Terms that are stoopid Flashcards
(112 cards)
1
Q
MHC class 1
A
- Major Histocompatability complex class 1
- Is an antigen
- Recognised on tumour cells by CD8+
2
Q
MHC class 2
A
- Present processed antigens to CD4+ Tcells
- Critical for initiation of antigen-specific imune response
3
Q
MIC-A, MIC-B, ULB
A
- Ligands (proteins) used to activate NKG2D receptors on NK cells, reactivating them
4
Q
IFN-Y, IL-15/12
A
- Cytokines (cytotoxic factors) that activate NK cells, increasing tumoricidal capacity
- Produced by tumour specific T-cells
5
Q
LAK
A
- Lymphokine activated killer cells
- Activated by IL-2
6
Q
TH1 cells
A
- Secrete IFN-Y in response to intracellular infection or tumor
- also produce IL-2 and TNF
- Activate macrophages and ingest and destroy microbes
7
Q
M1 and M2 macrophages
A
- IFN-Y can differentiate macrophages into M1 type and promote inflamation by secreting pro-inflamatory cytokines (IL6,12 and TNF-Alpha) (THESE BADBOIS KILL TUMORS)
- IL-4 (produced by TH2 cells) can convert macrophages into M2 type macrophages that inhibit inflamation (CAN PROMOTE TUMOR GROWTH - SECRETE VEGF and TGF-B)
8
Q
Cyclin dependent kinase 4, B-Catenin, Caspase-8, MAGE-1/3
A
TUMOR ANTIGENS
9
Q
APC
A
- Antigen presenting cell
- Can activate OR inhibit T-cells
- inhibiting could be PD-L1 released onto PD-1 receptor
- activating could be CD40 onto CD40L
10
Q
Antigenicity
A
- Capability of antigen to bind to T and B cells
- increased antigenicity = more antigens on tumor = better outcome
11
Q
Neoantigen
A
Antigen newly formed due to mutation - a peptide brought about due to mutation
12
Q
CTL
A
Cytotoxic Lymphocytes - Also known as CD8+ cells
13
Q
Epitope
A
Epitope
14
Q
HLA
A
Human Leukocyte Antigen - Protein marker on most cells of body: used to recognise which cells belong to your body and which cells do not
15
Q
MDSC
A
- Myeloid Derived Supressor cell
- possess strong immunosupressive activities
- Facilitate angiogenesis
- Drive tumor invasion and metastases
(NOT ALL BAD THOUGH - Can lower BSL, Reduce insulin tolerance and increase maternal-foetal tolerance and embryo implantation)
16
Q
CD4+ vs CD8+
A
- CD4+ = T Helper cells = Lead the fight against infection
- CD8+ = Cytotoxic T cells = Kill cancer cells
17
Q
Treg cell
A
- T-Regulatory cells = Suppress the immune response
- Patients with tumours = Higher Treg cell presentation
18
Q
EGFR
A
Epidermal Growth Factor
19
Q
Immunogenic
A
Ability to mount an immune response
20
Q
CTLA-4
A
a receptor which downregulates the immune response when activated
21
Q
PD-1
A
“programmed cell death protein-1”
a receptor found on T-cells which downregulates the immune response when activated (suppresses T cell)
22
Q
PD-L1
A
- a ligand binding to PD-1 receptor
- B7 family protein
- expressed on many tumors and APC’s
23
Q
TGF-B
A
- Transforming Growth Factor Beta
- Cytokine
- Inhibits proliferation and induces apoptosis
24
Q
CAR genes
A
Genes for “recombinant Chimeric Antigen Receptors” on T cells
They are composed of receptor domains specific for tumor antigens & signaling domains (ie. ITAMS, these promote robust T cell activation)
25
what ligand binds to:
a. ) CTLA4
b. ) PDL1 (this can be receptor somehow)
c. ) PD1
a. ) CD80, CD86
b. ) CD80
c. ) PDL1, PDL2
these all cause inhibition T cell
(this is all that Mauro said to know for this big slide)
26
activated T cell makes ___ which increases PD-L1 expression, in effort to regulate immune system
IFN-Y
27
state a type of anti-CTLA4 antibody?
ipillimumab, or Nivolamb
28
state a type of anti-PDL1 antibody?
Pembrolizumab
29
MMP
- Matrix Metallo-Proteinases (MMP)
| - Tumors use this substance to degrade the ECM
30
4 Most common destinations for tumor metastases
lung, liver, lymph nodes, bone
31
COX2
tumor cells have lots of an enzyme called COX2, COX2 produces prostalgandin-E2, which promotes inflammation
(note: PgE2 also inactivates T cells)
32
abscopal effect
- Phenomenon within treatment of metastatic cancer where localized treatment of tumor causes shrinkage of not only this tumor, but also tumors in different compartments around the tumor
- Usually applies to single-tumor with localised ratiation therapy
- Occurs extremely rarely
33
Where are the most microbes in our immune system found?
- Mostly in large intestine, but different groups of microbes prefer different areas
34
Autoimmune disease examples
rheumatoid arthritis, lupus, celiac, diabetes
35
3 events of immunoservailance
Escape, Equilibration, Elimination
36
IHD
Ischaemic heart disease
| - Most common end result = Heart Failure
37
Stenosis
narrowing of passage
38
Angina
Chest Pain
39
AMI
- Acute Myocardial Infarction (AKA A DAMN HEART ATTACK)
- reduction in coronary artery blood supply leading to formation of necrotic myocardium - reduction may be sudden, absolute or relative
- Caused usually by thrombosis or hemorrhage within atheromatous plaque in a coronary artery
- Symptoms: Chest pain, Nausea/vommiting, Profuse sweating
40
IHD and AMI (their relationship)
Atherosclerosis causes IHD which causes AMI
41
coronary artery anastomoses
Only in intramural part! (mural means 'wall', thus within heart wall only not major CA's)
42
mural thrombosis
many layers of thrombosis in infarcted area "The formation of an abnormal endothelial surface following infarction, occurring in interval of 1 week or more" - google
43
CHID
Chronic Ischemic Heart Disease
| - Symptoms: Angina (during exercise), Impaired ventricular function
44
SADS
Sudden adult (arrhythmic) death syndrome
45
heart failure
General term used to describe the end-result of various types of cardiac dysfunction leading to inadequate perfusion of heart tissue
- Prognosis = Roughly 3 years to live
46
Cor pulmonale
- AKA: right sided Heart Failure
| - alteration in structure and function of right ventricle
47
dysponea
shortness of breath (SOB)
| - First symptom of Heart Failure
48
orthopnea
shortness of breath whilst supine - caused by increased VR to lungs in this position
49
paroxysmal nocturnal dysponea
sudden urgent SOB during sleep
50
CAD
coronary artery disease
51
NO
most common endothelium-dependent relaxing factor for the dilation of coronaries
(so drug, ie. ACh --> effects NO in wall --> dilation)
- Produced by endothelial cells (Type III NO snythase)
52
resistance arteries
arterioles; small diameter BV's
53
EDHF
Endothelium dependent hyperpolarisation factor
- Hyperpolariszes vascular smooth muscle causing dilation
- Produced from endothelium
- Opens calcium dependant potassium channels
54
Prostacyclin and Prostaglandins
Vasodilates coronaries
55
aneurysm
Excessive localised swelling in the wall of an artery
56
hypertension
Hypertension or elevated blood pressure is a sustained increase in the pressure exerted on vessel walls during the heart's normal contraction and relaxation
57
claudication
Pain in the body, most commonly the legs due to lack f blood supply, typically indicative of peripheral vascular disease.
58
arteriosclerosis vs atherosclerosis
arteriosclerosis: Degenerative thickening of the arteries, making them less elastic
atherosclerosis: Deposition of material in the vessel wall leading to plaque formation
59
atheroma
Accumulation of lipid in the intima of the blood vessel
| - Leads to formation of plaque
60
oxidative modification hypothesis
The current oxidative modification or stress hypothesis of atherosclerosis predicts that LDL oxidation is an early, essential event in atherosclerosis and that Ox-LDL does contribute to both initiation and progression of atherosclerosis.
61
unstable angina
Chest pain due to poor blood flow and oxygen to the heart. Without treatment can lead to heart attack
62
OSA
Obstructive Sleep Apnea:
- occurs due to collapsed airway
- causes loud snoring, breathing ceases periodically
- linked to CVS disease
63
Kupffer cells
Liver macrophages
64
Humoral Immunity
- occurs within body humor (fluid)
- innate and adaptive
- mediated by soluble (cell-free) proteins (antibodies) in plasma/ interstitial fluids and mucosal secretions
65
cellular immune response
- innate and adaptive
- mediated by cells of immune system
- particularly effective against intra-cellular pathogens
66
MAC
Membrane attack complex
67
Complement System
- Proteins made in liver
- Is antibody mediated
1. Lyse bacteria by forming MAC.
2. Tag pathogens - enhancing recognition and destruction by phagocytes (opsonization)
3. Activate inflammatory response by triggering release of histamine from mast cells.
4. Enhance clearance of antigen-antibody complexes.
68
Naive mature B
Upon exposure to antigen, a niave mature B cell will differentiate into either a plasma B cell or a memory B cell
69
plasma cell
Produce & secrete antibodies
70
Which are the certain immunoglobins that require the help of T cells
IgG, IgA, IgE
71
Which immunoglobin can be produced by B cells independent of T cell help?
IgM
72
Long lived memory B cells produce which immunoglobins?
| Do these require T cell help for manufacture?
IgG, IgA, IgE, these all require T cell help for manufacture
73
Short lived memory B cells produce which immunoglobins?
| Do these require T cell help for manufacture?
IgM, this does not require T cell help
74
IgD
Primary B cell receptor
75
IgM
- Primary B cell receptor
| - Agglutination
76
IgG3
Broad complement cell activation
77
IgG1
Broad complement cell activation
78
IgA1
Mucosal antibodies
79
IgG2
Opsonophagocytosis complex antigens
80
IgE
Activation of mast cells and eosinophils
81
chemotaxis
movement of an organism in response to a chemical stimulus
82
phagocytic cells
1. Neutrophils
2. Dendritic cells (conventional, plasmacytoid)
3. Macrophages
4. Monocytes
83
Lysosome vs Peroxisome
- Peroxisome = used for breaking down hydrogen peroxide, large chain fatty acids, forming bile acids and controlling free radicals
- Lysomes are simps
84
Plasmacytoid dendritic cells (what they make?)
Production of type 1 interferons
85
primary lymphoid tissue
bone marrow, thymus
86
secondary lymphoid tissue
lymph nodes, spleen
87
apoptosis
programmed cell death
88
TH1 and TH2
TH1 - Type IV hypersensitivity. Macrophage activation, inflamation (mauro said Cytotoxic)
TH2- Type I, II, III Hypersensitivity (Allergic and helminth responses) (helps B-cells)
89
Type I
Immediate hypersensitivity:
- mediated IgE, mast cells involved
- reaction occurs within 30 mins exposure
90
Type II
Cytotoxic/ cytolytic hypersensitivity:
1. mediated IgG or IgM binding to antigens on cell surface
2. this activates complement cascade
3. leads to cell destruction
91
Type III
Lytic enzymes:
1. mediated IgG or IgM binding to antigens on cell surface (forming Ag-IgM or Ag-IgG complex)
2. complex activates complement cascade
3. granulocytes (ie. neutrophils) attracted to site of activation
4. damage caused by release of lytic enzymes
(reaction occurs within hours of challenge to antigen)
92
Type IV
Delayed-type hypersensitivity:
- no antibodies involved, instead cytotoxic T cells (CD8+) and Th1 cells (CD4+)
1. mediated by Th1 cells, upon their activation they release cytokines
2. causes accumulation and activation macrophages, plus activation cytotoxic T cells
3. these macrophages and cytotoxic T cells cause local damage
93
ILC 1 vs ILC 2
ILC 1 - Fights bacteria, tissue resident, non cytotoxic
| ILC 2 - Non allergic asthma, secrete IL5 and IL13 (type 2 cytokines)
94
Physiologically, what occurs when IgE and antigen bind?
1. IgE-antigen complex (immune complex) forms
2. this crosslinks FcεRI
3. causes release chemical mediatiors from mast cell
4. leads to allergic reaction
95
Allergic reaction steps
1. Sensitisation (Antigen on mucosal surface activates TH2 cells which release IL4 and 13 which act on B-cells differentiating them into plasma cells that will that will produce IgE)
2. Activation (IgE goes to FcεRI receptor on Mast cell, crosslink occurs, activating mast cell)
3. Effector (Mast cell produces 1. Preformed mediators - Histamine, and 2. Synthesised mediators - Prostaglandins, Leukotrines and PAF - Platelett activating factor)
96
FcεRI
a high affinity IgE receptor
97
which cells dominate in late phase allergic reaction?
eosinophils
98
what factors recruit eosinophils, making them migrate to site of allergic reaction?
IL-4, chemokines
99
state the main TH2 cytokines?
IL-4, IL-13
100
difference between IgG and IgM?
IgG is more specific to antigen, prevalent in late phase, memory antibody
IgM has greater avidity (strength), prevalent in early phase
101
Interleukin-3 (IL-3)
promotes growth and differentiation of eosinophils
102
state the function of the following cytokine:
| Chemokines
recruits eosinophils causing them to migrate
103
multiple sclerosis - what type of hypersensitivity?
type IV, an autoimmune disease which is cell mediated
104
is multiple sclerosis cell mediated or humoral? What substances or cells are involved?
- cell mediated
- T cells (T helper CD4, cytotoxic CD8)
- APC's
- B cells
105
Leukocyte recruitment stages
1. Margination (selectins)
2. Stable adhesions (Integrins)
3. Transmigration (chemokines)
4. Chemotaxis (WBC will travel within tissue to site of injury (Chemokines)
106
State the main WBC in blood, and there % prevalence?
"Never let monkeys eat bananas"
```
Neutrophils - 60%
Lymphocytes - 30%
Monocytes - 6%
Eosinophils - 3%
Basophils - 1%
```
107
granulocytes
- eosinophils
- basophils
- neutrophils
108
A macrophage in the bloodstream is known as?
a monocyte
109
What is pus
a collection of neutrophils and necrotic cells
110
myeloperoxidase
a enzyme involved in phagocytosis
111
which cells produce growth factors for repair?
macrophages and platelets at site of injury
112
chronic inflammation is characterized by?
activated macrophages and lymphocytes
