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ASC171 - Final exam modules > Immune system > Flashcards

Immune system Flashcards

1
Q

Major functions of the immune system…?

A

defence against invading pathogens (viruses, bacteria, fungi, parasites)
removal of old RBCs & tissue debris
I.D. & destroy abnormal/mutant cells
rejection of foreign cells
inappropriate response - allergies (normally harmless substance); autoimmune diseases

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2
Q

Organs & tissues of the immune system…?

A 
WBCs
thymus
lymph nodes
spleen
tonsils
adenoids
Peyer's patches - ileum (SI)
appendix
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3
Q

A bit about the innate immune system…?

A

RAPIDLY asserted upon exposure to threatening agent
DOES NOT depend on prior exposure to the agent
carried out by all animals

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4
Q

A bit about the adaptive (acquired) immune system…?

A

SELECTIVELY TARGET foreign material after 1st exposure
DELAYED response
found in JAWED vertebrates

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5
Q

Immune cells coordinate their actions via signal molecules called…?

A

cytokines

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6
Q

What are the circulating leukocytes (WBCs)? Briefly describe each one.

A

neutrophils - highly mobile
eosinophils - secrete chemicals -> destroy parasitic worms; involved in allergic responses
basophils - release histamine & heparin
monocytes - transformed into macrophages
NK cells - destroy virus-infected host cells & cancer cells
lymphocytes - primary cells of adaptive/acquired immunity

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7
Q

Localised leucocyte derivatives…?

A

mast cells - localised in barrier tissue, sense invasion -> secrete histamine
dendritic cells - same localisation

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8
Q

Almost all leucocytes originate from…?

A

stem cells in the bone marrow

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9
Q

1st line of defence innate immunity…?

A

barrier tissues & glands

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10
Q

2nd line of defence innate immunity…?

A

inflammation

complement system

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11
Q

Innate immunity comprises…?

A 
barrier tissues
inflammation
complement system
interferon
NK cells
symbiotic bacteria
- includes all non-specific immune responses
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12
Q

What can activate innate immunity…?

A

noxious material
infectious agents
chemical material
tissue injury/trauma/burns

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13
Q

Non-specific immune responses include…?

A 
inflammation
fever
interferon
complement systems
NK cells
symbiotic bacteria
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14
Q

Role of barrier tissues as 1st line of defence…?

A

form passive walls with active defence mechanisms via integument (skin) - largest organ in the body
MECHANICAL BARRIER - dynamically involved in defence
EXOCRINE GLANDS in skin - sweat glands (thermoreg & secrete antimicrobial peptides, dermicidin); sebaceous glands (produce oily sebum helps inhibit microbial growth

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15
Q

Apart from integument, other barrier tissues…?

A
  • digestive tract (saliva, stomach acid, gut associated lymphoid tissue GALT)
  • genitourinary tract (acidic urine, vaginal secretions, mucus)
  • Resp. system (nasal hairs, lymphoid tonsils & adenoids, cilia, cough/sneeze)
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16
Q

A bit about innate immunity - inflammation…?

A

2nd line of defence
caused by - microbial infections, physical agents, tissue necrosis thru inadequate blood flow
FUNDAMENTAL AIM of response - recruit phagocytes & plasma proteins -> tissue repair
also -> isolate, destroy, inactivate invaders; remove debris; prep. for healing & repair

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17
Q

9 mammalian inflamm. responses…?

A
  1. PHAGOCYTOSIS - foreign microbes by macrophages
  2. HISTAMINE RELEASE - via mast cells -> redness, swelling, pain
  3. FIBRIN FORMATION - > clotting
  4. EMIGRATION OF LEUKOCYTES - (eg. neutrophils) -> tissues attracted by chemotaxins
  5. PHAGOCYTIC DESTRUCTION - tagged & untagged bacteria
  6. NON-PHAGOCYTIC DESTRUCTION - tagged & untagged bacteria
  7. TISSUE REPAIR - increased cell division -> scar tissue
  8. MEDIATION OF INFLAMMATION - by phagocyte-secreted chemicals
  9. ENDOGENOUS PYROGENS -> FEVER
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18
Q

Principle effectes of inflammation…?

A

REDNESS - due to dilation of small blood vessels at damaged area -> blood flow -> HEAT
HEAT - increased temp. at periphery (skin)
SWELLING - from oedema -> stretches & distorts tissue (pus under pressure) -> PAIN

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19
Q

Drugs to suppress immune response…?

A

NSAIDs - aspirin, ibuprofen -> decreases histamine release -> inhibits clotting & fever via PGE inhibition
GLUCOCORTICOIDS - similar to cortisol -> suppress most aspects of inflamm. response -> destroys lymphocytes & reduces

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20
Q

Characteristics of the complement system…?

A
  • 2nd line of defence
  • 2 methods of activation - CHO chains on surface of microorgs. (alternative pathway); Ab’s produced against specific foreign invader (classical pathway)
  • sequential activation of 9 plasma proteins (C1-C9) -> membrane attack complex (MAC) -> into microorgs. & forms pores -> lysis & pathogen death
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21
Q

Properties of natural killer (NK) cells…?

A

Non-specifically destroys VIRUS-INFECTED CELLS & CANCER CELLS via chemicals released -> lyse membranes of infected cells upon 1st exposure to them

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22
Q

Properties of interferon…?

A

released from virus-infected cells
briefly interferes viral replication
enhances action of NK cells
slows cell division & tumour growth

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23
Q

A bit on aquired immunity…? Which 2 branches of immunity does acquired immunity involve…? 2 key features…?

A

3rd line of defence in jawed vertebrates
Selectively targets foreign material (Ag’s)
Involves - HUMORAL (Ab-MEDIATED) immunity (tranforms B lymphocytes -> plasma cells -> secrete Ab’s
CELL-MEDIATED IMMUNITY - Cytotoxic T-lymphocytes destroy virus-invaded & cancer cells
SPECIFICITY & MEMORY

24
Q

When does acquired (adaptive) immunity occur…?

A

when body exposed to pathogen (naturally or artificially)

NOT IMMEDIATE response of 1st exposure to pathogen

25
Q

What are integrating signals?

A

aid both humoral & cell-mediated immunity via helper T cells (activate effector cells) & T-reg. cells (supress immune response)

26
Q

Function of lymphoid tissues…? What are the lymphoid tissues…?

A

store, produce & process lymphocytes

lymph nodes, spleen, thymus, tonsils, bone marrow, lining of digestive tract, skin

27
Q

Where are lymphocytes produced? What do they form…?

A

stem cells in bone marrow -> B cells
immature lymphocytes in thymus -> T cells
thymus also -> thymosin

28
Q

Presence of … enables … & … cells to distinguish “non-self” cells from “self”

A

antigens, B cells, T cells

29
Q

What happens when B cells are exposed to antigens…?

A

B cells receptors (BCRs) bind with Ag -> B cells divide & turn into active plasma cells & dormant memory cells -> active plasma cells -> produce Ab’s -> into blood as Ig’s

30
Q

Antibody structure & classification…?

A

2 heavy chains & 2 light chains
arm region - specificity
tail region - functional properties
DRAW & LEARN DIAGRAM!

31
Q

Antibody subclasses & function of subclasses…?

A

remember G.A.M.E.D.
IgG - most abundant (enhance phagocytosis
IgA - secretions of digestive, resp., genitourinary systems
IgM - B-cell receptor
IgE - histaminE -> allergic responses & worms
IgD - surface of many B cells

32
Q

Functions of antibodies…?

A
  • Antigen destruction via NEUTRALISATION (combine with bacterial toxin & virus to prevent interaction with host cells); AGGLUTINATION (Ab’s cross-link Ag’s -> clumping)
  • amplify innate immune responses (via complement, phagocytosis, NK cells)
33
Q

Describe clonal selection theory…?

A

Remember diagram on slide 41

explain out loud

34
Q

Define primary & secondary immune responses…?

A

Primary response - INITIAL CONTACT with foreign Ag delayed for several days…plasma cells formed…Ab prod. peaks in few weeks
Secondary response - same Ag reappears later -> memory cells -> more rapid, potent & longer response (prevent & minimise infection; vaccination/immunisation
SLIDE 44

35
Q

LEARN SLIDE 44 BACK TO FRONT!!!

A

DRAW IT!!!

36
Q

Describe active vs passive immunity and the 3 ways it can be generated…?

A

Active immunity - prod. of Ab’s from exposure to an Ag (eg. vaccination)
passive immunity - transfer of preformed Ab’s from one animal to another (eg.s mother (IgG) -> foetus via placenta; colostrum IgM, IgA, IgG) broken down in < month

37
Q

Artificial immunity…?

A

vaccination - safe way animals prod. Ab’s to a pathogen

immunisation - developed immunity to pathogen, but not necessarily via vaccination

38
Q

A bit on vaccines…?

A

Vaccines mimic immunisation (prod. of Ab’s) -> immune sys. recognises Ag (not capable of prod. disease) -> Ab prod. specific to that particular Ag

39
Q

What are 2 kinds of vaccines…?

A

Live vaccines - weakened, non-virulent strains of disease-causing organism (mild form of disease)
Inactivated (killed) vaccines - contain killed disease organism or parts of toxins that prod. symptoms & stimulate Ab prod.

40
Q

Describe vaccination of animals…?

A

takes 2 weeks to produce initial response after vax.
level of immunity then decreases
livestock - 2 initial doses 4-6 weeks apart, then annual booster

41
Q

Name some diseases the cattle vaccines target…?

A
  • clostridial disease
  • leptospirosis
  • vibriosis
42
Q

Name some diseases the sheep & goat vaccines target…?

A 
Sheep:
- clostridial disease
- scabby mouth
- cheesy gland
Goats: clostridial disease
43
Q

Properties of T lymphocytes…?

A
  • CELL-MEDIATED IMMUNITY
  • DIRECT CONTACT with target via receptors called forming IMMUNOSYNAPSE
  • undergo GENETIC RECOMBINATION, CLONAL & Ag-SPECIFIC
  • immature lymphocytes get T-cell receptors in THYMUS
  • only activated when FOREIGN ANTIGEN & SELF-ANTIGEN present
  • display PRIMARY & SECONDARY responses
44
Q

What are self-antigens also called?

A

major histocompatibility complex (MHC)

45
Q

Types of T-lymphocytes…?

A

Cytotoxic T cells - destroy host cells with foreign Ag
Helper T cells - modulate power of activated lymphocytes & macrophages
Regulatory T cells - supress immune response

46
Q

More on cytotoxic T cells…?

A

release perforins -> lyse target cell
release granzymes -> self-destruct (target cell)
does not occur in neurons (cannot be replaced)

47
Q

More on helper T cells…?

A

secrete cytokines -> augment immune response

AIDS (HIV) invades T cells -> stopping immune response

48
Q

What are antigen presenting cells (APC’s)? How do they work?

A

consist of macrophages, dendritic cells, B cells
DENDRITIC CELLS - found in barrier tissues
1. bactrium engulfed by dendritic cells
2. foreign Ag bound to MHC proteins
3. both added to membrane for presentation to T CELLS
4. Dendritic cells -> lymph nodes
Slide 64 explains it well!

49
Q

What are self-antigens…?

A

plasma-membrane-bound GLYCOPROTEINS arising from MHC gene (most variable in mammals)
Class I MHC glycoproteins - surface of ALL BODY CELLS. present viral & cancer proteins to cytotoxic T cells
Class II MHC glycoproteins - surface of dendritic cells, macrophages, B cells. present foreign Ag’s to helper T cells

50
Q

T-cells immune surveillance…?

A

Recognis & destroy potentially cancerous tumour cells

involves - NK cells (1st line), cytotoxic T cells, macrophages, interferon

51
Q

Why do cancer cells survive?

A

due to blocking antibodies that interfere with T cell function

52
Q

Describe autoimmune disease…? Give examples of some…?

A

immune system FAILS TO DISTINGUISH SELF FROM NON-SELF -> attacks body’s own tissues
M.S, type I diabetes mellitus, rheumatoid arthritis

53
Q

How can AIDS arise?

A
  • exposure during injury of previously sequestered Ag’s
  • mod. of self-Ag’s by external chemicals, viruses, mutations
  • exposure of T cells to foreign Ag similar to self-Ag
54
Q

How does the nervous & endocrine system control the immune system…?

A

via a regulatory loop
stress -> increased cortisol secretion (mobilises nutrient stores, AAs, & suppresses immune sys
thus, long-term stress linked to infections & cancer

55
Q

The SNS innervates which organs?

A

thymus, spleen, lymph nodes

ASC171 - Final exam modules (7 decks)

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