Introduction to Immunology Flashcards
1
Q
What is the speed of response in the innate immune system?
A
Immediate (minutes to hours) upon infection.
2
Q
What type of specificity does the innate immune system have?
A
Recognizes broad pathogen-associated molecular patterns (PAMPs); not highly specific to a single epitope.
3
Q
Does the innate immune system have immunologic memory?
A
No immunologic memory; repeated exposures to the same pathogen do not generally enhance the response.
4
Q
List the primary components of the innate immune system.
A
- 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.
5
Q
What is the main function of the innate immune system?
A
Provides an immediate line of defense; activates and shapes the adaptive immune system.
6
Q
What is the speed of response in the adaptive immune system?
A
Slower on first exposure (days to weeks), but quicker on subsequent exposures.
7
Q
How specific is the adaptive immune system?
A
Highly specific to individual antigens and epitopes.
8
Q
Does the adaptive immune system have immunologic memory?
A
Long-lasting immunologic memory ensures faster and more robust responses on re-exposure.
9
Q
List the primary components of the adaptive immune system.
A
- Cellular components: B and T lymphocytes (Helper T cells, Cytotoxic T cells, Regulatory T cells).
- Humoral components: Antibodies (immunoglobulins).
10
Q
What is the main function of the adaptive immune system?
A
Eliminates or neutralizes specific pathogens, provides long-term protection.
11
Q
Define active immunity.
A
Immunity generated by the individual’s own immune system in response to exposure to an antigen.
12
Q
What mechanisms are involved in active immunity?
A
Involves B-cell and T-cell activation, clonal expansion, and formation of memory cells.
13
Q
What is the duration of active immunity?
A
Often long-lasting (years to lifelong).
14
Q
Give an example of natural active immunity.
A
Infection with a pathogen (e.g., recovery from measles confers immunity).
15
Q
Give an example of artificial active immunity.
A
Vaccination (e.g., administration of an inactivated or attenuated pathogen).
16
Q
Define passive immunity.
A
Immunity conferred by transferring antibodies or immune cells from an immune individual to a non-immune individual.
17
Q
What mechanism is involved in passive immunity?
A
Does not require the recipient’s immune system to mount its own response; relies on exogenous antibodies/cells.
18
Q
What is the duration of passive immunity?
A
Temporary; protection wanes as transferred antibodies degrade (weeks to a few months).
19
Q
Give an example of natural passive immunity.
A
Maternal IgG crossing the placenta or IgA in breast milk.
20
Q
Give an example of artificial passive immunity.
A
Administration of intravenous immunoglobulins (IVIG) or monoclonal antibodies.
21
Q
What occurs during the primary immune response?
A
Occurs upon the first contact with a particular antigen.
22
Q
What is the lag phase in the primary immune response?
A
Longer delay before a detectable immune response (often 5–7 days or more).
23
Q
What is the peak response in the primary immune response?
A
Generally lower magnitude of antibody titer and effector cell function.
24
Q
What is the initial antibody isotype in the primary immune response?
A
IgM, followed by class switching to other isotypes (IgG, IgA, etc.).
25
What occurs during the secondary immune response?
Occurs upon subsequent contacts with the same antigen.
26
What is the lag phase in the secondary immune response?
Much shorter due to presence of memory cells.
27
What is the peak response in the secondary immune response?
Higher and more rapid production of antibodies (often dominated by IgG, especially in serum).
28
What is a key feature of antibodies in the secondary immune response?
Antibodies have undergone affinity maturation, leading to stronger binding and greater efficacy.
29
What clinical relevance does the secondary immune response have?
Underpins the principle of booster vaccinations.
30
Describe the morphology of B lymphocytes.
Small lymphocytes with large nucleus, sparse cytoplasm; have surface immunoglobulin (B-cell receptor).
31
What is the main function of B lymphocytes?
Produce antibodies, present antigen to helper T cells, differentiate into plasma cells (antibody-secreting) and memory B cells.
32
Describe the morphology of T lymphocytes.
Similar to B cells in appearance but with T-cell receptors (TCRs).
33
List the subsets of T lymphocytes.
* 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.
34
Describe the morphology of natural killer (NK) cells.
Larger granular lymphocytes with cytotoxic granules.
35
What is the main function of NK cells?
Kill virus-infected cells and tumor cells without prior sensitization.
36
Describe the morphology of neutrophils.
Granulocytes with multilobed nucleus and abundant cytoplasmic granules.
37
What is the main function of neutrophils?
First responders to acute bacterial infection; phagocytic; release reactive oxygen species and granule enzymes to kill pathogens.
38
Describe the morphology of mast cells.
Tissue-resident cells with abundant granules containing histamine and other mediators.
39
What is the main function of mast cells?
Crucial in allergic reactions (Type I hypersensitivity); degranulation triggered by cross-linking of surface-bound IgE.
40
Describe the morphology of eosinophils.
Bilobed nucleus, cytoplasmic granules containing major basic protein.
41
What is the main function of eosinophils?
Important in parasitic infections and allergic responses; release cytotoxic proteins that damage parasite membranes.
42
Describe the morphology of monocytes.
Large leukocytes in circulation with kidney-shaped nucleus.
43
What is the main function of monocytes?
Differentiate into macrophages or dendritic cells upon entering tissues; phagocytic and cytokine-producing.
44
Describe the morphology of macrophages.
Tissue-resident phagocytes derived from monocytes; have pseudopods and large vacuoles.
45
What is the main function of macrophages?
Phagocytosis and digestion of pathogens, antigen presentation to T cells, release of inflammatory cytokines.
46
Describe the morphology of dendritic cells.
“Stellate” cells with dendritic processes; found in tissues interfacing with the external environment.
47
What is the main function of dendritic cells?
Professional antigen-presenting cells (APCs); capture antigen in periphery and migrate to lymph nodes to activate T cells.
48
What are exogenous antigens?
Antigens that enter the body from outside, such as bacteria, viruses, fungi, allergens, and toxins.
49
What are endogenous antigens?
Antigens generated within cells due to infection or abnormal cellular proteins like tumor antigens.
50
Define autoantigens.
The body’s own molecules that can trigger autoimmunity under certain conditions.
51
What are alloantigens?
Antigens from other members of the same species, such as blood group antigens and transplanted organ antigens.
52
What are xenoantigens?
Antigens from different species, such as pig heart valves in xenotransplantation.
53
Describe the structure of IgG.
Monomer; consists of four subclasses (IgG1–IgG4).
54
What are the properties of IgG?
* Crosses the placenta
* Opsonization
* Complement activation
* Neutralization of toxins/viruses
55
What is the structure of IgM?
Pentamer consisting of 5 monomers linked by a J chain.
56
What properties are associated with IgM?
* First antibody produced during primary response
* Highly efficient in complement activation
* Agglutination
57
Describe the structure of IgA.
Monomer in serum; dimer in secretions linked by J chain and secretory component.
58
What are the properties of IgA?
* Found in mucosal areas (GI tract, respiratory tract)
* Present in breast milk
* Protects mucosal surfaces by neutralizing pathogens
59
What is the structure of IgE?
Monomer.
60
What properties are associated with IgE?
* Binds to mast cells and basophils
* Involved in Type I hypersensitivity
* Defense against parasites
61
What is the structure of IgD?
Monomer.
62
What are the properties of IgD?
Primarily membrane-bound on naive B cells; role in B-cell activation is less well-defined.
63
What is the principle of ELISA?
Detects antigen or antibody via enzyme-labeled secondary antibody and a colorimetric reaction.
64
What are some applications of ELISA?
* Quantification of hormones
* HIV test
* Detection of specific proteins in serum
65
Describe the principle of Western Blot.
Proteins are separated by electrophoresis, transferred to a membrane, and probed with specific antibodies; visualization by enzyme or chemiluminescence.
66
What are some applications of Western Blot?
* Confirmatory test for HIV
* Detection of specific protein expression
67
What is the principle of immunofluorescence?
Fluorescently labeled antibodies bind to specific antigens in tissues or cells and are visualized under a fluorescence microscope.
68
What are some applications of immunofluorescence?
* Autoantibody detection (e.g., in lupus)
* Viral antigen detection
* Research staining
69
Describe the principle of flow cytometry.
Cells are tagged with fluorescent antibodies to cell-surface or intracellular antigens, then passed through a laser beam for analysis of fluorescence.
70
What are some applications of flow cytometry?
* Immunophenotyping (CD4 counts in HIV)
* Identification of abnormal cell populations in leukemia/lymphoma
71
What is the principle of agglutination tests?
Visible clumping occurs when particulate antigen binds to specific antibodies.
72
What are some applications of agglutination tests?
* Blood typing
* Detection of rheumatoid factor
* Identification of bacterial antigens
73
Define monoclonal antibodies (mAbs).
Uniform antibodies derived from a single B-cell clone, each recognizing the same epitope.
74
What are the advantages of monoclonal antibodies?
High specificity and consistent batch-to-batch reactivity.
75
What is a hybridoma?
A cell line produced by the fusion of an antibody-producing B lymphocyte with a myeloma cell.
76
Define fully human antibodies.
Antibodies with both variable and constant regions derived entirely from human immunoglobulin sequences.
77
What are humanized antibodies?
Mostly human antibody framework with complementarity-determining regions (CDRs) from a non-human source.
78
Define chimeric antibodies.
Antibodies where the variable regions are from one species and the constant region from another.
79
What is an application of mAbs in cancer therapy?
Rituximab (anti-CD20) for certain B-cell malignancies.
80
What is an application of mAbs in autoimmune diseases?
Infliximab (anti-TNF-α) for rheumatoid arthritis.
81
How are mAbs used in transplant rejection prevention?
Basiliximab (anti-IL-2 receptor) is used to prevent acute rejection.
82
What is an application of mAbs in infectious diseases?
Palivizumab (anti-RSV F protein) for high-risk infants against respiratory syncytial virus.
83
What are the structural features of Class I MHC?
Consists of a heavy α chain (three domains: α1, α2, α3) non-covalently associated with β2-microglobulin
## Footnote
Class I MHC includes HLA-A, -B, -C in humans.
84
What is the peptide-binding groove formed by in Class I MHC?
Formed by α1 and α2 domains
85
Where is Class I MHC expressed?
All nucleated cells (and platelets)
86
What type of peptides does Class I MHC present?
Endogenous (intracellular) peptides to CD8⁺ T cells
87
What are the structural features of Class II MHC?
Composed of two chains (α and β), each with two domains (α1, α2 and β1, β2)
88
What is the peptide-binding groove formed by in Class II MHC?
Formed by α1 and β1 domains
89
Where is Class II MHC primarily expressed?
Primarily on professional antigen-presenting cells (APCs) like dendritic cells, macrophages, B cells
90
What type of peptides does Class II MHC present?
Exogenous (extracellular) peptides to CD4⁺ T cells
91
What is MHC polymorphism?
Multiple variants (alleles) of each MHC gene in a population
92
What is the result of MHC polymorphism?
Increases the range of peptides that can be presented by the population as a whole; enhances survival against diverse pathogens
93
What is MHC polygeny?
Multiple MHC genes encoding different class I and class II molecules in each individual
94
What is the significance of MHC diversity for immune defense?
High MHC diversity makes it less likely that a single pathogen can evade the entire human population
95
What is the clinical implication of MHC restriction?
T cells generally do not respond to peptide antigens presented by non-self MHC, complicating allograft acceptance
96
What is the peptide origin for Class I MHC?
Intracellular proteins (viral, cytosolic)
97
What is the processing pathway for Class I MHC?
Proteasome degrades proteins → peptides transported into ER via TAP → loaded onto class I
98
What is the typical peptide length for Class I MHC?
Typically 8–10 amino acids in length
99
What is the peptide origin for Class II MHC?
Extracellular proteins taken up via endocytosis
100
What is the processing pathway for Class II MHC?
Antigen is degraded in endosomal/lysosomal compartments; class II is assembled in ER with invariant chain → invariant chain is removed in endosome → peptide loaded
101
What is the typical peptide length for Class II MHC?
Longer (usually 13–25 amino acids)
102
What are T-Cell Receptors (TCRs)?
Heterodimer of α and β chains (or γ and δ in fewer T cells) that recognize peptide bound to MHC
103
What are surface B-cell receptors?
Membrane-bound form of antibodies on B cells
104
What do CD4 and CD8 coreceptors bind?
CD4 binds MHC II, CD8 binds MHC I
105
What are Pattern Recognition Receptors (PRRs)?
Receptors in innate immunity that recognize PAMPs
106
Name a pro-inflammatory cytokine.
IL-1, IL-6, TNF-α
107
Name an anti-inflammatory cytokine.
IL-10, TGF-β
108
What are hematopoietic growth factors?
Cytokines like GM-CSF that influence blood cell production
109
What are Type I interferons?
IFN-α and IFN-β
110
What are the main functions of cytokines?
* Regulate immune cell activation, proliferation, and differentiation
* Mediate inflammation
* Influence hematopoiesis
* Antiviral defense
111
What is pleiotropy in cytokines?
One cytokine can have different effects on different cell types
112
What is redundancy in cytokines?
Different cytokines can exert similar biological effects
113
What does synergy and antagonism mean in cytokines?
Cytokines can work together or counteract each other
114
How can cytokines act?
Can act paracrine, autocrine, or endocrine
115
Where do T-cell precursors originate?
Bone marrow
## Footnote
T-cell precursors migrate to the thymus for development.
116
What are the major stages of T-cell development?
* Double-Negative (DN) Stage
* Double-Positive (DP) Stage
* Single-Positive (SP) Stage
117
Define double-positive thymocytes
Thymocytes that express both CD4 and CD8 co-receptors (CD4⁺CD8⁺)
## Footnote
Occur during the Double-Positive (DP) Stage.
118
Define single-positive thymocytes
Thymocytes that differentiate into either CD4⁺ or CD8⁺ T cells
## Footnote
This differentiation depends on TCR specificity for MHC II or MHC I.
119
What is positive selection in T lymphocyte development?
DP thymocytes that can weakly recognize self-MHC I or II survive
## Footnote
Ensures T cells can interact with self-MHC (MHC restriction).
120
What happens to T cells that do not recognize MHC during positive selection?
Undergo apoptosis
121
What is negative selection in T lymphocyte development?
T cells that strongly bind self-antigen presented on MHC undergo apoptosis
## Footnote
This process removes autoreactive T cells and induces self-tolerance.
122
What is the consequence if highly self-reactive T cells escape deletion?
Autoimmune pathology
123
What is the first step in naive T-cell activation?
Antigen Recognition
## Footnote
Naive T cells bind specific peptide-MHC complexes on APCs via the TCR.
124
What is required for co-stimulation during T-cell activation?
CD28 (on T cell) binding to B7-1/B7-2 (CD80/CD86 on APC)
125
What influences T-cell differentiation during activation?
APC-derived cytokines (e.g., IL-12)
126
What is clonal expansion in T-cell activation?
Activated T cells proliferate and differentiate into effector and memory cells
127
List the cytokines produced by TH1 cells
* IFN-γ
* IL-2
* TNF-β
128
What is the main function of TH1 cells?
Activate macrophages and support cell-mediated immunity against intracellular pathogens
129
What key transcription factor is associated with TH1 cells?
T-bet
130
List the cytokines produced by TH2 cells
* IL-4
* IL-5
* IL-13
131
What is the main function of TH2 cells?
Help B cells produce antibodies, especially IgE
132
What key transcription factor is associated with TH2 cells?
GATA-3
133
List the cytokines produced by TH17 cells
* IL-17
* IL-22
134
What is the main function of TH17 cells?
Recruit neutrophils and combat extracellular bacteria/fungi
135
What key transcription factor is associated with TH17 cells?
RORγt
136
What cytokines do Cytotoxic T Lymphocytes (CTLs) produce?
* IFN-γ (some)
* Perforin
* Granzymes
137
What is the main function of CTLs?
Direct killing of virus-infected cells or tumor cells
138
What marks the Pro-B Cell stage in B-cell development?
Begins rearrangement of immunoglobulin heavy chain; no surface immunoglobulin
139
What is expressed on the surface of Pre-B Cells?
μ heavy chain with surrogate light chain (Pre-BCR)
140
What characterizes Immature B Cells?
Expression of complete IgM on surface
141
What defines Mature (Naive) B Cells?
Co-expression of IgM and IgD on surface
142
What happens to activated B cells after antigen encounter?
Undergo class switching, affinity maturation, and differentiation into plasma or memory B cells
143
What is positive selection in B lymphocyte development?
B cells that successfully rearrange and express functional BCR move to the next stage
144
How is negative selection achieved in B lymphocytes?
Immature B cells that bind self-antigens strongly either undergo apoptosis or receptor editing
145
What do naive T cells require for activation?
APCs presenting antigen on MHC molecules along with co-stimulatory signals
146
What is the role of helper T cells in B cell activation?
Provide signals (CD40L on T cell binds CD40 on B cell) plus cytokines
147
What are T-dependent antigens typically composed of?
Proteins
148
What is the outcome of T-dependent B cell activation?
Isotype switching, affinity maturation, robust memory response
149
What are T-independent antigens often composed of?
Polysaccharides or repeating epitopes
150
What is the mechanism of T-independent B cell activation?
Cross-linking of multiple BCRs leads to direct activation without T-cell help
151
What is the outcome of T-independent B cell activation?
Mainly IgM response, limited immunologic memory
152
What is the mechanism of Type I hypersensitivity?
IgE-mediated mast cell degranulation.
## Footnote
Examples include allergic rhinitis, anaphylaxis, and asthma.
153
List examples of Type I hypersensitivity reactions.
* Allergic rhinitis
* Anaphylaxis
* Asthma
154
What is the mechanism of Type II hypersensitivity?
IgG or IgM antibodies directed against cell-surface or extracellular matrix antigens → complement activation or opsonization.
## Footnote
Examples include hemolytic anemia, Goodpasture’s syndrome, and some forms of myasthenia gravis.
155
List examples of Type II hypersensitivity reactions.
* Hemolytic anemia
* Goodpasture’s syndrome
* Myasthenia gravis (some forms)
156
What is the mechanism of Type III hypersensitivity?
Antigen-antibody (IgG) complexes deposit in tissues → complement activation and inflammation.
## Footnote
Examples include serum sickness, Arthus reaction, and certain forms of vasculitis.
157
List examples of Type III hypersensitivity reactions.
* Serum sickness
* Arthus reaction
* Certain forms of vasculitis
158
What is the mechanism of Type IV hypersensitivity?
T-cell mediated; either CD4⁺ T helper cells (Th1) activate macrophages or CD8⁺ cytotoxic T cells kill target cells.
## Footnote
Examples include contact dermatitis, tuberculin skin test, and type 1 diabetes.
159
List examples of Type IV hypersensitivity reactions.
* Contact dermatitis (e.g., poison ivy)
* Tuberculin skin test
* Type 1 diabetes (β-cell destruction)
160
What genetic factors predispose individuals to allergies?
Atopic individuals have a predisposition leading to higher IgE production and increased Th2 responses.
## Footnote
Polymorphisms in cytokines (IL-4, IL-13) or their receptors can enhance IgE class switching.
161
What environmental factors contribute to increasing allergy prevalence?
* Hygiene Hypothesis
* Exposure to pollutants
* Diet changes
* Antibiotic overuse
162
What does the Hygiene Hypothesis suggest?
Reduced childhood infections may lead to an under-stimulated Th1 response, skewing toward Th2 and atopy.
163
What is the Skin Prick Test (SPT)?
Allergen extracts placed on skin → pricked → wheal-and-flare response indicates sensitization.
164
What are serologic tests used for in allergy identification?
Specific IgE Measurement (e.g., RAST, ImmunoCAP) detects allergen-specific IgE in patient serum.
165
What is the purpose of elimination/challenge testing?
To identify food allergies by removing suspect foods from the diet and then reintroducing under controlled conditions.
166
Define anaphylaxis.
Severe, systemic allergic reaction triggered by widespread mast cell and basophil degranulation.
167
List clinical features of anaphylaxis.
* Hypotension (shock)
* Bronchoconstriction (wheezing)
* Laryngeal edema
* Urticaria
* GI symptoms
168
What is the first-line therapy for anaphylaxis?
Epinephrine (adrenaline) IM injection.
169
What additional treatments may be needed for anaphylaxis?
* Antihistamines
* Corticosteroids
* IV fluids
* Oxygen support as needed
170
What is the action of antihistamines?
Block histamine receptors (e.g., diphenhydramine, cetirizine).
171
What do mast cell stabilizers do?
Prevent degranulation (e.g., cromolyn sodium).
172
What is the action of leukotriene receptor antagonists?
Reduce leukotriene-mediated inflammation (e.g., montelukast).
173
What is the function of corticosteroids in allergy treatment?
Suppress inflammatory gene expression (e.g., prednisone, fluticasone).
174
What do anti-IgE antibodies do?
Bind circulating IgE, preventing its interaction with mast cells/basophils (e.g., omalizumab).
175
What are natural autoantibodies?
Low-affinity, polyreactive antibodies often present at low levels
## Footnote
Natural autoantibodies are typically produced by the immune system and can be found in healthy individuals.
176
What role do autoreactive T cells play in healthy individuals?
Low-level autoreactive T cells can exist but are kept in check by regulatory mechanisms
## Footnote
These regulatory mechanisms prevent autoreactive T cells from causing autoimmune diseases.
177
What is the Fas-FasL mechanism?
Continuous peripheral deletion of self-reactive lymphocytes
## Footnote
This mechanism is crucial for maintaining immune tolerance.
178
What is central tolerance in the immune system?
T cells in the thymus undergo negative selection and B cells in bone marrow undergo clonal deletion or receptor editing
## Footnote
Central tolerance is a critical process to prevent autoimmunity.
179
What is anergy in the context of peripheral tolerance?
Lack of co-stimulatory signals leads to non-responsiveness
## Footnote
Anergy prevents T cells from becoming activated in the presence of self-antigens.
180
How do regulatory T cells maintain tolerance?
They secrete immunosuppressive cytokines (IL-10, TGF-β)
## Footnote
These cytokines help to inhibit immune responses against self-antigens.
181
What is 'ignorance' in the context of immune tolerance?
Self-antigens may be sequestered in immune-privileged sites (brain, eye, testes)
## Footnote
This sequestration helps prevent immune recognition and response.
182
What is molecular mimicry?
Infectious agents share epitopes with self-antigens leading to cross-reactivity
## Footnote
This can trigger an autoimmune response as the immune system mistakenly targets self-tissues.
183
What is epitope spreading?
Tissue damage exposes hidden self-epitopes
## Footnote
This phenomenon can lead to the development of new autoantibodies against previously ignored self-antigens.
184
How do certain MHC alleles contribute to genetic susceptibility in autoimmunity?
Certain MHC alleles predispose individuals to autoimmunity
## Footnote
The association of specific MHC alleles with autoimmune diseases is well established in medical research.
185
What are the genetic factors associated with Type 1 Diabetes (T1D)?
Strong association with certain HLA class II alleles (e.g., HLA-DR3, DR4)
## Footnote
These genetic markers indicate a higher risk for developing T1D.
186
What environmental triggers are associated with Type 1 Diabetes?
Viral infections (e.g., coxsackie virus), gut microbiome factors
## Footnote
These triggers can initiate or exacerbate the autoimmune process in genetically susceptible individuals.
187
What mechanism leads to insulin deficiency in Type 1 Diabetes?
Autoreactive T cells attack pancreatic β-cells
## Footnote
This destruction of β-cells is the primary cause of insulin deficiency in T1D.
188
What genetic factors are predominant in Celiac Disease?
Predominantly HLA-DQ2 or DQ8 haplotypes
## Footnote
These haplotypes are critical for the development of Celiac Disease.
189
What environmental trigger is associated with Celiac Disease?
Dietary gluten (gliadin component)
## Footnote
Exposure to gluten in genetically predisposed individuals can trigger the autoimmune response.
190
What mechanism leads to damage in Celiac Disease?
Immune-mediated damage to small intestinal villi
## Footnote
This damage results in malabsorption and other gastrointestinal symptoms.
191
What genetic factors are associated with Systemic Lupus Erythematosus (SLE)?
Multiple genes (HLA-DR2/DR3); complement deficiencies (C1q, C2, C4)
## Footnote
These genetic predispositions play a significant role in the development of SLE.
192
What environmental factors can exacerbate Systemic Lupus Erythematosus?
UV light, sex hormones (estrogen), infections
## Footnote
These factors can trigger flares in individuals with SLE.
193
What mechanism leads to autoantibody production in SLE?
Loss of tolerance leads to autoantibody production (especially anti-nuclear antibodies) and immune complex deposition
## Footnote
This process is characteristic of SLE and contributes to its pathology.
194
How are immunofluorescence tests used to detect autoantibodies?
Patient serum applied to substrate tissue (e.g., HEp-2 cells), autoantibodies bind, then detected by fluorescently labeled anti-human Ig
## Footnote
This technique is widely used in clinical diagnostics for autoimmune diseases.
195
What is the process of ELISA in detecting autoantibodies?
Antigens coated on a plate → patient serum added → enzyme-labeled anti-human IgG → colorimetric readout
## Footnote
ELISA is a sensitive method for quantifying autoantibodies in serum.
196
What is the definition of primary immunodeficiencies?
Genetic or developmental defects resulting in defective immune function.
## Footnote
Examples include SCID, DiGeorge syndrome, and Bruton's agammaglobulinemia.
197
When does primary immunodeficiency typically onset?
Often in early childhood with recurrent, severe infections.
198
What is the definition of secondary immunodeficiencies?
Result from external factors such as HIV infection, chemotherapy, or malnutrition.
199
When can secondary immunodeficiency occur?
Can occur at any age depending on exposure or underlying disease.
200
What types of infections are T-Cell disorder patients more susceptible to?
Intracellular pathogens, including:
* Viruses
* Fungi
* Opportunistic organisms (e.g., Pneumocystis jirovecii)
* Certain intracellular bacteria (e.g., mycobacteria)
201
What types of infections are B-Cell (Humoral) disorder patients more susceptible to?
Recurrent pyogenic bacterial infections, especially:
* Streptococcus pneumoniae
* Haemophilus influenzae
Also struggle with some viruses that rely on neutralizing antibodies (e.g., enteroviruses).
202
What is the function of CD4⁺ T Cells?
Orchestrate immune responses via cytokine secretion; essential for B-cell antibody production and macrophage activation.
203
What role do CD4⁺ T Cells play in HIV infection?
Main target for HIV binding via gp120; progressive depletion leads to immunodeficiency (AIDS).
204
What is the function of macrophages and dendritic cells?
Antigen presentation, phagocytosis, and immunoregulation.
205
What role do macrophages and dendritic cells play in HIV infection?
Act as reservoirs; HIV can infect these cells via CCR5 co-receptor, allowing for persistent infection and spread.
206
What is the importance of CD4⁺ T-Cell Count in monitoring HIV infection?
Critical for determining degree of immunosuppression and opportunistic infection risk.
207
What does the viral load (HIV RNA PCR) indicate in HIV monitoring?
Level of active viral replication; used to monitor response to antiretroviral therapy (ART).
208
What is included in clinical monitoring of a patient with HIV infection?
Track opportunistic infections, overall health, and medication side effects.
209
What other laboratory tests are important for monitoring HIV patients?
Complete blood counts, liver and renal function tests to monitor ART toxicity or comorbidities.
210
What genetic factors affect the course of HIV infection?
* CCR5∆32 mutation confers resistance or slower disease progression
* HLA types can influence immune response effectiveness.
211
How do co-infections and comorbidities affect HIV infection progression?
Certain infections (e.g., TB, hepatitis) can exacerbate or accelerate progression.
212
What is the impact of immune status and nutrition on HIV infection outcomes?
Malnutrition or other immunocompromising conditions worsen outcomes.
213
How does adherence to ART affect HIV infection progression?
Poor adherence leads to higher viral loads and more rapid disease progression.
214
What are Tumor-Specific Antigens (TSAs)?
Unique to tumor cells (e.g., mutated oncogenes or viral antigens)
## Footnote
TSAs are critical for the immune system to distinguish tumor cells from normal cells.
215
What are Tumor-Associated Antigens (TAAs)?
Overexpressed or re-expressed normal proteins (e.g., prostate-specific antigen)
## Footnote
TAAs can be found in both tumor and normal cells but are typically present at higher levels in tumors.
216
What is one strategy tumors use to evade the immune response?
Reduced MHC Expression
## Footnote
Tumor cells downregulate MHC I to avoid recognition by cytotoxic T lymphocytes (CTLs).
217
What role do immunosuppressive molecules play in tumor evasion?
Secretion of TGF-β and IL-10 to inhibit T-cell function
## Footnote
These cytokines can create a suppressive tumor microenvironment.
218
Name a mechanism by which tumors upregulate immune checkpoints.
Upregulation of PD-L1 or CTLA-4 pathways
## Footnote
This dampens T-cell activity and helps the tumor escape immune detection.
219
What occurs to host oncogenes (proto-oncogenes) leading to cancer?
Mutations or overexpression convert them into oncogenes → uncontrolled cell proliferation
## Footnote
This process is a key step in malignant transformation.
220
How do viral oncogenes contribute to cancer?
Introduce or activate oncogenes or inactivate tumor suppressor genes (e.g., p53, Rb)
## Footnote
Viruses like HPV and EBV play significant roles in oncogenesis.
221
What is the interaction between viral infection and host susceptibility?
Viral infection can initiate or promote oncogenic processes in a genetically susceptible host
## Footnote
This leads to malignant transformation.
222
What are checkpoint inhibitors in cancer immunotherapy?
Antibodies blocking PD-1/PD-L1 or CTLA-4, reactivating T cells against tumors
## Footnote
Examples include nivolumab and pembrolizumab.
223
What is CAR T-Cell Therapy?
Engineering patient T cells with chimeric antigen receptors targeting tumor-specific antigens
## Footnote
An example is targeting CD19 in B-cell malignancies.
224
What is the purpose of cancer vaccines?
Elicit antitumor immunity
## Footnote
They can be prophylactic (e.g., HPV vaccine) or therapeutic.
225
What is the function of monoclonal antibodies in cancer treatment?
Direct tumor targeting or immune modulation
## Footnote
Examples include rituximab and trastuzumab.
226
What is Adoptive Cell Transfer (ACT)?
Expansion of tumor-infiltrating lymphocytes (TILs) ex vivo and re-infusion to the patient
## Footnote
This approach aims to enhance the body's immune response against tumors.
227
What is the mechanism of action of vaccines?
Vaccines introduce antigens that mimic infection, prompting the immune system to generate a protective adaptive response without causing the full-blown disease.
## Footnote
This includes antibody production and the formation of memory B/T cells.
228
What is immunologic memory in the context of vaccination?
Upon real exposure to the pathogen, the immune response is rapid and prevents clinical disease.
## Footnote
This is due to the memory B/T cells created by the vaccine.
229
What are live attenuated vaccines?
Weakened forms of the pathogen that induce robust immunity but can be contraindicated in immunocompromised individuals.
## Footnote
Examples include measles, mumps, rubella, and varicella.
230
What defines inactivated (killed) vaccines?
Pathogens killed by chemicals or heat, generally safer and often requiring boosters.
## Footnote
Examples include inactivated polio and hepatitis A vaccines.
231
What are subunit/conjugate vaccines?
Vaccines that contain only essential antigens, reducing the risk of adverse effects and may require adjuvants.
## Footnote
Examples include hepatitis B surface antigen and pneumococcal conjugate vaccines.
232
What are toxoid vaccines?
Inactivated bacterial toxins that elicit neutralizing antibodies against the toxin.
## Footnote
Examples include tetanus and diphtheria vaccines.
233
What is the function of mRNA vaccines?
They encode antigenic proteins and stimulate robust B- and T-cell responses.
## Footnote
An example is the COVID-19 vaccines.
234
What is the safety profile of live attenuated vaccines?
Risk of reversion to virulence is extremely low but possible; contraindicated in immunosuppression or pregnancy.
## Footnote
Example includes the MMR vaccine.
235
What is the efficacy of live attenuated vaccines?
Induces strong, long-lasting immunity, often with a single dose.
## Footnote
This makes them highly effective.
236
What is the safety profile of inactivated vaccines?
Cannot replicate; minimal risk even in immunocompromised individuals.
## Footnote
Example includes the Inactivated Poliovirus Vaccine (IPV).
237
What is the efficacy of inactivated vaccines?
Often requires multiple doses and boosters; immunity may be less robust compared to live vaccines.
## Footnote
This can make their overall effectiveness lower.
238
What is the safety profile of subunit/conjugate vaccines?
Extremely safe due to containing only specific antigens.
## Footnote
Examples include Hepatitis B and Pneumococcal Conjugate vaccines.
239
What is the efficacy of subunit/conjugate vaccines?
Generally good; immunogenicity can be enhanced by conjugating the antigen to a carrier protein and/or adding adjuvants.
## Footnote
Often require booster doses.
240
What is an autograft?
Transplant from one site to another on the same individual (e.g., skin graft)
## Footnote
Autografts are often used in surgical procedures to promote healing.
241
What is an isograft?
Transplant between genetically identical individuals (e.g., identical twins)
## Footnote
Isografts are less likely to be rejected due to genetic similarity.
242
What is an allograft?
Transplant between different individuals of the same species
## Footnote
Allografts are the most common type of transplant in clinical practice.
243
What is a xenograft?
Transplant between different species (e.g., pig to human)
## Footnote
Xenografts are used in experimental settings and face unique challenges.
244
List some commonly transplanted organs.
* Kidney
* Liver
* Heart
* Lung
* Pancreas
* Cornea
* Bone marrow/stem cells
## Footnote
These organs are frequently required in transplant surgeries due to various diseases.
245
What is hyperacute rejection?
Rejection occurring minutes to hours after transplant due to pre-formed antibodies
## Footnote
This type of rejection is often fatal and occurs very rapidly.
246
What is the timing of acute rejection?
Days to weeks (or months) post-transplant
## Footnote
Acute rejection is a significant concern and requires monitoring.
247
What is chronic rejection?
Rejection occurring months to years post-transplant due to low-level immune response
## Footnote
Chronic rejection leads to gradual organ failure and is difficult to manage.
248
How does stem cell transplantation differ from solid organ transplant?
Stem cell transplant replaces hematopoietic and immune system; solid organ transplant replaces a specific organ
## Footnote
The mechanisms and complications associated with these transplants differ significantly.
249
What major complication is associated with stem cell transplants?
Graft-versus-Host Disease (GVHD)
## Footnote
GVHD occurs when donor T cells attack recipient's tissues.
250
What is the primary concern in solid organ transplants?
Host-versus-Graft Reactions
## Footnote
The recipient's immune system may reject the donor organ.
251
What is one problem that needs to be overcome for xenotransplantation to be safe?
Hyperacute rejection due to pre-existing natural antibodies to animal epitopes
## Footnote
This is a significant barrier to the successful use of xenografts.
252
What are zoonotic infections in the context of xenotransplantation?
Potential cross-species transmission of viruses (e.g., porcine endogenous retroviruses)
## Footnote
These infections pose a public health risk.
253
What physiological challenge must be addressed in xenotransplantation?
Physiological and size mismatch
## Footnote
Transplanted organs must function adequately in a human environment.
254
What ethical concerns are associated with xenotransplantation?
Pathogen control, public health risk, and acceptance
## Footnote
Ethical concerns must be carefully evaluated before proceeding with xenotransplantation.
