Specific Immunity Flashcards

1
Q

Categories of Specific Immunities

A

natural v artificial, passive v active

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2
Q

natural

A

what you find in nature; 250 years and below

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3
Q

artificial

A

what you find in a hospital

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4
Q

passive

A

give someone antibodies

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5
Q

characteristics of passive

A

Works immediately but does not last long and helps immune system (3-6 months)

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6
Q

Natural passive

A

breast milk

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7
Q

artificial passive

A

acquiring antibodies in hospital (immunotherapy)

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8
Q

Colostrum

A

antibodies in breastmilk

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9
Q

active

A

when immune system is stimulated by an antigen

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10
Q

what must you have for active immunity to work

A

Must have immunocompetency

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11
Q

Immunocompetency

A

immune system is healthy; takes longer (2 weeks)

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12
Q

natural active

A

getting sick

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13
Q

artificial active

A

vaccine

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14
Q

human Leukocyte Antigens (HLAs)

A

important in Self-recognition by the immune system and Tissue compatibility (organ donation)

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15
Q

Major Histocompatibility Complexes are a group of (MHCs/HLAs)

A

group of cell surface receptors

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16
Q

3 classes of MHCs

A

MHC class 1,2,3

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17
Q

MHC Class I

A

self recognition

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18
Q

location of MHC Class I

A

surface of virtually all nucleated cells (except red blood cells)

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19
Q

function of MHC Class I

A

determine recognition of “self” molecules and cells.

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20
Q

absence of MHC class I molecules

A

triggering an immune response

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21
Q

MHC Class II

A

Foreign Antigen Presentation

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22
Q

location of MHC Class II

A

surface of macrophages, dendritic cells, and B cells (white blood cells)

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23
Q

function of MHC Class II

A

React with foreign antigens and present them to T cells

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24
Q

MHC Class III

A

Encode secreted complement components

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25
Q

B Cell Lymphocyte Receptors Antigen Binding

A

bind to free floating antigens

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26
Q

B Cell Lymphocyte Receptors structure

A

Y-shaped protein; two heavy chains and two light chains (four polypeptide chains)

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27
Q

Fc Region

A

constant region that binds to B cells and triggers activation.

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28
Q

Gene Regions of Immunoglobulins

A

Heavy chain genes have V, D, J, and C regions; light chain genes have V, J, and C regions

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29
Q

Variability

A

The V and D regions (in heavy chains) are responsible for the vast diversity of antigen-binding sites.

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30
Q

Immunoglobulin mechanism

A

Each B cell randomly selects one gene from each region during development producing only one type of antibody

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31
Q

Constant Region (C)

A

determines the antibody’s class (e.g., IgG, IgM) and its function

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32
Q

T Cell Lymphocyte Receptors binding

A

Bind only to processed antigens

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33
Q

structure T Cell Lymphocyte Receptors

A

Structurally different from B cell receptors

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34
Q

T-Cell Receptors vs. B-Cell Receptors

A

T-cell lymphocyte receptor (TCR) which binds to antigens are secreted, TCRs are smaller than immunoglobulins, TCRs are always membrane bound while immunoglobulins are membrane bound/secreted into blood plasma, TCR one binding site and immunoglobulin 2 binding sites

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35
Q

The Clonal Selection Theory

A

explains how the immune system can recognize millions of different antigens without attacking the body’s own cells

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36
Q

stages of clonal selection theory

A
  1. Proliferative Stage (Fetal Development)
  2. Clonal Deletion Stage (Fetal Development):
  3. Clonal Selection and Expansion Stage (Post-Birth):
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37
Q

Proliferative Stage (Fetal Development)

A

Millions of different B cells are generated during fetal development. Each B cell randomly selects specific V, D, J, and C genes to create a unique immunoglobulin; occurs in fetal bone marrow

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38
Q

Clonal Deletion Stage (Fetal Development)

A

B cells producing antibodies that recognize self-antigens (molecules in fetal tissue) are eliminated through apoptosis (programmed cell death). This process ensures that only B cells recognizing non-self antigens survive.

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39
Q

Clonal Selection and Expansion Stage (Post-Birth)

A

After birth, if a B cell encounters an antigen that its antibody recognizes, it is stimulated to proliferate (clone itself) and produce large quantities of its specific antibody. These antibodies are secreted into the blood plasma to target the foreign antigen.

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40
Q

T cell maturation

A

Produced in the bone marrow, but mature in the thymus. Different types of T cells exist, classified by their CD markers (e.g., CD4 helper T cells, CD8 cytotoxic T cells). Both migrate throughout the body via the bloodstream and lymphatic system.

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41
Q

B cell maturation

A

Produced and mature in the bone marrow, then released into circulation.

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42
Q

Antigens

A

provoke an immune response by binding to antibodies or T-cell receptors

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43
Q

common antigen types

A

Proteins (most common), Lipoproteins, Glycoproteins, Nucleoproteins,
Some polysaccharides

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44
Q

antigen characteristics

A

Smaller antigens are less effective, Larger, more complex antigens are more immunogenic

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45
Q

Epitopes

A

specific regions on an antigen where antibodies bind

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46
Q

antigen types

A

Haptens, Autoantigens, Alloantigens, Superantigens, Allergens

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47
Q

Haptens

A

requires large carrier molecule to stimulate immune response

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48
Q

Autoantigens

A

Antigens from your own body. These are problematic as they trigger autoimmune diseases. They often originate from immune-privileged sites (e.g., eye, thyroid, testes) that are shielded from the immune system during fetal development.

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49
Q

Alloantigens

A

Antigens from other organisms of the same species. These are encountered during organ transplantation.

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50
Q

Superantigens

A

Potent antigens (from bacteria and viruses) that over-activate T cells, leading to excessive cytokine release and potentially causing significant tissue damage, toxic shock syndrome, multi-organ failure, and autoimmune diseases.

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51
Q

Allergens

A

Antigens from non-pathogenic sources (e.g., pollen, pet dander) that trigger allergic reactions.

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52
Q

Antigen-presenting cells (APCs)

A

crucial for initiating an adaptive immune response

53
Q

key APCs

A

Macrophages
Dendritic cells
B cells

54
Q

APC process

A
  1. engulfing 2. processing 3. presentation 4. T cell activation
55
Q

Engulfment

A

APCs engulf antigens through phagocytosis.

56
Q

Processing

A

Antigens are broken down and modified to enhance immunogenicity

57
Q

Presentation

A

Processed antigens are loaded onto Major Histocompatibility Complex (MHC) molecules (MHC class I or MHC class II) and displayed on the APC’s surface

58
Q

T Cell Activation

A

The APC presents the antigen to T cells, specifically helper T cells (via MHC class II and CD4 interaction). The APC searches for the specific helper T cell with a T cell receptor that recognizes the presented antigen.

59
Q

importance of APC process

A

vital for initiating a targeted immune response against specific pathogens; ensures only the appropriate T cells are activated.

60
Q

(APCs) and Helper T Cells

A

Dendritic cells, phagocytosis, Antigen Presentation, Interleukin-12 (IL-12), Interleukin-2 (IL-2)

61
Q

Phagocytosis

A

Dendritic cells engulf the invader, forming a phagosome which fuses with a lysosome (phagolysosome). The invader is destroyed.

62
Q

Antigen Presentation

A

dendritic cell processes foreign molecules and presents them to matching helper t cell

63
Q

Interleukin-12 (IL-12)

A

Once the correct helper T cell is found, the APC releases IL-12, signaling “You’re the one!”

64
Q

Interleukin-2 (IL-2)

A

helper T cell confirms it received the message and will activate the specific immune response

65
Q

Once activated, the helper T cell

A

Divides and Stimulates other cells

66
Q

divides

A

Creating various helper T cell lines, including memory helper T cells (for future infections) and T regulatory cells (which we’ll discuss later).

67
Q

stimulates other cells

A

Including B cells. Helper T cells act as coordinators, directing the immune response.

68
Q

what are b cells primarily activated by

A

helper T cells or free-floating antigens

69
Q

Helper T cell activation

A

primary method of B cell activation. The helper T cell signals the B cell to begin working.

70
Q

Independent B cell activation

A

B cell lymphocytes can float freely and bind to free-floating antigens without needing helper T cell activation.

71
Q

Once activated, B cells:

A

divide, produce plasma b cells, then produce memory b cells

72
Q

b cell activation divide

A

Producing plasma B cells and memory B cells.

73
Q

b cell activation plasma b cells

A

Produce large amounts of antibodies (immunoglobulins) of various types. These cells and their antibodies exist for only a few months.

74
Q

b cell activation memory b cells

A

Divide slowly, producing fewer antibodies. They are crucial for a faster response to future encounters with the same antigen.

75
Q

antibody functions

A

Complement fixation, Opsonization, Neutralization, Agglutination and precipitation

76
Q

Complement fixation

A

Enhances the complement system, leading to more efficient pathogen destruction

77
Q

Opsonization

A

Coats target cells, enhancing phagocytosis.

78
Q

Neutralization

A

Covers viral particles or toxins, preventing them from binding to host cells.

79
Q

Agglutination and precipitation

A

Clumps cells or molecules together, rendering them inactive.

80
Q

Monoclonal Antibodies

A

target particular cells or molecules; used in research, diagnostics (like pregnancy tests), and therapeutics (treating conditions like coronavirus and cancer).

81
Q

T cells are activated by

A

only by antigen-presenting cells

82
Q

CD8+ T cells (Cytotoxic T cells)

A

cells directly kill infected, cancerous, or foreign cells

83
Q

what do CD8+ T cells (Cytotoxic T cells) release

A

perforins and granzymes

84
Q

perforins

A

create holes in target cell membranes

85
Q

granzymes

A

induce apoptosis – programmed cell death

86
Q

CD4+ T cells (Helper T cells)

A

coordinate the immune response by activating other immune cells

87
Q

types of CD4+ T cells (Helper T cells)

A

Th1, Th2, Th17, Tregs

88
Q

Th1

A

Activated by dendritic cells and interleukin-12 (IL-12). Involved in delayed hypersensitivity (e.g., poison ivy reaction)

89
Q

Th2

A

Activated by other interleukins and APCs. Activate B cells and contribute to humoral immunity.

90
Q

Th17

A

Promote inflammation.

91
Q

Tregs

A

Suppress immune responses, preventing autoimmunity and excessive inflammation. They maintain tolerance to self-antigens and commensal microbiota.

92
Q

Natural Killer (NK) cells

A

Lack antigen specificity; part of the innate immune system. Kill infected or cancerous cells.

93
Q

Natural Killer T (NKT) cells

A

Recognize lipid antigens; produce cytokines, granzymes, and perforins.

94
Q

passive immunization

A

Immunotherapy involves providing a patient with pre-formed antibodie

95
Q

immunotherapy antibodies characteristics

A

molecules that cannot replicate; their effectiveness lasts only as long as the molecules remain intact and active in the body—typically a few months. The immediate benefit is their rapid action.

96
Q

types of immunotherapy

A

immune Serum Globulin (ISG), Specific Immune Globulin (SIG), Monoclonal Antibodies, Animal-Derived Antisera

97
Q

Immune Serum Globulin (ISG)

A

support immune-deficient patients or provide antibodies when the body cannot produce them efficiently. It’s effective against various diseases, including measles and Hepatitis A.

98
Q

Specific Immune Globulin (SIG)

A

contains high titers of antibodies specific to that infection; derived from the serum of individuals recovering (convalescent) from a specific infection, such as tetanus, chickenpox, pertussis, or Hepatitis B

99
Q

Monoclonal Antibodies

A

single type of antibody highly specific to a particular infectious disease

100
Q

Animal-Derived Antisera

A

Used when human immunoglobulin is unavailable, particularly for potent toxins like diphtheria, botulinum toxin, and snake or spider venom. These are often derived from horses, which are injected with inactivated toxins to produce antisera. However, these can cause allergic reactions.

101
Q

goal of vaccine

A

teach the immune system to recognize and fight a pathogen without causing the disease itself.

102
Q

Weakened (attenuated) pathogen vaccines

A

Use a live but weakened version of the pathogen.

103
Q

Inactivated pathogen vaccines

A

Use a killed version of the pathogen

104
Q

Subunit, recombinant, polysaccharide, and conjugate vaccines

A

Use specific components of the pathogen (e.g., proteins, sugars) rather than the whole pathogen.

105
Q

three most common vaccine design mechanisms

A

killed/inactivated viruses, live attenuated viruses, and vaccines from microbial parts

106
Q

Killed/Inactivated Viruses

A

use whole pathogens that have been killed in a lab setting, preserving their antigens; Common methods for inactivation include radiation, chemicals, or heat

107
Q

example of killed/inactivated viruses

A

Hepatitis A vaccine, flu shot (inactivated), Salk polio vaccine, rabies vaccine

108
Q

advantages of killed/inactivated viruses

A

No risk of causing the disease,Safe for individuals with compromised immune systems, Doesn’t require special storage conditions

109
Q

disadvantages of killed/inactivated viruses

A

Requires a larger dose or booster shots because the antigens aren’t self-replicating, Growing pathogens in a lab (often requiring BSL-2, BSL-3, or even BSL-4 facilities) can be costly and risky.

110
Q

mechanisms Live Attenuated Viruses

A

weakened, live versions of the pathogen; they are alive but have reduced virulence

111
Q

example of live attenuated viruses

A

MMR vaccine (measles, mumps, rubella), smallpox vaccine (weakened version), Sabin oral polio vaccine, chickenpox vaccine, yellow fever vaccine, nasal flu spray.

112
Q

advantages live attenuated viruses

A

Easy to grow in a lab, requiring less stringent safety measures, usually requires a smaller dose because the attenuated virus can replicate within the body amplifying the immune response,
Can provide longer-lasting immunity.

113
Q

disadvantages live attenuated viruses

A

Potential for transmission to others (though this can also be beneficial for herd immunity).
Risk of causing disease in immunocompromised individuals.
Requires special storage to maintain the viability of the attenuated pathogen.
Risk of reversion to wild-type virulence, especially with single-point mutations.

114
Q

Vaccines from Microbial Parts/subunit vaccine mechanisms

A

use only the antigenic determinants (epitopes) of the pathogen, not the whole pathogen. This requires identifying the specific antigens responsible for triggering an immune response.

115
Q

examples of subunit vaccines

A

HPV vaccine, shingles vaccine, DTaP (diphtheria, tetanus, pertussis) vaccine, Tdap (adult version of DTaP).

116
Q

advantages of subunit vaccine

A

Easy to grow and produce in labs.
Generally don’t require special storage.
Very safe, as they don’t contain any live components of the pathogen.

117
Q

disadvantages of subunit vaccine

A

Requires extensive research to identify the relevant antigens.
May require multiple doses or adjuvants (substances that enhance the immune response) to achieve effective immunity.

118
Q

recombinant vaccines mechanisms

A

use genetically engineered microbes or antigens

119
Q

examples of recombinant vaccines

A

hepatitis B vaccine, mRNA vaccines

120
Q

advantages of recombinant vaccines

A

can be produced in large quantities, highly specific and safe

121
Q

disadvantages of recombinant vaccines

A

requires advanced genetic engineering techniques, can be expensive

122
Q

vaccine administeration

A

injection, nasal spray, oral

123
Q

Adjuvants

A

compounds that enhance immunogenicity by prolonging antigen retention in the bloodstream or tissues

124
Q

common vaccine side effects

A

local and systemic reactions

125
Q

local reactions

A

Redness, swelling, and aching at the injection site (inflammatory response) around 1 day

126
Q

systemic reactions

A

Fever (systemic response to the antigen). This is a desired effect, indicating the immune system is actively responding.

127
Q

rare vaccine side effects

A

Bowel Obstruction, febrile seizures

128
Q
A