflammation and diseases like systemic lupus erythematosus (SLE) and serum sickness.
130
What is an Arthus reaction?
A localized Type III hypersensitivity reaction caused by immune complex deposition in tissues, leading to inflammation.
131
What causes contact dermatitis?
Type IV hypersensitivity triggered by T-cell activation in response to allergens like poison ivy or nickel.
132
What precipitates serum sickness?
Systemic immune complex deposition (Type III) due to foreign proteins, such as after monoclonal antibody therapy or antiserum injections.
133
What is a granuloma?
A chronic Type IV hypersensitivity reaction where macrophages surround a pathogen, forming a mass of immune cells.
134
Can you name examples for each type of hypersensitivity reaction?
- Type I: Anaphylaxis, asthma, allergic rhinitis.
- Type II: Hemolytic anemia, Myasthenia gravis, Rheumatic fever.
- Type III: Serum sickness, Lupus, Arthus reaction.
- Type IV: Contact dermatitis, Tuberculosis, Type 1 Diabetes.
135
Can you identify the type of hypersensitivity for various diseases?
- Asthma → Type I
- Goodpasture Syndrome → Type II
- Systemic Lupus Erythematosus (SLE) → Type III
- Tuberculosis → Type IV
136
What are the clinical manifestations and molecular events that activate the reactions?
- Type I: Wheezing, rash, hypotension (Histamine and leukotrienes released by mast cells).
- Type II: Hemolysis, organ dysfunction (Antibody binding to cells → Complement activation).
- Type III: Vasculitis, arthritis (Immune complex deposition → Neutrophil activation).
- Type IV: Induration, granulomas (T-cell activation → Cytokine release).
137
What is the principle and application of agglutination assays?
Agglutination involves the clumping of particles (e.g., RBCs or bacteria) due to antigen-antibody interactions. Used for blood typing and bacterial identification.
138
What is the principle and application of precipitation assays?
Precipitation occurs when soluble antigen and antibody form an insoluble complex. Used in immunodiffusion tests like radial immunodiffusion.
139
What is the principle and application of the Ouchterlony assay?
A double diffusion gel technique where antigen and antibody diffuse toward each other to form a precipitin line. Used to identify antigenic relationships.
140
What is the principle and application of immunofluorescence assays?
Uses fluorescent-labeled antibodies to detect specific antigens in tissues or cells. Used in autoimmune disease testing and pathogen detection.
141
What is the principle and application of radioimmunoassay (RIA)?
Uses radiolabeled antibodies or antigens to measure concentrations of substances like hormones. Highly sensitive but requires radioactive handling.
142
What is the principle and application of flow cytometry?
Uses fluorescently labeled antibodies to detect and quantify specific cell populations based on size and granularity. Used for immunophenotyping and cancer diagnosis.
143
What is the principle and application of ELISA?
Enzyme-linked immunosorbent assay detects and quantifies antigens or antibodies using an enzyme-substrate reaction. Used in disease diagnostics (e.g., HIV, COVID-19).
144
What is the principle and application of Western blot?
Proteins are separated by gel electrophoresis, transferred to a membrane, and detected using antibodies. Used to confirm HIV and Lyme disease diagnoses.
145
What is the principle and application of complement fixation or complement inhibition assays?
Measures the presence of antibodies by detecting complement activation. Used in diagnosing infections like syphilis.
146
How would you read and interpret the results of immunological assays?
Interpretation depends on the assay type:
- Agglutination: Presence of clumps indicates a positive reaction.
- Precipitation: A visible line or ring indicates antigen-antibody interaction.
- ELISA: Color change correlates with antigen/antibody concentration.
- Western blot: Bands at specific molecular weights confirm protein presence.
147
What are the three zones of agglutination/precipitation reactions?
1. Prozone: Excess antibody prevents cross-linking.
2. Equivalence Zone: Optimal antigen-antibody ratio leads to maximum precipitation.
3. Postzone: Excess antigen prevents lattice formation.
148
What is a titer, and what does it tell us?
A titer is the highest dilution of a sample where a reaction still occurs. It indicates the concentration of antibodies in a patient’s serum, useful for diagnosing infections and assessing immunity.
149
Which disease has been eradicated by vaccination?
Smallpox.
150
How does vaccination enhance immunity? What is the difference between primary and secondary responses?
Vaccination exposes the immune system to an antigen, generating memory cells for faster response in future exposures. The primary response is slow, with a low antibody concentration, while the secondary response is rapid and strong due to memory cells.
151
What are the methods for making vaccines?
• Live attenuated (weakened pathogen)
• Inactivated (killed pathogen)
• Subunit (specific antigen parts)
• Toxoid (inactivated toxins)
• mRNA (delivers genetic instructions for antigen production)
• Viral vector (harmless virus delivers antigen-producing genes)
152
How are RNA vaccines made, and how do they work?
mRNA vaccines contain genetic instructions for cells to produce an antigen, stimulating an immune response. The mRNA degrades after protein synthesis.
153
What are the advantages and disadvantages of live and acellular (subunit) vaccines?
• Live vaccines: Strong immune response but may cause mild infection and are unsafe for immunocompromised individuals.
• Subunit vaccines: Safer, but require boosters due to weaker immune activation.
154
What is contact immunity (Sabin polio vaccine)?
The live oral polio vaccine can spread to others via fecal-oral transmission, indirectly immunizing unvaccinated individuals.
155
What is herd immunity?
When enough people are vaccinated, disease transmission decreases, protecting those who cannot be vaccinated.
156
What are some side effects of vaccines?
Common side effects include pain at the injection site, fever, fatigue, and mild allergic reactions. Severe allergic reactions are rare.
157
What kind of vaccines should not be given to individuals (especially infants) with known or suspected weakened immune systems?
Live vaccines (e.g., MMR, varicella, oral polio) due to the risk of uncontrolled infection.
158
Which is the only vaccine against a disease that is not contagious?
The tetanus vaccine. Tetanus is caused by a toxin from Clostridium tetani, not person-to-person transmission.
159
Are there non-self molecules recognizable by the immune system on tumors? What self-molecules can cause cancer, and are they recognizable?
Tumor-associated antigens (TAA) and tumor-specific antigens (TSA) can be recognized. Mutated or overexpressed proteins (e.g., HER2 in breast cancer) may contribute to cancer.
160
How does the immune system react to cancer cells? What is immunoediting?
The immune system eliminates or suppresses tumor cells, but some escape by evolving resistance. Immunoediting consists of elimination, equilibrium, and escape phases.
161
What are NK cells, and when are they activated?
Natural Killer (NK) cells detect and destroy abnormal cells without needing prior sensitization. Activated by stress signals or low MHC-I expression.
162
How do NK cells complement cytotoxic T lymphocytes (CTLs)? What is the missing self-model?
NK cells attack cells with low MHC-I, whereas CTLs require MHC-I for antigen recognition. The missing self-model suggests NK cells kill cells lacking MHC-I expression.
163
What immune mechanisms (cells & cytokines) eliminate cancer?
CTLs (CD8+), NK cells, macrophages, IFN-γ, and perforin-granzyme pathways.
164
What can be expected in the tumor microenvironment?
Suppressive cytokines (TGF-β, IL-10), regulatory T cells (Tregs), and hypoxia, all of which support tumor survival.
165
What immune mechanisms are double-edged?
Inflammation can promote cancer (chronic inflammation fuels mutations), while it can also help eliminate tumors.
166
What immune responses (cells & cytokines) help cancer escape elimination?
Tregs, M2 macrophages, IL-10, and TGF-β suppress immune responses, aiding tumor survival.
167
Are anti-tumor antibodies always protective? Why?
No. Some tumor antibodies may form immune complexes that block immune clearance.
168
What are the different forms of cancer immunotherapies? What are their mechanisms?
• Checkpoint inhibitors (block PD-1/PD-L1, CTLA-4)
• CAR-T cells (engineered T cells targeting specific antigens)
• Monoclonal antibodies (target tumor antigens)
• Cytokine therapy (boosts immune activation, e.g., IL-2)
169
What is checkpoint therapy, and what molecules does it block? What is its downside?
Checkpoint inhibitors (e.g., anti-PD-1, anti-CTLA-4) prevent immune suppression but may cause autoimmune reactions.
170
What are signs that suggest an immunodeficiency disorder?
Recurrent infections, poor wound healing, failure to thrive, and opportunistic infections.
171
What susceptibilities are associated with different types of immunodeficiencies?
• B-cell defects: Bacterial infections
• T-cell defects: Viral, fungal, and intracellular bacterial infections
• Complement defects: Encapsulated bacterial infections
172
What tests are used to detect immunodeficiencies?
• Flow cytometry (cell counts)
• Serum immunoglobulin levels
• Complement assays (CH50 test)
• Genetic testing
173
What defects and mutations lead to immunodeficiencies?
• SCID: Defective IL-2 receptor or ADA deficiency
• X-linked agammaglobulinemia: BTK mutation
• Chronic granulomatous disease: Defective NADPH oxidase
174
How are immunodeficiencies treated?
• IVIG (Intravenous Immunoglobulin)
• Antibiotics
• Bone marrow transplant
• Gene therapy
175
Why are immune deficiencies often associated with autoimmunity?
Some defects (e.g., in regulatory T cells) impair tolerance mechanisms, leading to autoimmunity.
