Week 10 Science and Scholarship: Immune System Flashcards
1
Q
name the 4 layers of immunity
A
static barriers
soluble barriers
cellular barriers
adaptive immunity
2
Q
what are static barriers
A
-continous barrier
-first layer of defence that consists of skin, mucosa, stomach acid, tears and microbiome
3
Q
what are soluble barriers
A
-work minutes/hours after exposure
-second layer of defence, consist of antimicrobial peptides, complements, opsonins and cytokines
4
Q
what are cellular barriers
A
-work minutes/hours after exposure
-third layer of defence, consist of macrophages, neutrophils, NKC’s, basophils and dendritic cells
5
Q
what is adaptive immunity
A
-works hours/days after exposure
-fourth layer of defence that consists of B and T cells
6
Q
Contrast innate vs adaptive immunity
A
-innate people are born with, adaptive people acquire
-innate is front line defence, adaptive develops later
-innate recognises common pathogens, adaptive recognises all pathogens
-innate has no memory, adaptive has memory
7
Q
name all the functions of the integumentary system
A
protection
immunity
sensation
thermoregulation
osmoregulation
Vitamin D production
8
Q
how does the integumentary system ‘protect’
A
protects the body from UV radiation, infection and physical injury
9
Q
how is the integumentary system involved with ‘immunity’
A
houses immune cells that help defend against pathogens and initiate immune responses
10
Q
how is the integumentary system involved with ‘sensation’
A
contains sensory receptors that allow us to detect temperature, touch, pressure and pain
11
Q
how is the integumentary system involved with ‘thermoregulation’
A
regulates body temperature via various mechanisms; sweating, vasodilation, vasoconstriction, shivering and
12
Q
how is the integumentary system involved with ‘osmoregulation’
A
helps maintain the balance of electrolytes and water in the body preventing dehydration or fluid overload
13
Q
how is the integumentary system involved with ‘Vitamin D production’
A
synthesis vitamin D when exposed to sunlight, aiding bone health and calcium absorption
14
Q
name components of integumentary system
A
skin
hair
sudoriferous and sebaceous glands
nails
15
Q
function of sweat and oil glands
A
-regulate body temperature
-antibacterial effects
-moisturise skin
16
Q
name the layers of skin
A
epidermis
dermis
hypodermis
17
Q
describe the epidermis
A
outermost layer that provides protection
-avascular
-renewed via epidermal turnover/desquamation
18
Q
describe the dermis
A
middle layer, contains CT and other structures (nerves, blood vessels, glands)
19
Q
describe the hypodermis
A
deepest layer, made of mainly fat tissue, proving insulation, connecting skin to underlying tissues and energy storage
20
Q
name the stratum of the epidermis
A
corneum
lucidium
granulosum
spinosum
basale
21
Q
describe corneum of epidermis
A
-ouermost layer
composed of dead keratinocytes
22
Q
describe lucidium of epidermis
A
thin, translucent layer that is only found in thick, hairless area eg palm
23
Q
describe the granulosum in epidermis
A
layer where keratinocytes begin to flatten and produce keratin
24
Q
describe spinosum in epidermis
A
layer in which keratinocytes increase in size and provide strength
25
describe basale in epidemris
deepest layer, site of rapid cell division
26
name the key cells of the epidermis
keratinocytes
langerhan cells
melanocytes
merkel cells
27
function of keratinocytes
epidermal cells that produces the protein keratin, which contribute to strength and water proofing skin
28
function of langerhan cells
specialised immune cells in the epidermis that play a role in antigen presentation and immune response activation
29
function of melanocytes
cells in the epidermis that produce the pigment melanin, responsible for skin, hair and eye colour as well as UV protection
30
function of merkel cells
specialised cells in epidermis that are involved in sensation, especially touch and pressure
31
whats keratinisation
-as keratinocytes migrate towards surface, keratin production increases, cells flatten and nuclei disappear
-this layer of keratinised cells forms the corneum
-keratin accumulates in cytoplasm and 'leaks' out surrounding corneum and providing protection
32
how long is the skin regeneration cycle
28 days
33
thick vs thin skin
-thick skin is found in areas of high friction and mechanical stress whereas thin skin is found everywhere else (more flexible)
-thick skin is has five epidermal layers (and a prominent lucidium) whereas thin skin has 4 layers (no lucidium)
-thick skin is hairless, thin is hairy
34
name the two layers of the dermis
papillary dermis
reticular dermis
35
describe papillary dermis
loose CT, allows for movement of molecules and exchange of waste/gases
36
describe reticular dermis
dense CT, thick collagen fibres and aids strength
37
name the accessory structures of the skin
nerves
hair follicles
sweat glands (merocrine)
sweat glands (apocrine)
38
function of nerves in skin
perceive stimuli and communicate with NS to maintain homeostasis
39
function of sweat glands (merocrine) in skin
secrete sweat onto body , glands are widely distributed
40
function of sweat glands (apocrine) in skin
secrete and move sweat through hair follicles (under armpits)
41
dermal blood vessels ___ to thermo (up) regulate
constrict
42
dermal blood vessels ___ to thermo (down) regulate
dilate
43
describe blood flow to achieve thermo (up) regulation
directed to deep regions
44
describe blood flow to achieve thermo (down) regulation
directed to superficial regions
45
arrestor pili muscle ___ to achieve thermo (up) regulation
contract (goosebumps)
46
arrestor pili muscle ___ to achieve thermo (down) regulation
expand/relax
47
how do antimicrobial peptides work
-for example defensins, are cationic proteins that disrupt bacterial cell membrane integrity or cell anabolism
-their positive charge allows them to bind to the negatively charged membranes of bacteria
-do not bind to mammalian membranes t/f ensuring they only target microbial invaders
48
what are complement pathways
a group of soluble factors that play a vital role in the immune response ; eliminate pathogens, enhance inflammation, promote clearance of cellular debris
49
name the different complement pathways
classical pathway
lectin pathway
alternative pathway
50
how does the classical complement pathway work
-initiated when antibodies bind to antigens on surface of pathogens
-leads to a series of enzymatic reactions, forming C3 convertase enzyme
-this enzyme cleaves the C3 protein to C3a and C3b fragments, initiating downstream complement events
-C3b acts as an opsonin, tagging pathogens for for recognition and phagocytosis
-also the membrane attack complex (MAC) lyses the pathogen
51
how does the alternative complement pathway work
-inititated when C3 is hydrolysed in the absence of specific antibodies or lectins
-C3 enzyme converts forms , initiating downstream complement events
-opsonisation, inflammation and pathogen lysis occurs
52
how does lectin complement pathway get initiated
lectin binds mannose (sugar) on pathogen
53
whats haematopoisesis
-the making of blood cells
-two lineages: myeloid and lymphoid
54
name the cells that a haematopoietic stem cell can differentiate into
B naive cell
CD8+ T cell
CD4+ T cell
natural killer cell
55
what is a B naive cell
differentiates in the bone marrow and expresses a B surface cell receptor
56
whats a CD8+ T cell
differentiates in the thymus and expresses a T surface cell receptor
57
whats a CD4+ T cell
differentiates in the thymus and expresses a T surface cell receptor
58
whats a natural killer cell
differentiates in the thymus, expresses no surface cell receptor, contains granules that enable cellular death against viral cells or tumours
59
what are the primary lymphoid organs
-it is where lymphocytes undergo synthesis
-the thymus and bone marrow
60
where does B cell ontogeny occur
bone marrow
61
where does T cell ontogeny occur
begins in bone marrow but concludes in thymus
62
where does fluid transfer from blood into tissue
capillaries and post capillary section
63
name secondary lymphoid organs
spleen and lymph nodes
64
function of bone marrow
production of B cells and T cells
-educates B cells and neutrophils, monocytes, eosinophils, and NKC's
65
function of thymus
maturation and education of T cells
66
function of lymph nodes
-filters lymph fluid,
-detects and eliminates foreign substances, filters tissue-borne antigens
-stores immune cells (B,T etc) for surveillance
67
function of spleen
-filters blood
-removes old or damaged RBC's
-reservoir for immune cells eg lymphocytes
-filters tissue-borne antigens
68
name the structural features that comprise the lymph node
-cortex and paracortex
-follicles
-medulla
-sinus
-antibodies
-afferent vessel
-efferent vessel
-trabecula
69
function of cortex and paracortex in lymph node
-cortex contains B cells and paracortex contains T cells
-facilitating the interaction between immune cells and the initiation of immune responses within the lymph nodes
70
function of follicles in lymph node
-areas in the cortex where B cells proliferate and produce antibodies as part of adaptive immune system
71
function of medulla in lymph node
-contains plasma cells that produce antibodies
-contains macrophages that phagocytose pathogens and cellular debris
72
function of sinus in lymph node
-spaces in lymph node where lymph circulates and immune cells meet antigens carried by lymph
-allows for immune surveillance and response
73
function of antibodies in lymph node
-produces by B cells, specifically target and neutralise pathogens, aiding immune response
74
function of afferent vessel in lymph node
bring lymph (along with pathogens and antigens) to lymph node for filtration and initiation of immune response
75
function of efferent vessel in lymph node
carry filtered lymph (along with immune cells and antibodies) to other parts of body
76
function of trabecula in lymph node
-fibrous CT partitions within lymph nodes
-provide structural support and contain blood vessels that supply nutrients to lymph node
77
what are cytokines
intercellular communicators,
-small proteins that are secreted to communicate with cells.
78
name the effects of cytokines
autocrine, paracrine, endocrine
79
name the cytokine classes
interleukins
interferons
chemokines
tumour necrosis factors
80
describe role of interleukins
-proteins produced by cells in response to viral infection or other immune stimuli
-involved in inhibiting viral replication and modulating immune response
81
describe role of interferons
-group of cytokines produced by various immune cells
-act as signalling molecules to regulate immune responses and allow communication between cells
82
describe role off chemokines
-small proteins that help recruit and guide immune cells to specific locations by attracting and directing their movement
83
describe role of tumour necrosis factors
-pro inflammatory cytokine that is involved in inflammation, cell death, immune system regulation in response to tumour development and infections
84
foul tasting/smelly mucous is indicative of
bronchiectasis
85
pink/frothy mucous is indicative of
pulmonary oedema
86
haemoptysis is indicative of
TB
lung cancer
pulmonary embolism
87
chest pain (irritation of parietal pleura) indicates
lobar pneumonia
pneumothorax
pulmonary embolism
88
voice hoarseness is indicative of
upper airway problems eg laryngitis, vocal cord tumours
89
fever is indicative of
viral/ bacterial infection
90
weight loss/ night sweats are indicative of
cancer/ infection
91
smoking is indicative of
COPD, emphysema, lung cancer
92
asthma can be indicative of
atopic triad (eczema, hay fever-allergic rhinitis)
93
wheezing indicative of
asthma,COPD
94
what can recent travel be indicative of
long flights/ immobilisation be indicative of pulmonary embolism, infections eg TB
95
chronic cough, chest pain radiating to throat and burning indicates
acid reflux
96
voice hoarseness, throat clearing cough and sore throat indicative of
post nasal drip
97
painful, persistent acute cough with voice hoarseness indicates
laryngitis
98
painful, persistent intense cough with stridor indicates
pertussis
99
cough, wheeze and rapid dyspnoea indicates
asthma
100
cough, wheeze and moderate dyspnoea indicates
tracheatis
101
cough, wheeze and long term dyspnoea that worsens in morning indicates
COPD
102
cough, wheeze and long term dyspnoea that has massive bleeding indicates
bronchial malignancy
103
cough with purulent (green sputum) and recent onset indicates
pneumonia
104
cough with purulent (green sputum), blood and fever indicates indicates
TB
105
cough with purulent (green sputum), blood and dyspnoea indicates
bronchiectasis
106
pink frothy sputum and cough indicates
pulmonary oedema
107
taking ACE inhibitors can be indicative of
dry scratchy, persistent and chronic cough
-normally has hypertension
108
worsening chronic cough and worsening dyspnoea indicates
interstitial lung disease
109
chest pain under breastbone indicates
pulmonary embolism
110
chest pain radiating on ipsilateral side indicates
pneumothorax
111
what is the significance of MHC markers
-T cells cannot recognise antigens in their natural form
-natural antigens are in the form of folded polypeptides, these are cleaved into shorter peptides, the peptides are presented on MHC molecules
t/f T cells can recognise the antigen
112
CD8 cells recognise which MHC marker
MHC class 1
113
CD4 cells recognise which MHC marker
MHC class 2
114
how do MHC class I present
presents endogenous peptides
115
how do MHC class II present
presents exogenous peptides
116
Describe antigen processing (MHC I)
-endogenous protein is synthesised within the body
-protein is digested into short peptides (8-10 AA)
-peptides enter the rough ER
-peptides are loaded onto MHC I
-MHC I are exported to surface via vesicular transport
-MHC I is expressed on a nucleated cell
117
Describe antigen processing (MHC II)
-exogenous proteins are taken up via pinocytosis, endocytosis or phagocytosis
-exogenous antigen is digested in the endosome by lysosomes
-MHC II travels from rough ER into endosome
-peptide loaded onto MHC II
-MHC II expressed on APC
118
How are intracellular pathogens/tumours managed by MHC
-CD8+ T cells are activated
-MHC I is activated
-T cytotoxic cell (Tc) is produced and apoptosis occurs
119
How are extracellular pathogens managed by MHC
-CD4+ T cells are activated
-MHC II is activated
-T helper (Th) is produced and phagocytosis occurs
120
what is immunoglobulin (Ig)
refers to the structure of a molecule
-Ig has a heavy and light chain
-Y shaped glycoproteins
-4 PP chains held by 4 disulphide bonds
-A.B.S
121
what does antibody (Ab) mean
refers to the function of a molecule
122
name the Ig isotopes
IgM,IgA,IgD,IgG,IgE (MADGE)
123
IgM
*structure
*# binding sites
*binding location
pentameric
10 binding sites
blood; tissue
124
IgA
*structure
*# binding sites
*binding location
Dimeric
4 binding sites
mucosa
125
IgD
*structure
*# binding sites
*binding location
monomeric
2 binding sites
blood; tissue
126
IgG
*structure
*# binding sites
*binding location
monomeric
2 binding sites
blood (neutrophil); tissue
127
IgE
*structure
*# binding sites
*binding location
monomeric/dimeric
2 binding sites
mucosa, GI tract and respiratory tract
128
whats an antigen
substance, usually a protein or carbohydrate that is capable of stimulating an immune response in the body
129
name the ways antibodies can act
neutralisation
agglutination
opsonisation
complement protein activation
(ACON)
130
how do antibodies 'neutralise'
antibody binds to the antigen, prevents antigen binding to body cells
131
how do antibodies 'agglutinate'
arms of antibodies bind to antigens, prevents colonisation
132
how do antibodies 'opsonise'
antigen recognises opsonin receptor and enhances phagocytosis
133
why do antibodies activate complement proteins
works in classical pathway, C3b deposition, forms membrane attack complex and cell death occurs
134
Describe humoral antibody response
-naive B cell sitting in secondary lymphoid tissue (lymph node)
-when antigen drains into lymph node it recognises a s+c naive B cell
-naive B cell is activated and proliferates to create a clone of itself
-proliferated B cell divides into plasma and memory cells
-plasma cells secrete IgM and memory cells secrete IgG
135
list the cells produced to ultimately form B memory cells
naive B cells -recognise
mature B cell-activate
mature B cells-proliferate
Plasma cells or memory cells-differentiate
136
Outline steps of primary immune response
1.lag period:first B cell must find its antigen after exposure
2.initial spike of IgM antibodies:plasma cell (IgM) production increases
3.following rise in IgG antibodies: memory B cell (IgG) production increases
4.IgM and IgG antibodies have achieved their function t/f concentrations decrease
137
Outline steps of secondary immune response
1.reduced lag period due to more cloned B memory cells to recognise antigen
2.initial spike of IgG due to B memory cells
3.spike of IgM due to plasma cells (immune response)
4.more B memory cells for priming future exposures
138
list the clinical relevances of B cells
-autoimmune disorders
-allergies
-B cell malignancies
139
how are autoimmune disorders linked to the clinical relevance of B cells
B cells can produce autoantibodies that mistakenly target and attack the body's own tissues leading to autoimmune disorders. eg RA, MS
140
how are allergies linked to the clinical relevance of B cells
B cells can be activated by allergens, leading to production of IgE antibodies, histamine is released and allergic symptoms occur
141
how are B cell malignancies linked to the clinical relevance of B cells
abnormal proliferation or dysfunction of B cells can lead to development of B cell lymphomas
142
name the ways B cells can be modulated
stem cell transplantation
therapeutic vaccines
143
how can stem cell transplantation be used to modulate B cells
in some cases, stem cells transplantation can be used to replace abnormal or dysfunctional immune cells with healthy cells
144
how can therapeutic vaccines be used to modulate B cells
vaccines can be designed to target specific antigens associated with diseases involving B cells, such as cancers, vaccines aim to stimulate an immune response against diseased cells
145
Outline the development of T cells
-early phase in the thymus
-production in bone marrow
-completion of development in thymus
-CD4+ and CD8+ T cells produced + migrate to lymph nodes
146
how are T cells activated
-T cells meet processed antigens (via MHC II) in lymphoid tissue
-naive T cells activated and differentiate
-MHC II allows for the antigen recognition by T cells
-clonal selection and expansion occurs
-T helper (CD4+)/T cytotoxic(CD8+) and T memory produced
147
Explain the processes involved in cell-mediated immunity in the adaptive immune response
1.APC's ingest pathogens and present them on cell via MHC
2.naive T cells recognise MHC via TCR's and co-stimulatory signals (become activated)
3.T cell undergoes clonal expansion
4.T cells differentiate into Tc cells, Th cells, Treg cells
5.effector T cells migrate to site of infection via chemotaxis guided by chemokine
6.Tc cells recognise and bind to infected cells that display antigen on MHC I
7.Tc cells release cytotoxic chemical eg perforins that lead to apoptosis of infected cell
8.Th cells release cytokines to amplify immune response, attract macrophages, activate B cells
9.some T cells divide into T memory cells for long term immunity
10. Tregs suppress excessive immune response, prevent autoimmunity and maintain homeostasis
148
list the clinical relevances of T cells
autoimmune disease
infectious diseases
transplant rejection
149
how are autoimmune diseases linked to the clinical relevancies of T cells
T cells mistakenly recognise self cells as foreign leading to responses against body cells
150
how are infectious diseases linked to the clinical relevancies of T cells
T cells are essential in responding to viral, fungal and bacterial infections, understanding them can aid drug and vaccine development
151
how are transplant rejections linked to the clinical relevancies of T cells
T cells are involved in allograft rejection, where the recipients immune system recognises organ as foreign and rejects it
152
name the way T cells can be modulated
cytokine therapies
T cell engineering
immune checkpoint inhibitors
153
how can cytokine therapies be used to modulate T cells
administration of cytokines eg interferons or interleukins modulates T cells and enhances there immunity against specific diseases
154
how can T cell engineering be used to modulate T cells
techniques like CAR T cell therapy, involves modifying patients T cells to express specific receptors against tumour antigens, enhancing anti cancer activity
155
how can immune checkpoint inhibitors be used to modulate T cells
drugs that block inhibitory receptors on T cells unleash their anti tumour responses by relieving immune suppression t/f enhance T cell activity against cancer cells
156
what is vaccination
the uptake of injection (orally or injection)
157
what is immunisation
process of getting the vaccine and subsequently getting immune to the disease
158
whats a vaccine
weak form (attenuated) or part of (protein or nucleic acid) an infectious agent
159
describe vaccination action
-they must activate CD4+ cells in the adaptive immune system by first passing the static, soluble and cellular barriers of innate system
160
function of MALT
filters mucosa-borne antigens
161
is natural immunity or vaccination preferred
natural immunity
162
name the vaccine types
live
inactivated
purified subunit
cloned
163
define live vaccine and give an example
antigen microbes are grown repeatedly in cell culture eg.mumps
164
define inactivated vaccine and give an example
antigen microbes are inactivated, exposed to heat, chemicals or radiation eg influenza
-HI only
165
define purified subunits vaccine and give an example
components of the microbe are isolated and proteins (+polysaccharide) are administered eg tetanus
-HI only
166
define cloned vaccine and give an example
genetic material of antigen is isolated and recombinant DNA is administered eg COVID 19
-HI only
167
attenuated and mRNA vaccines differ to other vaccines because
they can enter the host cell t/f stimulates cell mediated and humoral response
-can undergo reversion
-only need one dose
168
Describe vaccination action
-first exposure
1.the vaccine is introduced to the body and injected under the skin
2.the vaccine is taken up and digested by DC, Toll-like receptors on surface of DC facilitate relocation to secondary lymphoid organs
3.vaccine is processed and presented on MHC II to naive CD4+ cell
4."line up" of CD4+ cells to find a complementary match
5.activation, proliferation and differentiation into Th cell
6.Th cells activate a B cell that recognises the vaccine
7.B cell activates, proliferates and differentiates, into IgM plasma cell, IgG memory cells
8.clones of B memory cells that can recognise infectious agents
169
Describe vaccination action
-second exposure
1.antigen is presented on MHC II, proliferation of B cell begins
2.surplus of B cells differentiate into IgM secreting plasma cells and IgG secreting memory cells (tops up memory)
170
whats an adjuvant
substance that enhances immune response in non living vaccines, act like a depot for slow vaccine release to prime immune response
171
what is passive immunity
transfer of ready made antibodies From one person to another
172
name the general steps of inflammation
initial insult
inflammation
inflammatory mediators
demolition, repair and result
173
name the types of inflammation
chronic and acute
174
Contrast acute vs chronic inflammation
-acute is an early response vs chronic is a later response
-acute inflammation is short vs chronic is long
-acute inflammation involves neutrophil, fibrin and oedematous exudate vs chronic involves macrophages, lymphocytes, plasma cells and fibrosis/scars
-acute is non specific vs chronic can be specific or non specific
175
what is acute inflammation
-occurs directly following insult/injury
-aims to deliver nutrients, defence cells, remove debris and destroy infections
176
what can acute inflammation lead to
resolution, repair or chronic inflammation
177
name the effects of acute inflammation
redness
heat
pain
swelling
loss of function
malaise
myalgia
leukocytosis
178
describe redness in inflammation
vasodilation and increased blood flow (hyperaemia)
179
describe heat in inflammation
heat released by hyperaemia
180
describe pain in inflammation
pressure effects on nerve endings and chemical factors eg prostaglandin
181
describe swelling in inflammation
accumulation of exudate and hyperaemia
182
describe function loss in inflammation
direct local damage and various factors eg swelling
183
describe malaise in inflammation
general feeling of unwellness
184
describe myalgia in inflammation
muscle aches and pains particularly in joints (arthralgia)
185
describe leukocytosis (WBC+) in inflammation
neutrophils in acute inflammation and macrophages in viral infection.
186
Outline sytsematic steps in acute inflammation
1. break in skin/injury introduces bacteria
2. macrophages engulf the pathogen and release chemotaxins (cytokine)
3. mast cells activated, release histamine
4. histamine dilates local blood vessels and widens capillary pores, some cytokines cause neutrophils and monocytes to stick to blood vessel wall
5. chemotaxins attract neutrophils and monocytes, increased leakiness moves exudate to site of injury
6. macrophages and neutrophils destroy bacteria
## Footnote
pain and swelling occur due to exudate itself
187
role of neutrophils
-respond most to bacterial infection
-phagocytotic
-destroy bacteria
-release free radicals
-release lysosomal digestive enzymes
188
role of monocytes
-leave circulation at site of inflammation
-phagocytose tissue debris and pathogens
-initiate immune response
189
role of macrophages
specialised functions eg dust cells, osteoclasts
-long living
190
whats exudate
-protein rich mixture of fluid and cellular debris that has escaped from blood vessels due to increased permeability of blood vessels
191
name the components of exudate
-plasma proteins
-inflammatory cells
-fluid/electrolytes
-cytokines
-enzymes
192
role of plasma proteins in inflammation
-eg fibrinogens, complements and immunoglobulins
involved in immune response
193
role of inflammatory cells in inflammation
-neutrophils, monocytes and macrophages
-involved in immune response
194
role of fluid/electrolytes in inflammation
provides nutrients for inflammation eg water, potassium, sodium and chloride
195
role of cytokines in inflammation
mediate inflammatory responses eg chemokine, interleukins, TNF
196
role of enzymes in inflammation
catalyse tissue repair and remodelling
197
name the systemic effects of chronic inflammation
arthralgia,myalgia
anxiety
depression
fever
mood disorders
leukopenia
chronic fatigue/insomnia
GI complications
weight gain/loss
frequent injections
198
whats chronic inflammation
-mononuclear cell infiltration (macrophages, lymphocytes and plasma cells
-tissue destruction
-fibrosis and angiogenesis to replace damaged CT
199
name the cells in chronic inflammation
-lymphocytes
-plasma cells
-fibroblasts
-endothelial cells
-eosinophils
200
lymphocyte role in chronic inflammation
release cytokines to activate macrophages, persistent + feedback loop until homeostasis
201
plasma cells role in chronic inflammation
B cells mediated by Th cells release antibodies
202
fibroblast role in chronic inflammation
produce and secrete components of the ECM, for immune response and healing
203
endothelial cells role in chronic inflammation
angiogenesis
204
eosinophil role in chronic inflammation
abundant in IgE responses (allergies); granules contain toxic components (they mediate them)
205
name stages of wound healing
reactive
reparative
remodeling
206
what happens in reactive stage of wound healing
-haemostasis
-inflammation:redness, heat, pain, swelling
-immune cell action
207
what happens in reparative stage of wound healing
-Granulation tissue formation
-angiogenesis
-epithelialisation
-contraction
208
what happens in remodelling stage of wound healing
-maturation of scar tissue
-scar formation
-continual vascular and cellular changes
209
primary vs secondary intention healing
-primary occurs in clean, well edged wounds vs secondary occurs in large, deep wounds
-primary the gap can be closed vs secondary has larger gap
-primary heals sequentially and systemically vs secondary heals bottom to top
-primary has smaller inflammatory response vs second has large and profound one
-primary is less complex and easy to manage vs secondary is complex and hard to manage
210
name the components of granulation tissue
fibroblasts
capillaries
ECM
inflammatory cells
myofibroblasts
211
what is hypersensitivity
reactions that are exaggerated/inappropriate response to antigens that leads to over inflammation and destruction of innocent cells
212
how many hypersensitivity reactions is there
4
213
Outline type I hypersensitivity
-'immediate'
-2 to 30 minute symptom onset
-allergen is the antigen
-IgE isotope
-effector is mast cell
-pathology eg is asthma
214
Outline type IV hypersensitivity
-'delayed type'
-more than 72h symptom onset
-antigen is haptens;bacteria
-no Ig isotope
-effector is T cell; macrophage
-pathology eg is dementia
215
Explain the concept of immunological tolerance
Each T cell receptor and B cell receptor is unique in that the portion that recognises the shape of the antigen is different, the shape to recognise the antigen is randomly generated because of this some TCR and BCR can be complementary and bind to self antigens
216
what is caused by a breach of tolerance to self
autoimmune diseases
217
what is the self antigen and immune effector for type 1 diabetes
self antigen=beta pancreatic cells
immune effector=auto antibodies and Th cells
218
what is the self antigen and immune effector for myasthenia gravis
self antigen=Ach receptors
immune effector=blocking auto antibodies
219
what is the self antigen and immune effector for multiple sclerosis
self antigen=brain white matter
immune effector=Th cells, Tc cells, auto antibodies
220
what is the self antigen and immune effector for rheumatoid arthritis
self antigen=CT,IgG
immune effector=auto antibodies
221
what is the self antigen and immune effector for sytemic lupus erythmatosus
self antigen=DNA, erythrocytes
immune effector=auto antibodies
222
