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
functions of antibodies
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
26
opsonization
coating of bact with antibodies and then macrophages that have Fc receptors bind to Fc stem of antibody - more efficient phagocytosis
27
complement activation
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
agglutination
antibodies stick bact together so that macrophage can eat many in one gulp - more efficient phagocytosis
29
neutralization
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
antibody-dependent cell-mediated cytotoxicity
natural killer cells with Fc receptors grap infected cells that have teh antibodies attahced to them and kill infected cell
31
stem region of Y shaped antibody monomer =
Fc region
32
serum
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
plasma
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
Ig
immunoglobulin = antibody
35
IgG
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
IgM
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
IgA
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
IgE
extremely LOW conc 0.0002% ALLERGIES (responsibel for allergies) binds Fc recpetors on mast cells + eosinophils important for parasite neutralization
39
IgD
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
first class of antibody synthesized, especially effective against microorganisms
IgM
41
antibodies transferred form mum to fetus
IgG
42
antibodes protect mucosal membranes + good reason to breast feet
IgA
43
focuses of diff antibody types
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
MHC
major histocompatibility complex also HLA present foreign particle/antigen to macrophages that come from infections with cell
45
MHC class I
all nucleated cells (self-marker) presents endogenous peptides (peptides made inside cell) activates CD8+ cytotoxic T cells
46
MHC class II
only APCs presents exogenous peptides (peptides not made in cell - foreign particles) activates CD4+ helper T cells
47
CD (from CD8+ or 4+)
cluster of differentiation different proteins on surface of cells used to characterize diff cell types in the body
48
mhc refers to
molec found in mice should be HLA
49
T lymphocytes
Cytotoxic T lymphocytes CD8+ Helper T lymphocytes CD4+ Regulatory T lymphocytes
50
cytotoxic T lymphocytes CD8+
target + directly kill virus-infected cells, tumour cells, or cells from tissue graft do the work ATTACK
51
helper T lymphocytes CD4+
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
regulatory T lymphocytes
can suppress other immune cells puts a stop/stopper on immune processes
53
T lymphocytes details
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
Activated cytotoxic T lymphocyte cells produce + secrete...
perforin + granzyme to kill cell needs cell contact to recognize recognize due to infection + cancer
55
activated Tc cells undergo
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
actiavted Helper T cells will secrete
cytokines (Th1) or act as B cell helpers (Th2)
57
activated Th cells undergo
clonal expasion majority remain in system as helper cells some become memory cells upon second encounter with same antigen + MHC II
58
partial immunodeficiency
loss of function or numbers patients highly prone to infections
59
auto-immunity
T cells unable to differentiate self from non-self hyper immune responses celiac disease, rheumatoid arthritis
60
severe immunodeficiency
severe combined immunodeficiency (SCID) fatal if untreated by bone marrow transplant
61
acquired immune deficiency syndrome
HIV hijack Th cells
62
how do immune cells kill infected cells?
apoptosis (programmed cell death) necrosis (death caused by cell injury, infection or toxins)
63
apoptosis
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
Necrosis
death of cell triggered by extrinsic factors detrimental to host + has inflammatory response UNNATURAL
65
humoral immunity
B cells + antibodies in blood + lymph
66
cell-mediated immunity
cytotoxic T cells + T helper cells
67
the innate and adaptive immunes systems are
not independent of each other, but interact + work together and overlap