Module 8A & 8B - Immune System Flashcards
1
Q
What is homeostasis in the immune system?
A
The process of removing dead cells and renewing tissues to maintain balance in the body.
2
Q
How does the immune system interact with the environment?
A
It recognizes and neutralizes harmful substances from the environment.
3
Q
What are the primary types of pathogens the immune system defends against?
A
Viruses, bacteria, fungi, and parasites.
4
Q
What is the role of neutrophils?
A
They are the first responders to infection and help by engulfing and destroying pathogens (phagocytosis).
5
Q
What is the function of eosinophils?
A
They are involved in allergic reactions and help fight parasitic infections.
6
Q
What do basophils do?
A
They release histamine and other chemicals during allergic and inflammatory responses.
7
Q
What is the function of lymphocytes?
A
They play a crucial role in adaptive immunity, including B cells (antibody production) and T cells (cell-mediated response).
8
Q
How do monocytes contribute to immunity?
A
They differentiate into macrophages and dendritic cells, which help in phagocytosis and antigen presentation.
9
Q
What is the role of macrophages in the immune system?
A
They engulf pathogens and dead cells and help activate adaptive immune responses.
10
Q
What do mast cells do?
A
They release histamine and are involved in allergic reactions and inflammation.
11
Q
What is the function of natural killer (NK) cells?
A
They kill virus-infected and cancerous cells without the need for prior exposure.
12
Q
What are examples of physical barriers in innate immunity?
A
Skin and mucous membranes.
13
Q
What are examples of chemical barriers in innate immunity?
A
Stomach acid, enzymes in tears, and skin oils.
14
Q
How do phagocytes contribute to innate immunity?
A
They engulf and digest pathogens.
15
Q
What triggers the inflammatory response?
A
The release of cytokines, which recruit immune cells to infection sites.
16
Q
Why is the inflammatory response important?
A
It helps isolate and destroy pathogens while initiating tissue repair.
17
Q
How does the adaptive immune system recognize pathogens?
A
Through specific antigens present on the pathogen’s surface.
18
Q
What are the two main types of lymphocytes in adaptive immunity?
A
T cells and B cells.
19
Q
What are the two main types of T cells?
A
Cytotoxic T cells (kill infected cells) and helper T cells (activate other immune cells).
20
Q
What is the function of B cells?
A
They produce antibodies that specifically bind to pathogens.
21
Q
How do memory cells help the immune system?
A
They allow for a faster and stronger response upon re-exposure to the same pathogen.
22
Q
What is the difference between humoral and cell-mediated immunity?
A
Humoral immunity involves antibodies produced by B cells, while cell-mediated immunity involves T cells directly attacking infected cells.
23
Q
What are antibodies?
A
Proteins produced by B cells that specifically bind to antigens to neutralize pathogens.
24
Q
What are the five classes of antibodies?
A
IgG, IgA, IgM, IgE, and IgD.
25
Which antibody is most abundant in the bloodstream?
IgG
26
Which antibody is involved in allergic reactions?
IgE
27
Which antibody is the first to be produced in response to an infection?
IgM
28
What is an autoimmune disease?
A condition where the immune system mistakenly attacks the body’s own cells.
29
Give an example of an autoimmune disease.
Rheumatoid arthritis, lupus, or type 1 diabetes.
30
What is immunodeficiency?
A condition where the immune system is weakened and cannot fight infections effectively.
31
What is an example of an immunodeficiency disorder?
HIV/AIDS.
32
What is hypersensitivity?
An exaggerated immune response to harmless substances, such as in allergies.
33
What happens in an allergic reaction?
The immune system overreacts to allergens, releasing histamine and causing symptoms like swelling, itching, and congestion.
34
How do vaccines work?
They expose the immune system to a harmless form of a pathogen, allowing it to develop memory cells for future protection.
35
What is herd immunity?
When a large portion of a population is immune to a disease, reducing its spread and protecting those who are not immune.
36
What is passive immunity?
Immunity gained from receiving antibodies from another source, such as from mother to baby through breast milk.
37
What is active immunity?
Immunity developed after exposure to a pathogen, either through infection or vaccination.
38
Which immune system responds immediately to infections?
The innate immune system.
39
Which immune system takes longer to respond but provides memory for future exposures?
The adaptive immune system.
40
How does the specificity of the innate and adaptive immune systems differ?
The innate immune system is non-specific, while the adaptive immune system is highly specific to a pathogen’s antigens.
41
Which immune system has memory?
The adaptive immune system.
42
How do the innate and adaptive immune systems work together?
The innate immune system captures and processes pathogens, presenting their antigens to adaptive immune cells to initiate a specific immune response.
43
What is the most abundant white blood cell (WBC) in the human body?
Neutrophils.
44
What is the primary function of neutrophils?
To respond to bacterial and fungal infections by engulfing pathogens (phagocytosis).
45
Which innate immune cell is involved in combating parasitic infections and allergic inflammation?
Eosinophils.
46
Which is the least common type of white blood cell?
Basophils
47
Which phagocytic cells differentiate into macrophages?
Monocytes.
48
What are the functions of macrophages in the immune system?
Engulfing pathogens, presenting antigens to adaptive immune cells, and releasing cytokines to regulate immunity.
49
Where are T lymphocytes (T cells) created and where do they mature?
Created in the bone marrow, mature in the thymus.
50
What are the main types of T cells?
Cytotoxic T cells (CD8+), helper T cells (CD4+), and regulatory T cells.
51
What is the function of cytotoxic T cells (CD8+)?
They directly kill infected or cancerous cells.
52
What do helper T cells (CD4+) do?
They release cytokines to amplify the immune response and assist other immune cells.
53
What are the subtypes of helper T cells?
TH1, TH2, and TH17 cells.
54
What is the role of memory T cells?
They persist in the body and enable a faster response upon re-exposure to the same antigen.
55
What is the function of B cells?
They produce antibodies and contribute to humoral immunity
56
Where do B cells mature?
In the bone marrow.
57
What are plasma cells, and what do they do?
Plasma cells are activated B cells that produce and secrete large amounts of antibodies.
58
What do memory B cells do?
They persist in the body for long-term immunity and provide a faster response upon re-exposure to an antigen.
59
What is an antigen?
A foreign substance that triggers an immune response.
60
What are common sources of antigens?
Pathogens (viruses, bacteria), allergens (pollen, food), and abnormal body cells (cancer cells).
61
What are the five classes of antibodies (immunoglobulins)?
gG, IgA, IgM, IgE, and IgD.
62
Which antibody is the most abundant in the blood?
IgG (~80%).
63
Which antibody is found in bodily secretions like saliva and tears?
IgA
64
Which antibody is the first produced in response to an infection?
IgM
65
Which antibody is associated with allergic reactions?
IgE
66
Which antibody is found on the surface of immature B cells?
IgD
67
What is the function of antigen-presenting cells (APCs)?
They capture microbial antigens and display them to lymphocytes to initiate an immune response.
68
What are the three main types of antigen-presenting cells?
Dendritic cells, macrophages, and B lymphocytes.
69
Which APC is most important for initiating T cell responses?
Dendritic cells.
70
Where are dendritic cells commonly found?
In tissues that have contact with the external environment, such as the skin (Langerhans cells), nasal and oral cavities, lungs, and gastrointestinal tract.
71
What type of antigens do dendritic cells present?
Exogenous antigens from extracellular sources like bacteria.
72
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What type of MHC molecule do APCs use to present antigens to helper T cells?
MHC class II
74
What are the three main classifications of immune system disorders?
Hypersensitivity, autoimmune diseases, and immunodeficiency.
75
What happens when the immune system malfunctions?
It can either overreact, attack the body’s own cells, or become too weak to fight infections.
76
What is hypersensitivity?
An excessive or harmful immune response to an antigen.
77
What are two sources of antigens that can trigger hypersensitivity reactions?
Exogenous (microbes, chemicals, food, pollen, dust, drugs) and endogenous (self-antigens).
78
What is another common name for hypersensitivity reactions caused by exogenous antigens?
Allergies.
79
What is a severe and potentially fatal hypersensitivity reaction?
Anaphylaxis.
80
What happens in a hypersensitivity reaction?
There is an imbalance between immune response activation and control mechanisms, leading to excessive, misdirected, or poorly controlled responses.
81
What are the four types of hypersensitivity reactions?
Type I (Immediate), Type II (Antibody-mediated), Type III (Immune complex-mediated), and Type IV (Cell-mediated).
82
Which hypersensitivity reaction is commonly referred to as allergies?
Type I (Immediate hypersensitivity).
83
How are hypersensitivity reactions categorized?
Based on the mechanism responsible for tissue injury.
84
True or False
Some immune diseases involve more than one type of hypersensitivity reaction.
True
85
What causes autoimmune diseases?
The immune system fails to distinguish self-antigens from foreign antigens.
86
What do autoantibodies do in autoimmune diseases?
They attack the body’s own cells and tissues.
87
What is self-tolerance, and how does its failure lead to autoimmune diseases?
Self-tolerance is the immune system’s ability to avoid attacking the body’s own cells. When this fails, autoimmune diseases develop.
88
What happens in immunodeficiency diseases?
The immune system is weakened or not functioning properly, making the body vulnerable to infections and diseases.
89
What are the two categories of immunodeficiency diseases?
Primary (congenital) and secondary (acquired).
90
What is the difference between primary and secondary immunodeficiency?
Primary immunodeficiency is present at birth due to genetic defects, while secondary immunodeficiency is acquired later due to infections, medications, or other conditions.
91
True or False
Hypersensitivity reactions are when the body’s immune system
causes a deficient response to identified antigens
False
92
True or False
Immunodeficient disorders can be due to a genetic abnormality or due to a viral infection.
True
93
What are other names for Type I hypersensitivity?
IgE hypersensitivity, allergies, immediate hypersensitivity.
94
Why can Type I hypersensitivity be life-threatening?
It can lead to anaphylaxis, a severe systemic allergic reaction.
95
What triggers Type I hypersensitivity reactions?
The binding of an allergen to IgE antibodies on mast cells.
96
Is Type I hypersensitivity a local or systemic reaction?
It is primarily local but can become systemic in severe cases.
97
What is an allergen?
A substance that causes an immune response and sensitization of mast cells.
98
What type of antibody is involved in Type I hypersensitivity?
IgE antibodies.
99
Which immune cells play a major role in Type I hypersensitivity?
Mast cells.
100
What chemical mediator is primarily responsible for allergic symptoms?
Histamine
101
What are the two main steps of Type I hypersensitivity?
Sensitization (first exposure) and re-exposure.
102
What happens during the sensitization step?
An APC presents the allergen to a naïve T helper cell, which differentiates into a TH2 cell, leading to IgE production.
103
What do IgE antibodies do after being produced?
They bind to mast cells, sensitizing them for future exposures.
104
What happens upon re-exposure to the allergen?
The allergen binds to sensitized mast cells, causing them to release chemical mediators.
105
What are the three main types of mediators released by mast cells?
Vasoactive amines, lipid mediators, and cytokines.
106
What is the main vasoactive amine released in Type I hypersensitivity?
Histamine.
107
What are the effects of histamine?
Vasodilation, increased vascular permeability, smooth muscle contraction, and increased mucus secretion.
108
What are the main lipid mediators in Type I hypersensitivity?
Prostaglandins and leukotrienes.
109
What do prostaglandins and leukotrienes cause?
Bronchospasm, increased mucus secretion, and increased vascular permeability.
110
What are the two phases of Type I hypersensitivity?
Immediate response and late-phase response.
111
When does the immediate response occur, and how long does it last?
Begins within 5-30 minutes and subsides in about 60 minutes.
112
What happens during the immediate response?
Vasodilation, increased vascular permeability, and smooth muscle contraction.
113
When does the late-phase response occur, and what does it cause?
Occurs 2-24 hours later and leads to inflammation and tissue damage.
114
Which immune cells are involved in the late-phase response?
Eosinophils and basophils.
115
What are common symptoms of Type I hypersensitivity?
Urticaria (hives), allergic rhinitis, allergic conjunctivitis, allergic asthma, and pruritus (itching).
116
What medications are used to treat Type I hypersensitivity?
Antihistamines (block histamine effects) and corticosteroids (reduce inflammation).
117
What is anaphylaxis?
A severe and systemic Type I hypersensitivity reaction.
118
What are common triggers for anaphylaxis?
Bee stings, food allergies, drug allergies.
119
Why does anaphylaxis cause a dangerous drop in blood pressure?
Massive vasodilation and increased vascular permeability lead to fluid loss from circulation.
120
What are the key symptoms of anaphylaxis?
Airway constriction, excessive mucus secretion, swelling (hives), low blood pressure, tachycardia, abdominal pain, vomiting, and diarrhea.
121
What is the immediate treatment for anaphylaxis?
Epinephrine (EpiPen).
122
Why must individuals with anaphylaxis seek medical attention even after using an EpiPen?
Symptoms may initially improve but can return in a second wave.
123
All of the options must occur for type 1 hypersensitivity reactions,
except?
• A) APCs must present antigen to T helper cells
• B) IgM antigens must bind to mast cells
• C) A person must have prior exposure to the antigen
• D) Mast cells must release histamine
B) IgM antigens must bind to mast cells
124
All the options are true regarding type 1 hypersensitivity reactions, except?
• A) Urticaria is a possible outcome
• B) Corticosteroids are a treatment option
• C) A complication of anaphylaxis is high blood pressure
• D) The majority of symptoms are a result of a massive secretion of histamine
C) A complication of anaphylaxis is high blood pressure
125
What are other names for Type II hypersensitivity?
Antibody-mediated hypersensitivity, cytotoxic hypersensitivity.
126
What antibodies are involved in Type II hypersensitivity?
IgG antibodies.
127
What do IgG antibodies bind to in Type II hypersensitivity?
Intrinsic (self) antigens or extrinsic (exogenous) antigens.
128
What happens when antibodies bind to these antigens?
It triggers immune system mechanisms that lead to cell damage and destruction.
129
What are the three main outcomes of Type II hypersensitivity?
Activation of the complement system, opsonization and phagocytosis, and interference with normal cellular functions.
130
Which of these outcomes are cytotoxic?
Opsonization and phagocytosis, complement activation, and antibody-dependent cell-mediated cytotoxicity (ADCC).
131
What does “cytotoxic” mean in this context?
It means the immune response leads to cell death.
132
Which mechanism of Type II hypersensitivity is non-cytotoxic?
Antibody-mediated cellular dysfunction.
133
What are the four mechanisms of Type II hypersensitivity?
Opsonization and phagocytosis, complement system activation, antibody-dependent cell-mediated cytotoxicity (ADCC), and antibody-mediated cellular dysfunction.
134
What happens in opsonization and phagocytosis?
Antibodies or C3b complement proteins mark a cell for destruction by phagocytosis.
135
How does the complement system contribute to Type II hypersensitivity?
It leads to inflammation, opsonization, and the formation of the membrane attack complex (MAC), which lyses cells.
136
What happens in antibody-dependent cell-mediated cytotoxicity (ADCC)?
Natural killer (NK) cells recognize antibody-coated cells and destroy them.
137
How does antibody-mediated cellular dysfunction differ from the other mechanisms?
It does not kill cells but instead disrupts their function by blocking or activating receptors.
138
What are some diseases associated with Type II hypersensitivity?
Autoimmune hemolytic anemia, Myasthenia gravis, Graves’ disease, Pernicious anemia, Vasculitis, Acute rheumatic fever, Goodpasture syndrome.
139
What happens in Myasthenia Gravis?
Antibodies block acetylcholine receptors at the neuromuscular junction, leading to muscle weakness.
140
What happens in Graves’ Disease?
Antibodies activate thyroid-stimulating hormone (TSH) receptors, leading to overproduction of thyroid hormones (hyperthyroidism).
141
What causes Autoimmune Hemolytic Anemia?
Antibodies target red blood cells, leading to their destruction and anemia.
142
What is Goodpasture Syndrome?
Antibodies attack the basement membrane in the kidneys and lungs, causing damage.
143
What option is TRUE regarding type II hypersensitivity reactions?
• A) It only involves self antigens
• B) It can lead to opsonization
• C) All the outcomes lead to cytotoxic processes
• D) All the options are tru
B) It can lead to opsonization
144
All of the options are true regarding type II hypersensitivity
reactions reactions, except?
• A) Cell lysis is a possible outcome
• B) Overactivation of a cellular receptor is a possible outcome
• C) All outcomes lead to cellular death
• D) Can lead to the formation of MAC
C) All outcomes lead to cellular death
145
What is another name for Type III hypersensitivity?
Immune Complex–Mediated Hypersensitivity.
146
What causes Type III hypersensitivity?
Antigen-antibody complexes (immune complexes) form in circulation and deposit in tissues, leading to complement activation and inflammation.
147
How is Type III hypersensitivity different from Type II hypersensitivity?
Type II involves antibodies binding to cell-surface antigens, while Type III involves immune complexes made of antibodies and soluble antigens in circulation that get deposited in tissues.
148
What are the main sites affected by Type III hypersensitivity?
Kidneys (glomerulonephritis), joints (arthritis), and small blood vessels (vasculitis).
149
Why do immune complexes tend to deposit in these areas?
These are areas where blood is filtered at high pressure, making them vulnerable to immune complex deposition.
150
What are the three steps/phases of Type III hypersensitivity?
Formation of immune complexes, deposition of immune complexes, and inflammatory response/tissue injury.
151
What happens in Step 1 (Formation of Immune Complexes)?
An antigen triggers an immune response, and antibodies bind to the antigen in circulation, forming antigen-antibody (immune) complexes.
152
What happens in Step 2 (Deposition of Immune Complexes)?
These immune complexes circulate and deposit in tissues, especially in organs where blood is filtered at high pressure (e.g., kidneys, joints, blood vessels).
153
What happens in Step 3 (Inflammation and Tissue Injury)?
The deposited immune complexes activate the complement system, leading to acute inflammation and tissue damage
154
What happens when immune complexes deposit in blood vessels?
It causes vasculitis
155
What happens when immune complexes deposit in the kidneys?
It causes glomerulonephritis (nephritis).
156
What happens when immune complexes deposit in joints?
It causes arthritis.
157
What are common diseases associated with Type III hypersensitivity?
Systemic lupus erythematosus (SLE), reactive arthritis, Arthus reaction, nephritis (glomerulonephritis), vasculitis.
158
What is true of type III hypersensitivity reactions?
• A) Involves antibodies binding to both cellular and soluble antigens
• B) When the antibody-antigen complexes are deposited, they activate the complement system
• C) A common location for the antibody-antigen complexes to be deposited is the heart
• D) None of the options are true
B) When the antibody-antigen complexes are deposited, they activate the complement system
159
All of the following options are common locations for the antibody-antigen
complexes to be deposited associated with type III hypersensitivity reactions, except?
• A) Kidney
• B) Liver
• C) Joint
• D) Small blood vessels
B) Liver
160
The difference between type II and type III hypersensitivity reactions is that type III
only binds to soluble antigens and type II only binds to cellular antigens?
• A) True
• B) False
A) True
161
What are other names for Type IV hypersensitivity?
• T cell-mediated hypersensitivity
• Delayed-type hypersensitivity (DTH)
162
163
How is Type IV hypersensitivity different from other hypersensitivity reactions?
• It is not antibody-mediated but cell-mediated (involves T lymphocytes instead of antibodies).
164
What immune cells are involved in Type IV hypersensitivity reactions?
• CD4+ T cells (Helper T Cells) → Release cytokines, causing inflammation.
• CD8+ T cells (Cytotoxic T Cells) → Directly kill target cells.
165
What are the two mechanisms of Type IV hypersensitivity?
• Cytokine-Mediated Inflammation (involves CD4+ T cells).
• Direct Cell Cytotoxicity (involves CD8+ T cells).
166
How does cytokine-mediated inflammation occur?
• APCs present antigens to CD4+ T cells, which differentiate into TH1 and TH17 effector cells.
• These cells release cytokines, leading to:
• Recruitment of macrophages.
• Activation of inflammatory mediators.
• Tissue damage due to chronic inflammation.
167
What are examples of cytokine-mediated inflammation?
• Delayed-Type Hypersensitivity (DTH) (e.g., tuberculin skin test).
• Contact Dermatitis (e.g., poison ivy).
168
Why is it called “Delayed-Type” Hypersensitivity?
• Because the response takes 24-48 hours to develop after exposure.
169
What happens in direct cell cytotoxicity?
• CD8+ T cells (Cytotoxic T Lymphocytes - CTLs) recognize infected or abnormal cells.
• CTLs directly kill the target cells by releasing:
• Perforins → Punch holes in the cell membrane.
• Granzymes → Trigger apoptosis (cell death).
170
What are examples of direct cell cytotoxicity?
• Viral infections (e.g., hepatitis).
• Graft rejection (transplant rejection).
171
What option is TRUE regarding cytokine–mediated inflammation reaction?
• A) Antibodies activate CD4+ cells
• B) There is recruitment of macrophages
• C) Cells are directly destroyed
• D) There is recruitment of neutrophils
B) There is recruitment of macrophages
172
All of the options are true regarding type IV hypersensitivity reactions, except?
• A) Activation of cytotoxic T cells leads to cellular death via perforins
• B) Macrophages release pro-inflammatory chemical mediators with cytokine-mediated
inflammation
• C) Both versions utilize antibodies to destroy foreign antigens in the body
• D) The reason there can be delayed type hypersensitivity is due to the time it takes for
leukocytes to be recruited and activated
C) Both versions utilize antibodies to destroy foreign antigens in the body
173
Negative selection occurs with peripheral tolerance?
• A) True
• B) False
B) False
174
A viral infection could be a variable that leads to the development
of an autoimmune disorder?
• A) True
• B) False
A) True
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