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MMI133 > MMI133_Lecture10 > Flashcards

MMI133_Lecture10 Flashcards

1
Q

SCID

A

severe combined immunodeficiency

bubble boy
cannot produce antibodies

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2
Q

innate immunity

A

non-specific defence

first line of defence against pathogens

= skin + gut microbiota
complement + phagocytosis of microorganisms + inflammation

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3
Q

adaptive immunity

A

specific defense

specialized immune cells
specific response
self/non-self recognition
memory generation

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4
Q

the adaptive immunity specificity is based on

A

antigen recognition

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5
Q

antigen

A

foreign molec recognized by adaptive immune cells
elicit immune response
most immunogenic = best ones = proteins

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6
Q

the innate and adaptive immune systems are

A

overlapping

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7
Q

vaccines work because

A

of the memory involved in teh adaptive immue system

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8
Q

adaptive immunity is mediated by

A

B lymphocytes (humoral)
T lymphocytes (cell-mediated)

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9
Q

humoral

A

body fluids, blood + lymph

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10
Q

summary of the innate immune system

A

antigen-independent
broad spectrum
immediate response
not antigen specific
no memory

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11
Q

summary of adaptive immune system

A

antigen-dependent
lag time in response
antigen specific
memory
specific

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12
Q

B lymphocytes

A

produce antibodies in response to specific antigens to fight infection

produce cytokines which produce chemical signals that can change behaviour of other cells

act as Antigen presenting cells (APC) to activate other immune cells to combat infection by cellular mechanisms

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13
Q

APC’s

A

antigen presenting cells

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14
Q

antigen

A

foreign moelc that can be recognized by adaptive immune cells + elicit an immune response

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15
Q

epitope

A

specific site on an antigen recognized by immune cells or antibodies

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16
Q

antibody

A

protein produced by B cells that recognizes a specific epitope on an antigen

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17
Q

B lymphocytes

A

produced in bone marrow
is antigen-independent

activation in peripheral lymphoid organs is antigen-dependent

differentiation into plasma or memory B cells within lymph glands is antigen-dependent

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18
Q

clonal expansion

A

rapid cell division + proliferation

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19
Q

TD

A

thymus-dependent antigens
PROTEINS

requiers T helper cell contact

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20
Q

TI

A

thymus-independent antigens (mostly other molecuels like cell wall components)
doesn’t require T helper cell

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21
Q

cytokines

A

soluble proteins secreted by immune cells
chemical signals that can change teh behaviour of other cells
can cause B cell prolifereation - clonal expansion - and class switching

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22
Q

class switching

A

changing Ig produced by B cell with no loss of antigen specificity
produces diff antibodies depending on cytokine environment arnd plasma cells

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23
Q

Fab region

A

the arms part of the Y antibody

variable region
antigen bidning sites
diff combinations at variable regions give rise to large repertoire of diff antigen specificity

the antigen binding site is on the ends of the Y arms

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24
Q

Fc region

A

stem region of the Y antibody shape

consant region
recognized by other immune cells that have a Fc receptor binding site

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25
Q

functions of antibodies

A

opsonization - coating of bact to make more efficient + tasty phagocytosis

complement activation OIL

agglutination - sticking bact tog for more efficient phagocytosis

neutralization - cover all attachment points of pathogen

antibody-dependent cell-mediated cytotoxicity - grap infected cell + kill it

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26
Q

opsonization

A

coating of bact with antibodies and then macrophages that have Fc receptors bind to Fc stem of antibody - more efficient phagocytosis

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27
Q

complement activation

A

anatibodies nidn to antigens on a bact = immune complex which activates classical complement pathway.

C3b split product of C activation binds to bact cell wall opsonin
formation of membrane attach complex MAC

28
Q

agglutination

A

antibodies stick bact together so that macrophage can eat many in one gulp - more efficient phagocytosis

29
Q

neutralization

A

for toxins or bact or viruses, antibodies cover up all attachment points on pathogen so that it cannot attach to host cell. deactivates it + neutralizes threat

30
Q

antibody-dependent cell-mediated cytotoxicity

A

natural killer cells with Fc receptors grap infected cells that have teh antibodies attahced to them and kill infected cell

31
Q

stem region of Y shaped antibody monomer =

A

Fc region

32
Q

serum

A

if blood is allowed to clot
yellow liquid above clotted blood
rich in proteins
mostly lab testing
contains no active blood clotting proteins bec all used up

33
Q

plasma

A

if anticoagulant added to blood so won’t clot
yellow fluid
contains intact blood clotting proteins that have not been activated
has more layers

34
Q

Ig

A

immunoglobulin = antibody

35
Q

IgG

A

most abundant antibody in serum = 80% of serum antibodies
mother - fetus via placenta = 6 months immunity
highly efficient to activate complement
high affinity for Fc receptors on phagocytic cell membranes _ mediate opsonization

36
Q

IgM

A

5-10%
1st produced in primary response
1st one synthesized by neonates, even in fetus
J oining chain J chain
more efficient to activate complement
secreted by pentamer

37
Q

IgA

A

10-15%
in breast milk (also other secretiosn - saliva, tears, mucus)
monomer + dimer J chain
protects newborn baby by mothers milk - dependent on types of antigens mum was exposed to

38
Q

IgE

A

extremely LOW conc 0.0002%
ALLERGIES (responsibel for allergies)
binds Fc recpetors on mast cells + eosinophils

important for parasite neutralization

39
Q

IgD

A

0.2%
expressed at cell surface of mature B cells along with IgM
biological funciton not really know

something to do with mucosal immunity

40
Q

first class of antibody synthesized, especially effective against microorganisms

A

IgM

41
Q

antibodies transferred form mum to fetus

A

IgG

42
Q

antibodes protect mucosal membranes + good reason to breast feet

A

IgA

43
Q

focuses of diff antibody types

A

IgG - mum - fetus placenta - lots of them - highly efficeint

IgM - 1st produced in primary + synthesized by neonates

IgA - breast milk + mucus secretions

IgE - low - ALLERGIES - paraiste neutralization

IgD - cell surface - not well understood - something to do with mucosal immunity

44
Q

MHC

A

major histocompatibility complex

also HLA

present foreign particle/antigen to macrophages that come from infections with cell

45
Q

MHC class I

A

all nucleated cells (self-marker)
presents endogenous peptides (peptides made inside cell)
activates CD8+ cytotoxic T cells

46
Q

MHC class II

A

only APCs
presents exogenous peptides (peptides not made in cell - foreign particles)
activates CD4+ helper T cells

47
Q

CD (from CD8+ or 4+)

A

cluster of differentiation

different proteins on surface of cells used to characterize diff cell types in the body

48
Q

mhc refers to

A

molec found in mice
should be HLA

49
Q

T lymphocytes

A

Cytotoxic T lymphocytes CD8+
Helper T lymphocytes CD4+
Regulatory T lymphocytes

50
Q

cytotoxic T lymphocytes CD8+

A

target + directly kill virus-infected cells, tumour cells, or cells from tissue graft

do the work
ATTACK

51
Q

helper T lymphocytes CD4+

A

produce cytokines that support inflammation + activates other immune cells
activate B cells which leads to antibody production
activate T cytotoxin cells

tells things to start workign
COMMUNICATION

52
Q

regulatory T lymphocytes

A

can suppress other immune cells

puts a stop/stopper on immune processes

53
Q

T lymphocytes details

A

develop in bone marrow + travel to thymus where dependent on MHC molecs + antigen
cells programmed so don’t auto-react to self

activated in peripheral lymphoid organs
is MHC + antigen dependent

differentation becomes effector cells (T helper or cytotoxic) or memory cells

54
Q

Activated cytotoxic T lymphocyte cells produce + secrete…

A

perforin + granzyme to kill cell

needs cell contact to recognize

recognize due to infection + cancer

55
Q

activated Tc cells undergo

A

clonal expansion where…

majority remian in system as killer cells and some become memory cells which can quickly activate after second encounter with same antigen + MHC I

56
Q

actiavted Helper T cells will secrete

A

cytokines (Th1) or act as B cell helpers (Th2)

57
Q

activated Th cells undergo

A

clonal expasion
majority remain in system as helper cells
some become memory cells upon second encounter with same antigen + MHC II

58
Q

partial immunodeficiency

A

loss of function or numbers
patients highly prone to infections

59
Q

auto-immunity

A

T cells unable to differentiate self from non-self
hyper immune responses
celiac disease, rheumatoid arthritis

60
Q

severe immunodeficiency

A

severe combined immunodeficiency (SCID)
fatal if untreated by bone marrow transplant

61
Q

acquired immune deficiency syndrome

A

HIV hijack Th cells

62
Q

how do immune cells kill infected cells?

A

apoptosis (programmed cell death)
necrosis (death caused by cell injury, infection or toxins)

63
Q

apoptosis

A

death of cells that occurs as normal part of development or as targeted event
doesn’t trigger inflammation since clean up of apoptotic bodies done by phagocytic cells

NATURAL

64
Q

Necrosis

A

death of cell triggered by extrinsic factors
detrimental to host + has inflammatory response

UNNATURAL

65
Q

humoral immunity

A

B cells + antibodies
in blood + lymph

66
Q

cell-mediated immunity

A

cytotoxic T cells + T helper cells

67
Q

the innate and adaptive immunes systems are

A

not independent of each other, but interact + work together and overlap

MMI133 (16 decks)

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