MODULE 9 Flashcards

(74 cards)

1
Q

whats the difference between immunology and imunity

A

immunology: the study of the immune system
immunity: the ability of an organism to resist infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

whats the difference between innate and adaptive immunology

A

innate: 1st and 2nd line of defence that prevents entry and spread of dangers
adaptive: 3rd line of defence provides a specific response to dangers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

innate immunity is ____-_______ and non-__________, it has a _____ response, physical and chemical ________, and ______ _______ previous exposure,

A

non inducible
specific
quick
barriers
doesn’t require

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

adaptive immunity happens when _______ ____, it has _______ recognition of pathogens, with a _____ process because its ______-_____. it also develops ______

A

innate fails
specific
slow
multi-step
memory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what are the 3 wasy your body can react to microbes

A
  • tolerate (friendy or harmless microbes)
  • segregate (keep them from where they cant go)
  • defend (immediate aggressive response)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what are the 3 non-specific innate defences

A

physical
chemical
cellular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what are 3 types of physical nonspecific innate immunity and examples

A
  • cellular barriers: skin, mucus
  • mechanical defence: shedding, pissing,
  • microbiome: resident bacteria of skin and intestinal tract
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are 3 types of chemical nonspecific innate defences and examples for 2

A
  • body fluids: pH regulation, enzymes
  • antimicrobial: peptides(AMPs), bile acids
  • cytokines
  • complement system
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is the complement system and how does it work

A
  • plasma proteins found in blood and fluids
  • they work together to: destroy pathogens, make pathogens easier to phagocytose, promote inflammation
  • protein activated when pathogen detected and (3 pathways can happen)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is the classical pathways of the cascade compliment activation

A
  • Links adaptive immunity to innate immunity
  • Triggered when antibodies (IgG or IgM) bind to antigens on a pathogen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is the lectin pathway of the cascade complement system

A
  • Triggered when mannose‑binding lectin (MBL) binds to sugars on pathogen surfaces
  • no antibodies required
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is the alternative pathway of the cascade compliment system

A
  • Triggered directly by pathogen surfaces
  • Activated continuously at a low level
  • Rapid first‑line defence
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are the 3 effects of the compliment system and what are their results

A
  • opsonisation(C3b): Faster and more efficient phagocytosis
  • inflammation(C3a, C5a): More immune cells reach the infected area
  • cell lysis: MAC creates pores in the pathogen’s cell membrane where water enters → cell bursts (lysis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what do cytokines and chemokines do in innate immunity

A

Both Chemical messangers that help coordinate immune response
- Cytokine - stimulate and binds to receptors signalling cascade leading to transcription activator
- Chemokines are a sub-class of cytokines that recruit circulating immune cells to site of injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what do interferons do and how are they different

A
  • Cytokine subtype that primes antiviral activity
  • doesnt have direct antiviral action itself, but instead is secreted by virus infected cells to signal other cells to start making antiviral factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

whats the difference between an autocrine, paracrine and endocrine

A
  • same cell recieves and secretes signals
  • cytokine signal released to nearby cell
  • signal secreted into blood stream and travels to distant cell
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what are the organs of immunity

A
  • blood: Allow circulation and distribution of immune cells
  • lymph (nodes): Lymph dumps antibodies and immune cells into the blood
  • MALT - mucosa associated lymphoid tissue
  • spleen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what are the cellular players of innate immunity

A
  • stem cells (HSCs): erythrocytes, leukocytes, platelets
  • monocytes: imature
  • granulocytes:
  • Granules that can be stained
  • Toxins and enzymes
  • Destroy their targets
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what are 7 cell types and their roles

A

dendric cells: APCs in skin and mucus
macrophages: APCs in tissues and organs (monitor and process invaders)
- neutrophils: in blood and bone marrow, kill extracellular bacateria
- eosinophils: protect against protozoa, has role in allergies
- mast cells: in tissues, allergic reaction and inflammation
- NK cells: kills virus infected and cancerous cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

phagocytosis is considered ______ immunity, whos purpose is to _______,

A

innate
destroy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what are PAMPs (pathogen associated molecular pattern) and PRRs (pattern recognition receptors)

A
  • PAMPs: unique microbe structures/patters detected by the PRRs on the cell surface
  • PRRs: receptors on or in host cells that recognise PAMPs.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

how do we kill without using phagocytosis

A
  • killing smthn bigger than u (parasites)- (eosinophils secreting toxic proteins that perforate parasite wall)
  • killing smthn within a cell (extracellular killing with NK cells, seek and destroy virus in cell
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

a healthy cell has _____ where as an infected cell doesnt, which triggers a response in the ____ cell to _______ the infected cell.

A

MHC1
NK
Kill

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what is inflammation

A

Normal biological response that promotes healing. Its characterized by: Redness (erythema), swelling (edema), Pain, Heat
- it produces activators like
* Pro-inflammatory molecules (histamine)
* Phagocytes and lymphocytes
* Induce vasodilation
* Increased vascular permeability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
TF an Influx of phagocytes means increased inflammation
T
26
what is a fever
inflammatory response induced by LPS (exogenous) and cytokines (endogenous) pyrogens {fever causers} that act on the hypothalmus to raise body temperature to help limit the growth of the pathogen.
27
what is the fever pathway
LPS--> leukocytes --> cytokines --> PGE2 --> hypothalmus --> fever
28
what can happen if cytokine release becomes excessive
excessive swelling --> toxic shock
29
what is considered a high grade fever
above 40 degrees celcius
30
what are the benefits of fever
- Slows the growth of temperature sensitive microbes - Reduce availability of nutrients used by microbes - Increase metabolic activity of phagocytic cells - Stimulate acute inflammation
31
what is the DDM of adaptive immunity
- Discriminate: distinguish between specific foreign molecules - Diversify: recognize many possible foreign molecules - Memorize: remember foreign molecules after 1st exposure
32
what are the 2 components to adaptive immunity
1. Humoral immunity - Antibodies produced by B-cells (Bone marrow lymphocytes) in response to antigens 2. Cell-mediated immunity - Activation of T-cells (Thymus lymphocytes) to control intracellular microbes (virus, bacteria, parasites)
33
what is an antigen
molecule/substance that interacts with antibodies or T Cell Receptor (TCR)
34
TF all antigen induce an immune response
F
35
what is an immunogen
induces an immune response (conjugate vaccines)
36
what is a hapten
small molec that binds to an antibody (doesnt induce immune response)
37
what are epitopes
section or specific regions of an antigen that are recognized
38
TF antibodies are like a bridge that connect antigens
T
39
what are antibodies
Antibodies are immunoglobulins — specialized proteins made by B cells (plasma cells) as part of the adaptive immune response. Their main job is to recognise and bind specific antigens. - exist as Y shaper monomer, - "light" chains on arms of Y (Fab region) - "heavy" chains on stem of Y (Fc region) - The two arms bind antigens the stem interacts with other immune components
40
what are the 5 functions of antibodies
Opsonization Complement activation Neutralization Agglutination Cell‑mediated cytotoxicity (ADCC)
41
what is opsonization
A macrophage binding a pathogen coated with antibodies, the macrophage has Fc receptors Pathogen is “tagged” and phagocytosis becomes much more efficient
42
what is Immune activation: complement activation
the classical complement pathway diagram
43
what is neutralization
Antibodies block: - Viral attachment to host cells - Toxin binding to receptors result - Pathogen or toxin becomes biologically inactive - No need for phagocytosis or complement
44
whats the function of Ig(A,D,E,G,M)
A = neutralization D = B-cell receptor E = Bind Fcto activate mast cells and basophils G = neutralization, agglutination, complement activation, opsonization, cell mediated toxicity M = neutalization, agglutination, complement activation
45
what are the properties of Ig(A,D,E,G,M)
A = major secretory antibodies D = activate B cells E = parasite immunity G = Major circulatory antibody M = first antibody to appear
46
the Major Histocompatibility Complex (MHC) important for
antigen presentation
47
what are MHC 1 and 2 found
on phospholipid bilayer surface of their respective cell types
48
where is the MHC 1 found specifically and what does it present
all nucleated cells self antigens and non self antigens
49
where is the MHC2 found specifically and what does it present
macrophages, dendritic and B cells present non self antigens
50
what are APCs (antigen presenting cells)
process antigens in cell and present to T cells on cells surface (MHC2) of macrophages, dendritic cells and B cells
51
what are immunodominant epitopes
Only peptides that: - Fit into the MHC II binding groove - Are stable enough are presented
52
Cell mediated immunity is driven by ______ to eliminates ________- with a microbe and kills __________and_________. they also regulate function of cells involved in ________
T cells infected cells abnormal cancer cells non-self tissues innate immunity
53
what is the purpose of T cell selection
Distinguish between: Self (host antigens) Non‑self (danger antigens) Prevent immune responses against self
54
what is positive and negative selecition when t cells bind antigens
+ve = weak(survive), no bind(die) -ve = strong interation (die)
55
what the difference between helper, regulatory, and cytotoxic T cells
- Helper: CD4, MHC2, humoral and cellular immunity - regulatory: CD4, MCH2, activate macrophage and NK cells - cytotoxic: CD8, MHC1, destroy cells with infected pathogens
56
what do TH1, TH2 and memory helper T cells do
- TH1 - stim cytotoxic T cell - TH2 - co stimulate B cells - Memory helper T cells - remember specific pathogens for reexposure
57
what the ket interactions of cytotoxic T cells with the infected cell
TCR ↔ antigen on MHC I CD8 ↔ MHC I (stabilizes the interaction)
58
how do B cells recognize one specific antigen and do not attack self (B cell selection)
Each B cell has a unique BCR that can bind 1 specific antigen
59
what is +ve and -ve B cell reception, and where does it occur
+ve = keep the good ones, B cells with a working BCR survive, If the receptor doesn’t work → the B cell dies -ve = remove dangerous ones, If a B cell binds strongly to self antigens it is eliminated - occurs in bone marrow
60
how do B cells stimulate the production of antibodies (T cell independent B cell activation)
occurs when repetitive antigens and PAMPs activate B cells directly, causing them to proliferate and produce mainly IgM antibodies.
61
How does B cell stimulation work when its T-cell dependant
- An antigen on a bacterium binds to the B cell receptor (BCR) (1st activation signal) - The B cell pulls the antigen inside and is broken into pieces - The B cell displays antigen fragments on MHC class II and a CD4⁺ helper T cell (TH2) recognizes the antigen - The helper T cell releases cytokines making B cell stronger and last longer - B cells divide, some become memory cells and some become plasma cells
62
what do CD4⁺ helper T cells decide
weather to use cell mediate or humoral immunity
63
What links innate and adaptive immunity?
Antigen presentation by APCs to CD4⁺ T cells via MHC II
64
What is humoral immunity?
Antibody‑mediated immunity by B cells
65
What is cell‑mediated immunity?
Killing of infected cells by CD8⁺ cytotoxic T cells
66
How do CD8⁺ T cells kill cells?
Perforin and granzymes → apoptosis
67
What do helper T cells do?
Release cytokines to direct immune responses
68
Q: Th1 vs Th2 functions?
Th1 → activates macrophages & CD8⁺ T cells Th2 → activates B cells & antibody production
69
Summarize adaptive immunity in one sentence.
APCs activate CD4⁺ T cells, which direct humoral immunity via B cells and cell‑mediated immunity via CD8⁺ cytotoxic T cells.
70
what are the mechanisms to aquire immunity
- passive natural (breast milk) - passive artificial (antibodies harvested from animal or human) - active natural (gained thru illness or recovery - active artificial (vaccine)
71
what are the vaccine types and their descriptions
Live attenuated (non pathogenic viable microbe) - whole inactivated (pathogen dead) - sub units (toxoid, cojugated, viral like particle) - viral vector (virus expressing antigen) - RNA (RNA strand thats translated)
72
why do we need booster shots ?
- Antibodies produced during the secondary response are more effective and bind with higher affinity - Plasma cells produced during secondary responses: live longer and the levels of antibody remain elevated for longer
73
what factors can affect vaccine efficiency
intrinsic extrinsic behavioural nutritional environmental administrative
74