Immunology Flashcards
1
Q
What are the two components that make up the immune system?
A
cellular and soluble
2
Q
What cells are in the cellular component?
A
neutrophils monocytes macrophages eosinophils basophils mast cells t lymphocytes B lymphocytes natural killer cell (9)
3
Q
what type of cells are all the cells in the cellular component?
A
white blood cells (or originate from white blood cells)
4
Q
what stem cell do all white blood cells come from?
A
haematopoietic pluripotent stem cell
5
Q
What is the role of a neutrophil?
A
phagocytic, engulf and destroy bacteria
6
Q
how many types of granules are in a neutrophil?
A
3
7
Q
describe the primary granules’ role and what they contain
A
role: antibacterial, digest by combining with the phagosome
contain: lysosomes, acid hydrolases, defensins, superoxides, complement receptors.
8
Q
what do superoxides do that assists break down of bacteria?
A
covert h2o2 to .oh which is a free radical which is toxic
9
Q
what do defensins do that assists break down of bacteria?
A
insert into membranes of bacteria so killing it
10
Q
describe the secondary granules’ role and what they contain
A
role: regulate inflammatory response
contain: lactoferrin and lysozyme
11
Q
describe the tertiary granules’ role and what they contain
A
role: facilitate insertion of proteins into cell membrane of bacteria
12
Q
describe the neutrophil nucleus
A
nucleus is multi lobar (2-5 lobes)
nuetrophils are polymorphonuclear leukocytes
13
Q
What is the role of a monocyte?
A
remove foreign or dead madterial by phagocytosis.
14
Q
how are monocytes important for both innate and adaptive immunity?
A
phagocytic - innate
antigen presenting cells- adaptive
15
Q
what can monocytes differentiate into?
A
monocytes are immature cells. they differentiate into macrophages or dendritric cells once they enter connective tissue
16
Q
where do macrophages live and what is their role?
A
in tissues
remove foreign microbes and dead/tumour self by phagocytosis
17
Q
how do macrophages and monocytes phagocytose?
A
by using their lysosomes that have peroxidase
18
Q
what are dendritic cells? give an example
A
fixed, differentiated macrophages
e.g. kupfer cells in liver
19
Q
describe the shape of the nucleus of a monocyte
A
kidney shaped
20
Q
what is the role of eosinophils?
A
phagocytose antigen-antibody complexes
are associated with parasitic infections
neutralise histamine so are also associated with allergic reactions
21
Q
are eosinophils granulocytes?
A
yes
22
Q
what do eosinophil granules contain?
A
major basic protein which is a potent toxin. it activates neutrophils, induces histamine release from mast cells
23
Q
describe the eosinophil neucleus
A
polymorphonuclear, 2-3 lobed nucleus
24
Q
what is the role of basophils?
A
main role in parasitic infections and allergic reactions
25
are basophils granulocytes?
yes
26
what do basophil granules contain?
histamine
27
how does histamine get released from basophils?
basophils have IgE receptors so when IgE binds to them degranulation occurs so histamine released from granules
28
describe the basophil nucleus?
polymorphonuclear but not multi-lobar
29
what cell has a similar role to basophils?
mast cells
30
where are mast cells found?
in tissues, their precursor (mast cell progenitor) is found in the blood
31
what is the role of mast cells?
parasitic infections
| allergic reactions
32
what do mast cells have that allows them to be involved in allergic reactions?
high-affinity IgE receptors
| histamine-containing granules
33
how do lymphocytes leave the blood? (3)
by extravasation they travel to infection site. mediated by:
1. rolling of lymphocytes along activated vascular endothelium
2. tight adhesion of lymphocytes
3. chemokines
34
how many lymphocytes are there that are involved in immunity? Name them
3
T cells
B cells
Natural killer cells
35
where are T cells matured?
thymus
36
what is T cells major role? (3)
recognising antigens displayed on antigen presenting cells, stimulate antibody production from B cells, help kill pathogens
37
how many types of T cells are there? name them
```
4
t helper 1 cell
t helper 2 cell
cytotoxic t cell
T regulator cell
```
38
what is the role of each of the T cells?
T helper 1: produce IFN gamma to kill intracellular pathogens (e.g. virus)
T helper 2: stimulates antibody production
cytotoxic t cell: kills intracellular pathogens directly
T regulator cell: inhibitory role and controls level and quality of immune response
39
describe the T cell receptors (TCR)
TCR have transmembrane proteins that make CD3 thus forming the CD3-TCR complex. this complex recognises antigens when they are with major histocompatibility complex. but recognition is not enough to activate T cell, other signal needed e.g. interleukin and co-stimulatory molecules
40
how many classes of major histocompatibility complex are there?
3
41
what cells recognise MHC class 1?
cytotoxic T cells that have CD8
42
what cells can present MHC class 1?
all cells except red blood cells
43
what type of antigens do MHC class 1 use?
intrinsic e.g. virus
44
what cells recognise MHC class 2?
T helper cells that have CD4
45
what cells can present MHC class 2?
antigen presenting cells
46
what type of antigens do MHC class 2 use?
extrinsic e.g. microbe phagocytosed and antigen on surface
47
what type of molecules are MHC class 3?
secreted proteins with immune function e.g components of complement system
48
where do B cells mature?
bone marrow
49
what is B cells role in adaptive immunity?
recognise antigens by antigen presenting cells
express membrane bound antibodies on surface
differentiate into plasma cells that make lots of antibodies
differentiate into memory cells
50
What are natural killer cells a type of?
type of lymphocyte
51
where are natural killer cells found?
spleen and tissues
52
what is natural killer cells' role in immunity?
innate immunity as they have no memory and need no prior activation. they kill virus infected cells and tumour cells by apoptosis.
53
what are the parts to the humoral component of immunity?
complement
antibodies
cytokines
54
what is the role of complements?
remove/destroy antigens by direct lysis or by opsonisation
55
define opsonisation
mechanism in which microbes become chemically modified to have stronger interactions with phagocytic cells
56
what are complements?
series of interacting plasma proteins that act as an enzymatic cascade i.e. they are mostly inactive and activation of one will lead to it activating the others.
57
what are the two steps in the activation of complement?
1) produce C3 convertase
| 2) C3 convertase cleave C3
58
how many pathways can produce C3 convertase? name them
3
classical
alternative
lectin
59
how does the classical pathway lead to C3 convertase?
activation by the antibody bound to the microbe
60
how does the alternative pathways lead to C3 convertase?
activation by the compliment binding to the bacterial cell wall
61
how does the lectin pathway lead to C3 convertase?
activation by mannose-binding lectin bound to the microbe (MBL promotes opsonisation)
62
what are some of the fragments produced from C3 cleavage?
C3a, C4a, C5a
C3b
C5, C6, C7, C8, C9
63
What is the most important and main fragment from C3 cleavage?
C3b
64
What do fragments C3a C4a C5a do?
involved in inflammation and immune cell recruitment
65
what does fragment C3b do?
involved in opsonisation and removal of immune complexes
66
what do fragments C5-C9 do?
involved in cell lysis
67
which fragments from c3 cleavage are involved in inflammation and immune cell recruitment?
c3a, c4a, c5a
68
which c3 cleavage fragment is involved in opsonisation?
c3b
69
which c3 cleavage fragments are involved in cell lysis?
c5-c9
70
are mast cells all the same? what is the name for this feature of mast cells?
no they are different slightly in different tissue types
| this is called heterogeneity
71
which cell is the main effector cell in allergies?
mast cell
72
give a difference between mast cells and basophils
mast cells are characterised by c-kit protein on their surface
73
what can mutation of c-kit proteins lead to?
cancer
| systemic mastocytosis
74
does IgE promote the compliment system?
no
75
what part of the antigen do antibodies bind to?
epitope
76
what does it mean that the antibodies are specific?
they only bind with the antigen which induced their synthesis
77
How many classes of antibodies are there? name them
```
5
IgG
IgA
IgM
IgD
IgE
```
78
which antibody can cross the placenta?
IgG
79
Which antibody is the predominant Ig in mucous secretion?
IgA
80
describe the structure of IgA
two molecules of basic units (dimers) linked by a joining (J) chain
81
describe the shape of IgM
pentamer shape (five units with lots of J chains)
82
which Ig can never cross the endothelium?
IgM, too big
83
which antibody mostly acts as a cell surface receptor on B cells for antigens?
IgD
84
which antibody's receptor is mostly expressed on basophils and mast cells?
IgE
85
which antibody is most associated with allergic reactions and parasitic infections?
IgE
86
what are cytokines?
proteins secreted to act as simulator or inhibitory signals between cells
87
what cells secrete cytokines?
immune cells and non-immune cells
88
what is a cytokine called if it is released from lymphocytes vs macrophages/monocytes?
lymphokines
| monokines
89
give 5 examples of cytokines
```
interferons
interkeukins
colony stimulating factor
tumour necrosis factors
chemokines
```
90
what do interferons do?
induce state of antiviral resistance in unaffected cells to limit spread of viral infection
91
how many types of interferons are there and where are they produced from?
3
IFN alpha and beta-produced by virus infected cells
IFN gamma- produced by activated T helper 1 cells
92
what do interleukins do?
cause cells to divide, differentiate and secrete factors
93
what is the difference between interleukin 1 and 2?
IL1- pro-inflammatory
| IL2- anti-inflammatory
94
what do colony stimulating factors do?
involved in directing the division and differentiation of bone marrow stem cells
95
what do tumour necrosis factors do?
mediate inflammation and cytotoxic reactions
96
what do chemokines do?
direct movement of leukocytes and other cells from blood to tissues or lymph nodes where infection or inflammation is occuring
97
where are chemokines produced?
site of inflammation/infection
98
what are some features all cytokines share? (4)
short half lives
rapid degradation
local action
may affect multiple organs
99
what are the two types of immunity we have?
innate and adaptive
100
give 10 features of the innate immune system
1. not specific
2. first line of defence
3. instinctive
4. primitive
5. independent of lymphocytes
6. provides barriers to antigens
7. doesn't have long lasting memory (only has evolutionary memory)
8. supplement to adaptive response
9. rapid response
10. can be evaded
101
give an example of an anatomical, physical, chemical and physiological barrier that the innate system provides
anatomical-skin
physical- mucociliary lining of resp tract
chemical- acidic stomach
physiological-temperature
102
what is PAMP and DAMP?
pathogen/ damage associated molecular patterns
103
describe the evolutionary memory of innate immunity
microorganisms have similar characteristics which are unchanging. infection is also associated with damage and trauma so through evolution and natural selection our immune system has memorised PAMP and DAMPs
104
what type of receptors does innate immunity use?
pattern recognition receptors
105
what do pattern recognition receptors detect?
all microbes that share a specific pattern or characteristic
106
what are the two divisions for pattern recognition receptors?
- secreted and circulate in the body
| - cell-associated
107
give four examples of types of secreted PRR
defensins
lectins
collectins
pentraxins
108
what are defensins?
antimicrobial peptides that are secreted in lining fluid from epithelium and phagocytes
109
what do lectins and collectins do?
they are carbohydrate-containing proteins that bind to carbohydrates or lipids in bacterial walls and can activate complements and improve phagocytosis
110
give an example of a lectin or collectin
mannose-binding lectin
111
what can pentraxins do?
activate complement and promote phagocytosis
112
give an example of a pentraxin
CRP
113
where are cell-associated PRR found?
cell membrane or cytosol of cell
114
what is the main family of cell-associated PRR?
Toll-like receptors
115
what do TLR1 and 2 recognise?
gram positive bacteria's lipopetides
116
what does TLR3 recognise (exogenous and endogenous)
exogenous-double stranded RNA
| endogenous- mRNA
117
what does TLR4 recognise (exogenous and endogenous)?
exogenous- viral proteins
| endogenous-heat shock proteins
118
what does TLR5 recognise?
flagellin of microorganism
119
what do TLR7 and 8 recognise?
single stranded RNA (exogenous)
120
what does TLR9 recognise?
endogenous DNA
121
what PRR are used for intracellular pathogens?
Nod like receptors
| Rig like receptors
122
what is PRR roles (3)?
recognition of PAMP recognition of DAMP
| haemostasis
123
how does PRR contribute to haemostasis
tlr4 signalling controls neutrophil numbers
| PRR can control number of commensal organsims
124
how does PRR contribute to damage recognition and repair?
PRR recognise substances not meant to be outside of their cell or in unfamiliar places so TLR activated
TLR activation can activate tissue repair
125
how does PRR contribute to adaptive immunity?
TLR can increase cytokine production by antigen presenting cells so increase t cell activation
126
give 5 features of adaptive immunity
1. specific
2. acquired
3. required immune recognition by lymphocytes
4. requires antibodies
5. has memory
127
why do we need adaptive immunity?
microbes can evade innate immunity
| we need memory for specific antigens so second response is faster
128
what are the two components of adaptive immunity?
```
cell mediated (t cells interacting with APC, MHC, antigens)
humoral (b cells)
```
129
what are three antigen presenting cells?
dendritic cells
macrophages
B cells
130
describe t cell selection, thymus tolerance
t cells that recognise and bind with low affinity to self-antigens are positively selected and mature
t cells that don't recognise self-antigens apoptosis occurs
t cells that are recognise and bind with high affinity to self-antigens are negatively selected and apoptosis occurs
131
what are the primary lymphoid organs?
thymus and bone marrow
132
what are secondary lymphoid organs?
those that have antigen reactive cells in the process of recirculating around the body
133
give three examples of secondary lymphoid organs?
lymph nodes
spleen
mucosa-associated lymphoid tissue
134
what is the difference between primary and secondary follicles in lymph nodes?
primary: B cells have more IgD and IgE
secondary: B cells have more IgG
135
how do primary follicles become secondary follicles in lymph nodes?
antigen challenged
136
how do antigens get presented?
antigen-presenting cell will phagocytose microbe. Antigen processed in golgi body to form complex with MHC. this complex goes to surface of APC.
137
how does a T cell interact with an APC?
T cell recognises antigen bound to MHC and binds.
| Co-stimulatory pathway also needed e.g. interleukin production
138
can antibodies be produced without an APC contributing? Why?
no, because for a T cell to recognise an antigen on a B cell it must have first bound to that antigen whilst it was on an APC
139
Which cell synthesises antibodies?
B cell
140
what is isotype switching?
B cell switch from making one type of antibody e.g. IgM, and make another e.g. IgG
141
What is required for isotype switching?
CD4 on B cell
CD4 ligand on activated T cell
interkeukin
142
How can a T cell recognise and activate a B cell for a specific antigen?
B cell must present antigen.
143
How does a B cell present an antigen?
```
IgM on B cell surface binds to antigen, internalises it.
antigen processed in golgi body to form complex with MHC class 2 that goes to surface.
```
144
What does the activation of B cells by T cells lead to the formation of?
```
Plasma cells (antibodies)
Memory cells
```
145
What are plasma cells?
B cells that all produce the same type of antibody for one specific antigen.
146
how are plasma cells made?
contact with antigen on surface of B cell and T cell and interleukin (produced by T cell)
147
What is the process called of making lots of memory and plasma cells?
clonal expansion
148
what can antibodies do to fight microbes?
neutralise toxins by binding to them
increase opsonisation so increase phagocytosis
activate complement cascade
149
what are the two ways of acquiring adaptive immunity?
passive and active immunity
150
what is passive immunity?
protection provided by transfer of antibodies from immune individuals to non-immune individuals
151
give three examples of passive immunity
across placenta/ via breast milk
transfusion of blood
injection of human immunoglobulin
152
give five infections that are protected against by antibodies that cross the placenta or enter individual via breast milk
```
tetanus
rubella
mumps
poliovirus
streptococcus
```
153
give three scenarios where passive immunity is provided
infection by toxins from tetatnus
infection from hepatitis, measles, rubella (antibodies given as prophylactic)
exposure to venom e.g. snake bite
154
what are two negative points to passive immunity?
protection temporary
| doesn't activate immunological memory
155
what is active immunity?
protection provided by an individual's own immune system
156
what substances are involved with active immunity?
cellular responses
| antibodies
157
give two benefits to active immunity
long-lasting protection
| immunological memory activated
158
what kind of immunity do vaccines provide?
active immunity
159
why do we use vaccinations to provide active immunity instead of natural infection?
vaccination provides similar immunity as infection naturally but without any risks from the actual disease
160
what are the first antibodies produced when first vaccinated? what are the second?
1. IgM
| 2. IgG
161
what can vaccinations be made from?
1. whole organism
2. subunits
3. recombinant components
162
what are the two ways of delivering whole organisms in vaccines?
inactivated/dead organism
| attenuated (altered so not harmful) live organism
163
what are the advantages of using inactivated whole organisms in vaccines?
no risk of infection
| less critical storage
164
what are the disadvantages of using inactivated whole organisms in vaccines?
lack of T cell involvement
| repeated booster needed
165
give three examples of vaccines that use inactivated whole organisms
cholera
hepatitis a
polio salk
166
what are the advantages of using whole attenuated live organisms in vaccines?
full natural immune response
prolonged contact with immune system
stimulates T and B cell memory
single immunisation needed
167
what are the disadvantages of using whole attenuated live organisms in vaccines?
immunosuppresed patients may become infected, attenuated can become virulent (harmful again), transport difficult because fridge needed
168
give four examples of vaccines that use whole attenuated live organisms
tuberculosis
measles
mumps
polio sabin
169
give four types of subunits that can be used in vaccines
secreted products from that organism e.g. exotoxins (heat treated toxins to remove toxicity)
antigenic extracts
capsular polysaccharide on cell wall
peptides
170
give advantages of using subunits in vaccines
safer than whole pathogen, no risk of infection, easy storage
171
give disadvantages of using subunits in vaccines
less powerful immunity, repeat vaccines needed, adjuvant needed
172
what are adjuvants
substances added to vaccines to stimulate immune system
173
give advantages of using recombinant components of organisms
create ideal, flexible, produces memory, safe in relation to live pathogen
174
give disadvantages of using recombinant components of organisms
requires fridge, can cause illness in immunosuppressed
175
why are booster vaccines needed?
some pathogens mutate regularly
some diseases have such rapid onset that even activated memory takes too long to be set off, so need constant high levels of antibodies
176
define allergy
abnormal response to harmless foreign material
177
what is allergy also known as
hypersensitivity
178
what is atopy?
hereditary tendency to develop immediate hypersensitive reaction against common environmental antigens.
179
What are the four things that are involved in allergic responses?
antibodies
genetics (immune and non-immune related genes)
cells
mediators
180
what is the main antibody involved in allergic reactions
IgE
| and IgG4, IgA
181
what cells are involved in allergic responses?
```
immune cells (mast cells, eosinophils, TH2, dendritic cells (APC))
non-immune (smooth muscle, fibroblasts, epithelia, neurons)
```
182
what makes a substance an allergen (4)
delivery of antigen (through respiratory system more likely to be allergen)
presence of PAMP
low doses makes substance allergen (high doses-desensitisation)
substance must induce TH2 formation
183
name the two types of receptors that IgE bind to
high affinity receptors (FcER1)
| low affinity receptors (FcER2)
184
where can high affinity receptors of IgE be found?
eosinophils, basophils, mast cells
185
what happens when IgE binds to a high affinity receptor on a mast cell?
more IgE will come and bind to the other receptors so that the mast cell becomes covered with IgE
186
What happens when an IgE (already bound to high affinity receptor via body) binds to an antigen
the high affinity receptors will cluster and receptor cross-linking will occur
187
what type of hypersensitivity reaction is the one mentioned of an antigen binding to an IgE bound to a mast cell?
type 1
188
describe type 1 hypersensitivity
immediate hypersensitivity due to antigen interacting with IgE bound to mast cell/basophil
OR
overproduction of IgE on mast cell/basophil
189
what happens after receptor cross-linking occurs?
cascade of signalling cellular events will be initiated which lead to degranulation
190
where are low affinity receptors found?
B cells, T cells, monocytes, eosinophils, platelets, neutrophils
191
what is FcER2 role?
regulate IgE synthesis
trigger cytokine release from monocytes
present antigens on cells
192
which IgE receptors mentioned don't cross-link?
FcER2 (low affinity receptors)
193
what are the three types of susbtances (or what event occurs) after/during granulation? and when are they released?
1. pre-formed compounds released (within seconds)
2. lipid derived mediators released (within minutes)
3. transcription/ translation occurs (within hours (of mast cell still alive and degranulating)
194
what are the four preformed compounds that are released from mast cells?
histamine
chemotactic factor
proteases
proteoglycans
195
what does histamine do?
lead to arteriole dilation
capillary leakage
bronchoconstriction
196
what do chemotactic factors do?
lead to eosinophil attraction and activation
197
give an example of two proteases released from mast cells during degranulation
tryptase
| chymase
198
give an example of a proteoglycan that is released from mast cells during degranulation
heparin
199
what do the proteoglycans do?
they were involved with the packaging of the granules
200
name three lipid derived mediators released from the mast cells during degranulation
leukotrienes
prostaglandin D2
platelet activating factor
201
what do leukotrienes do?
capillary endothelial contraction
| vascular leakage
202
what does prostaglandin D2 to?
smooth muscle contraction
203
what does platelet activating factor do?
increased platelet aggregation
degranulation
activation of neutrophil secretion
204
what is being transcribed, translated during the transcription event that occurs within hours of degranulation?
new proteins: forms of mediators to control wider immune system
cytokines (leads to more IgE so more mast cell activation)
205
what can activate mast cells?
indirect and direct activators
206
give three classes for indirect activators
allergens
bacterial/viral antigens
phagocytosis of enterobacteria
207
how do indirect activators work?
via IgE and high affinity receptors, prior sensitisation is required
208
give six examples of allergens
```
latex
wasp venom
foods
drugs
pollen
house dust mite faeces
```
209
give three examples of direct activators
cold/mechanical deformation
aspirin
preservatives
210
give three examples of allergic diseases
anaphylaxis
allergic asthma
allergic rhinitis hay fever
211
what happens during anaphylaxis
vasodialtion, low BP, bronchial constriction
rashes- urticarial
swelling- oedema because more vascular permeability
pain
vomiting
212
how many classes of hypersensitivity are there, name them
```
4
type 1: immediate hypersensitivity
type 2: antibody to cell-bound antigen
type 3: immune complex reaction
type 4: delayed hypersensitivity mediated by T cells
```
213
describe type 2 hypersensitivity
antibody to cell-bound antigen
antibodies bind to antigenic determinants on cell membrane
(e.g. drug incorporated into RBC so antibody binds to drug (so cell-bound antigen)) and causes bystander lysis (damage to RBC)
214
what type of hypersensitivity does autoimmunity use?
type 2
215
what antibodies are involved in type 2 hypersensitivity?
IgM and IgG
216
give an example of type 2 hypersensitivity
RBC in autoimmune haemolytic anaemia
217
describe type 3 hypersensitivity
immune complex reaction
| deposition of immune complexes (e.g. antigen-antibody complex) in tissues
218
give an example of type 3 hypersensitivity
nephritis
219
describe type 4 hypersensitivity
delayed hypersensitivity mediated by T cells
T cells sensitised to antigen during primary exposure and produce interleukin 2 etc. in secondary exposure there is a delay before action.
delay can be 2-3 days and involves inflammatory responses
220
give an example of type 4 hypersensitivity
contact dermatitis
221
what does immunodeficiency present as?
specific,
persistent,
unusual,
recurrent infection (SPUR)
222
what is the reason for immunodeficiency?
missing or reduced or malfunctioning vital parts of the immune system (specific and/or non-specific)
223
what are the two types of defects that can cause immunodeficiency
primary and secondary defects
224
what are primary defects due to?
intrinsic defects with immune system
225
what are the three types of primary defects?
primary antibody deficiencies
primary cell-mediated immunity defects
primary defects of phagocytic function
226
what is primary antibody deficiency?
defects in synthesis of all classes of antibodies or only in some (selective deficiency)
227
what signs will patients with primary antibody deficiency have? (4)
recurrent respiratory tract bacterial infections
skin sepsis -boils
gut infections
meningitis
228
what is the most common family that infects patients with primary antibody deficiency? give an example
pyogenic bacterial
| streptococcus pneumonia
229
why do viral/fungi infections not commonly occur with patients with primary antibody deficiency?
cell-mediated is fine
230
do primary cell-mediated immunity defects occur on its own?
mostly occurs with B cell defects because t cells needed to activate B cells
231
do primary phagocytic cell defects occur on their own?
antibody synthesis usually occurs too
| phagocytic cells are needed to removeantigen-antibody complexes
232
give an example of a disease that is caused by primary phagocytic defects. explain
chronic granulomatous disease
inability to produce radical oxygen species during phagocytosis
caused by staphylococcus aureus commonly
233
what causes secondary defects?
underlying conditions
234
what can the underlying conditions do to cause immunodeficiency
decreased production of vital parts of immune system
| increased loss of vital parts of immune system
235
give three examples of conditions that cause decreased production of vital parts of immune system
malnutrition (protein-energy malnutrition)
infections : HIV, measles, rubella
bone marrow infiltration
236
give three examples of conditions that cause increased loss of vital parts of immune system
nephrotic syndrome
protein-losing enteropathy
inflammatory disease- crohn's disease, ulcerative colitis
237
what is hypogammaglobulinemia?
reduction in antibodies
238
what is autoimmunity
immune response to self-antigens, breakdown of tolerance to self-antigens
239
what is autoimmune disease?
damage to tissues or disturbed physiological function after autoimmune response
240
what method does autoimmunity use to attack self-antigens
same as that for any immune response for non-self antigens
241
what are the two types of autoimmunity
organ specific
| non-organ specific
242
what is organ specific autoimmunity
restricted to a single organ, usually involved endocrine organs
243
what are the common antigens for organ specific autoimmunity
```
surface proteins e.g. hormone receptors
intracellular molecules (intracellular enzymes)
```
244
what is non-organ specific autoimmunity
involves auto-antigens widely distributed all around the body
245
what antigens are commonly used for non-organ specific autoimmunity
molecules invpolved in translation and transcription of DNA
246
what is t cell tolerance
down-regulation or removing T cells that react to self-antigens
247
what is thymus tolerance
positive and negative selection
248
why do we need periphery tolerance
because in thymus not all self-antigens are present to negatively select T cells against e.g. self-antigens in brain
249
how does periphery tolerance occur? (4)
1. some self-antigens in avascular areas away from immune cells
2. MHC2 needed for T cell recognising antigens so MHC2 presentation only occurs on antigen presenting cells
3. self-antigens kept away from antigen presenting cells by debris from cell death being cleared quickly
4. self-reactive T cells inhibited by T regulator cells
250
give three examples of autoimmune diseases?
multiple sclerosis
rheumatoid arthritis
insulin-dependent diabetes (type 1)
251
how fast does anaphylaxis occur and for how long
```
within minutes (or hours if allergen exposure via GI)
lasts 1-2 hours
```
252
what is anaphylactoid reactions?
non-immune anaphylaxis
| direct mast cell degranulation without previous exposure
