Week 3 - Immunology Flashcards

1
Q

Who is Robert Koch?

A

1st person to identify microbes as causing disease

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2
Q

Koch’s Postulates

(used in disease identification)

A
  1. Pathogen must be found in every host + ever case
  2. Same pathogen must be isolated from the host and grown in pure culture
  3. When placed in a healthy host, that pathogen must cause the same disease
  4. When the pathogen is isolated from the new host, it has to be proven to be the original pathogen
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3
Q

Endemic Disease

A

normally found within the population

ex. common cold

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4
Q

Epidemic Disease

A

many people acquire disease over a short period of time

ex. COVID

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5
Q

Antibiotics

A

chemical subtances derived from mold or bacteria that cure infections
-pathogen causing disease must be bacterial in order for antibiotics to work

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6
Q

Immunity

A

the ability of a body to resist or eliminate potentially harmful, foreign materials or abnormal cells

immune system plays a key role in this

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7
Q

How does the immune system play a key role in immunity?

A

-defends against invading pathogens
-removes worn out cells
-identifies and destroys abnormal cells

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8
Q

Inappropriate immune responses lead to:

A

allergies + autoimmune diseases

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9
Q

Primary pathogens that activate the immune system:

A

-bacteria
-viruses: 94% of febrile illnesses; noncellular

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10
Q

Leukocytes

A

immune system effectors arising from stem cells in bone marrow
-neutrophils
-eosinophils
-basophils
-monocytes
-lymphocytes

(all destroy bacteria by phagocytosis)

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11
Q

Neutrophils

Leukocytes

A

highly mobile phagocytes engulf/destroy unwanted cells

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12
Q

Eosinophils

Leukocytes

A

secrete chemicals to fight parasites; also involved in allergic reactions

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13
Q

Basophils

Leukocytes

A

release histamine and heparin; also involved in allergic reactions

similar to mast cells

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14
Q

Monocytes

Leukocytes

A

are transformed into macrophages; tissue bound, phagocytic

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15
Q

B Lymphocytes

Adaptive Immunity

A

antibody-mediated immunity (adaptive)
-differentiate into plasma cells (stimulated by antigens to produce antibodies) + memory cells (lay dormant to prevent future infections)

stored/processed in bone marrow

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16
Q

Memory Cells

(B Lymphocytes)

Adaptive Immunity

A

lay dormant to prevent future infections

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17
Q

Plasma Cells

(B Lymphocytes)

Adaptive Immunity

A

stimulated by antigens to produce antibodies

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18
Q

T Lymphocytes

Adaptive Immunity

A

cell mediated immunity (adaptive)
-maintained by Thymosin
-antigen induces immune response against itself
-do not secrete antibodies; directly bind to target
-clonal/antigen specific
-slow response time
-two types: Cytotoxic + Helper

stored/processed in Thymus

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19
Q

Sites of Lymphoid Tissues

store, produce + process lymphocytes

A

-bone marrow (B lymphocytes)
-Thymus (T lymphocytes)
-lymph nodes
-spleen
-tonsils
-adenoids
-appendix
-Peyer’s patches (digestive tract)

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20
Q

Pathogens that enter the immune system are filtered by:

A

lymph nodes

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21
Q

What serve as macrophages within the lymph nodes?

A

lymphocytes

(spleen performs a similar role in the blood)

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22
Q

Innate (non-specific) Immunity Characteristics

Innate Immunity

A

1st line of defense from foreign pathogen
-cannot recognize a specific pathogen (non-selectively defends)
-natural killer cells, neutrophils, macrophages, dendritic cells, mast cells, basophils, eosinophils
-binds to pathogenic markers
-rapid but limited
-works immediately upon exposure to threatening agent
-respond to phagocytic cells by TLRs (toll-like receptors) - generic traits

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23
Q

4 Innate Immunity Defenses

Innate Immunity

A
  1. Interferon
  2. Natural T killer cells
  3. Complement system
  4. Inflammation
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24
Q

What is Inflammation?

Innate Immunity

A

non-specific response to tissue injury
-goal: bring phagocytes & plasma proteins to invaded or injured area

(same no matter what triggering event)

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25
Characteristics of Inflammation ## Footnote Innate Immunity
-defense by macrophages -redness -swelling -interstitial clots -immigration of leukocytes -pus -heat
26
**Inflammation**: Process ## Footnote Innate Immunity
-Resident **macrophages defend** against bacteria (hour 1) -**Arterioles dilate** (redness) -Histamine is released to **increase capillary permeability** (swelling) -**Plasma proteins leave blood** to enter inflamed area - leakage of plasma and fluid (edema) -**Fibrin walls off the area** from surrounding tissues (interstitial clots) -Neutrophils or monocytes emigrate from blood to area (adhere by **margination**, enter space by **diapedesis**, guided by **chemotaxis**) -Within a few hours, **leukocytes proliferate** (pus) -Increase in neutrophils 4/5x than normal -**Opsonins mark bacteria** for destruction -Antibody binds to foreign cells to make more susceptible to phagocytosis -> complement system activated -Inflammatory process repairs tissue
27
Phagocyte Secreted Chemicals | (Inflammation) ## Footnote Innate Immunity
-**Nitric Oxide** (macrophages) -**Lactoferrin** (neutrophils) -**Histamine** (increase capillary permeability) -**Kinins** (from kininogens) -**Endogenous pyrogen** (fever development) -**Leukocyte Endogenous Mediator** (decreases plasma iron) -**Acute phase proteins** (liver)
28
Margination | (Inflammation) ## Footnote Innate Immunity
neutrphils/monocytes adhere to surface of capillaries
29
Diapedesis | (Inflammation) ## Footnote Innate Immunity
neutrophils enter interstitial space
30
Chemotaxis | (Inflammation) ## Footnote Innate Immunity
Neutrophils are guided to area in need
31
Opsonins | (Inflammation) ## Footnote Innate Immunity
mark bacteria for destruction | (activated proteins of complement system)
32
Where does scar tissue form? | (Inflammation) ## Footnote Innate Immunity
non-regenerative tissues (ex. nerve + muscle)
33
Drugs that suppress inflammatory process: ## Footnote Innate Immunity
-**NSAIDS** (aspirin - inhibits histamine release; ibuprofen) -**Glucocorticoids** (suppress all aspects to resist infection) -**Infliximab (Remicade)/Humira** (autoimmune diseases) -**Chemotherapy** (methotrexate, azathioprine, 6-mercaptourine) -> decreases WBCs -**Interferon** (inhibits multiplication of viruses)
34
Interferon ## Footnote Innate Immunity
**triggers production of virus blocking enzymes** -enzymes inactive unless attacked by virus -released nonspecifically from any cell when virus attacks -induces immunity to many viruses -warns other cells of viral attack -slows cell division -anticancer effects
35
Natural Killer Cells ## Footnote Innate Immunity
**naturally occuring lymphocyte cells** -lyse membranes -1st line of defense against cancer -destory cancer and virus infected cells -provide an immediate non-specific defense -release chemicals to destroy target cells
36
Complement System ## Footnote Innate Immunity
**non-specific response consisting of plasma proteins produced by the liver** -activated by exposure to carbohydrate chains (identification markers) on microbial surface + antibodies produced by foreign invaders -cascade (C1-C4) reinforces general inflammatory tactics | (forms membrane attack complex C5-C9 to form holes in victim cells)
37
Membrane Attack Complex | (MAC) ## Footnote Innate Immunity
-C5 starts the membrane attack complex -forms pore in membrane of the invader -foreign particle is recognized by antibody -complex attaches to foreign body & causes lysis -formed by C5-C9 | occurs towards the outer end of complement cascade
38
**Membrane Attack Complex**: Process | (MAC) ## Footnote Innate Immunity
1. Antibody molecules attach to the antigens on the pathogen's membrane 2. Complement proteins link two antibody molecules 3. Activated complement proteins attach to the pathogen's membrane in step by step sequence, forming membrane attack complex (MAC) 4. MAC pores in the membrane cause lysis
39
**Membrane Attack Complex**: C5-C9 | (MAC) ## Footnote Innate Immunity
1. C5 binds with C6 and C7 2. C567 complex binds to membrane via C7 3. C8 binds to complex and inserts into cell membrane 4. C9 molecules bind to complex and polymerize 5. 1-16 molecules of C9 bind to form a pore in the membrane
40
Adaptive (Specific) Immunity ## Footnote Adaptive Immunity
**2nd line of defense** **-learn from exposure (ex. vaccine or familiar pathogen)** -fast and strong but takes more time (prepares for attack) -**two types**: cell mediated and antibody mediated (humoral)
41
Antibody Mediated (Humoral) Immunity ## Footnote Adaptive Immunity
production of antibodies by B-Lymphocytes -> plasma cells -> antibodies
42
Cell Mediated Immunity ## Footnote Adaptive Immunity
production of T-Lymphocytes to directly attack unwanted cells
43
What allows T + B cells to recognize invaders? | (distinguish between antigenic and normal cells) ## Footnote Adaptive Immunity
**Ag (antigen ) presence** -surface receptors for binding with one possible type of antigen
44
Recognition of an antigen stimulates... ## Footnote Adaptive Immunity
B cells to convert to plasma cells, then into antibodies
45
All antibodies eventually enter where?
blood or lymph
46
What are antibodies? | (Ab) ## Footnote Adaptive Immunity
**immunoglobulins** -globular proteins found in blood serum (Ig) -"arms" attach to antigens by agglutination -amplify immune response to promote antigen destruction -mark and identify foreign material for destruction -activate MAC (membrane attack complex)
47
Types of Antibodies | (G. A. M. E. D) ## Footnote Adaptive Immunity
-IgG -IgA -IgM -IgE -IgD
48
IgM | (Antibody) ## Footnote Adaptive immunity
B cell surface receptor for antigen attachment
49
IgG | (Antibody) ## Footnote Adaptive Immunity
most abundant | produced in large amounts
50
IgE | (Antibody) ## Footnote Adaptive Immunity
protection against parasitic worms/allergies
51
IgA | (Antibody) ## Footnote Adaptive Immunity
found in G.I., G.U., respiratory secretions
52
IgD | (Antibody) ## Footnote Adaptive Immunity
uncertain function; found on many B cell surfaces
53
Toll-Like Receptors (TLRs) ## Footnote Adaptive + Innate Immunity
**act as a bridge between adaptive and innate immunity by mediating activation of pathogen specific T Lymphocytes** -activate signaling pathways, inducing overlap of inflammation | dual functioning
54
**TLRs**: role in adaptive immunity
recognize generic traits of all microbes
55
**TLRs**: role in innate immunity
**TLRs recognize pathogens + generate an immediate defense by producing pro-inflammatory cytokines** (destroy or limit invading pathogens)
56
**Antibody**: Composition | (tail + arms) ## Footnote Adaptive Immunity
**composed of 5 interlinked polypeptide chains** -2 long chains -2 short chains -arranged in "Y" shape -**tail** = classification region (determine function) + binding sites for mediators -**arms** = determine specificity of antibody with antigen binding sites present (unique)
57
Antibody attachment to antigen identifies foreign material for destruction, leading to:
cascade leads to formation of membrane attack complex | by phagocytosis + stimulation of killer cells
58
Polyclonal Antibodies
mixed antibody group, each bind to a separate epitope | usually made within our bodies
59
Monoclonal Antibodies
recognizes and binds to only **one** epitope of an antigen | commonly made in lab using mice or cell cultures
60
Immune Complex Disease ## Footnote Acitivation of Complement System
**overzealous antigen-antibody response causes damage to normal and invading foreign cell** -occasionally exaggerated response -> tissue damage -bacterial, viral or parasitic infections -damage to kidneys, joints, brain (ex. Glomerulonephritis following strep infection or Rheumatoid Arthritis) | (Ag-Ab-Complexes)
61
**Differentiation of B Cells**: Plasma Cells
**produce and secrete IgG antibodies (Ab) and each antibody combines with antigen (Ag) marking it for destruction** -Ab response delayed during initial contact with Ag (plasma cells formed during delay) -**peak** = a couple weeks after primary response when Ab concentration decreases
62
**Differentiation of B Cells**: Memory Cells
**small percentage of B lymphocytes that become a specific cell** - remain dormant and expand a specific clone -secondary response is faster, more potent and longer lasting -**re-exposed to same antigen** = memory cells ready for immune response (adaptive immunity) | can be induced by a disease or vaccine
63
Active v. Passive Immunity
**active**: results from exposure to Ag (antigen) **passive**: from transfer of preformed Ab (antibodies) - ex. from mother to fetus (borrowed immunity)
64
Blood Groups are named by....
the presence of antigens on the surface of erythrocytes | (type of passive immunity)
65
Blood Type A
A antigen, B antibody | (anti-B antibody)
66
Blood Type B
B antigen, A antibody | (anti-A antibody)
67
Blood Type AB
A + B antigens, No antibodies | universal recipient / no antibodies
68
Blood Type O
No antigens, anti-A and anti-B antibodies | universal donor
69
Agglutination | (Transfusion Reaction)
**If Ag of the donor and Ab of recipient match by letter, the donated RBCs can agglutinate in recipient's blood** -cells burst | result of transfusion reaction
70
RH +
individual with RH factor | 85% of population
71
RH -
**individual without RH factor** -produce anti-RH antibodies when first exposed to RH factor -mother receives Rho-gam if pregnant and RH -
72
Erythroblastosis Fetalis
**mother's blood exchanges with 1st fetus during childbirth, producing anti-RH antibodies** -affects second pregnancy/childbirth -results in ischemia + agglutination | (hemolytic disease of the newborn - HDN)
73
Antigen | (Ag)
**foreign proteins that initiate the immune response** -found on: viruses, bacteria, parasitic worms, fungi, etc.
74
Surface Cell Proteins ## Footnote Lymphocytes
**present on all cells, ex. bacteria, fungi, yeast** -cell to cell recognition -facilitated diffusion -active transport
75
Major Histocompatability Complex (MHC) ## Footnote Lymphocytes
**cell surface molecules that bind to peptide fragments derived from pathogens + display them on cell surface for recognition by appropriate T cells** -no two people will have the same type of MHC glycoproteins on cell surface -> rejection after organ transplant -mature lymphocytes bear receptors specific to different MHC (undergo apoptosis to keep the body safe from its own defense mechanism) | human leukocyte antigens controlling major part of immune system
76
MHC: Class 1 Glycoproteins | (Human Leukocyte Antigens) ## Footnote Lymphocytes
**found on all nucleated cells; non-professional antigen presenting cells** -help **Cytotoxic T Cells** respond to foreign antigens | genes found on Chromosome 6
77
MHC: Class 2 Glycoproteins | (Human Leukocyte Antigens) ## Footnote Lymphocytes
**found on macrophages, B + T cells; professional antigen presenting** -recognized by **Helper T cells** & are confined to surfaces of special types of immune cells -make up the interior of Thymus | genes found on Chromosome 6
78
MHC Molecule Function
**present antigens that cells may be housing due to an infection or intrusion by foreign tissues to T cells** -plasma membrane glycoproteins that block T cell binding
79
Epitopes ## Footnote Lymphocytes
specific shape/size/sub-shape on an antigen (Ag) | antibodies recognize epitopes for antigen binding
80
Lymphocytes only respond to antigens presented to them by: ## Footnote Lymphocytes
**ANTIGEN PRESENTING CELLS** -**Macrophages**: cluster around B cell clone; each bind to MHC molecule; engulfs microbe into antigenic peptides; MHC transports bound antigen to cell surface -**Phagocytosis**: process and present antigen & expose on macrophage surface
81
Interleukin Secretion ## Footnote Lymphocytes
**secreted by antigen presenting cells (macrophages + dendritic cells)** -chemical mediator enhances the differentiation + proliferation of the now activated B cell clone
82
Antigen Presenting Cells
Dendritic Cells + Macrophages
83
Cytotoxic T Cells ## Footnote Cell Mediated Immune Response
**secrete chemicals (perforin) to destroy targets before virus can enter the nucelus and replicate** -bind to foreign antigens only, not MHC self-antigens (protection from self immune attack) -respond in association with **Class 1 MHC glycoproteins** when combined with foreign peptide -protect against virus-induced cancer | create Memory T Cells
84
Helper T Cells
**secrete chemicals that amplify the activity of other immune cells w/ cytokines** -recognize **MHC Class 2 glycoproteins** -release Cytokines | create Memory Helper T Cells
85
Cytokines
**chemicals secreted by Helper T Cells that message other immune cells to ward off invaders** -B cell growth factor -interleukin 2 -chemotaxins -macrophage-migration inhibition factor | amplify or reduce the activity of other immune cells
86
Primary v. Secondary Immune Response
-**Primary**: B or T cells activate 1st time + produce memory cells -**Secondary**: same antigen encountered again; memory cells produce a faster response and long lasting
87
Immune System is regulated by Endocrine + Nervous Systems by...
negative feedback loops | ex. cortisol mobilizes storage of metabolic fuel
88
Cancer Cells
have counter productive blocking antibodies that interfere with T Cell function
89
Immune System Tolerance
**preventing the immune system from attacking its own tissues** -dysfunction may result in autoimmune disease | normally tolerant of self-antigens
90
Clonal Deletion ## Footnote Immune System Tolerance
**self antigens seen in early development** -apoptosis prevents from interaction with body's own proteins | (major mechanism)
91
Clonal Allergy ## Footnote Immune System Tolerance
**single signal will turn off compatible T cell so it does not attack itself** -lymphocyte must receive two specific signals at the same time for activation
92
Receptor Editing ## Footnote Immune System Tolerance
B cell with a receptor for one of the body's own antigens changes its receptor to a non-self version if it encounters a self-antigen | makes sure B and T cells do not attack each other
93
B Ag Sequestering ## Footnote Immune System Tolerance
self molecules are hidden from the immune system | seen with eyes and testes
94
Autoimmune Disease
**arise from the loss of tolerance of self-antigens or exposure to a foreign antigen almost structurally identical to a self-antigen** -result of abnormal functioning immune system -may be related to pregnancy - arising from lingering fetal cells post pregnancy
95
What cells are lacking in severe immunodeficiency?
B and T cells
96
HIV
virus invades and incapacitates helper T cells
97
Allergies
**acquisition of inappropriate specific immune reactivity (hypersensitivity) to a normally harmless substance** -immediate or delayed -antibody mediated
98
Chemical Mediators of Allergic Reactions
-histamines -slow reactive substance of anaphalaxis (SRS-A) - leukotriene similar to prostaglandins -eosinophil chemotactic factor
99
Allergens bind to and ellicit synthesis of...
IgE antibodies -tail portions attached to mast cells and basophils -these cells produce and store inflammatory chemicals (histamine)