Immunology Flashcards

0
Q

Antibody

A

Protein made by body’s immune system that reacts wit specific antigens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

Antigen

A

Any subs that produces an immune response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

MAC

A

Membrane attack complexes

Pores on pathogen surfaces causing osmotic lysis of bac/virus
Made by complements

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Complement pathways

A

Classical (conplement activated by antibody/antigen complexes)
Alternative (initiated by foreign cell surfaces)
Lectin ( recognise mannose on pathogens)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Neutrophil

A

Most abundant type of WBC

Phagocytose bac/fungi

Can kill bac by NET

Key thing in ACUTE INFLAMMATION

has multilobed nucleus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Basophils

A

Secrete histamines during inflammtion

Similar to mast cells in allergies

Targets big parasites like eosinophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Eosinophils

A

Involved in allergic inflammation responses

Targets larger parasites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Mast cells

A

Involved in allergic response

Upon stimulation wit allergen, release stuff like histamine, interleukin
To create local repsonses eg increase permeability of blood vessles, increase mucus production etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Opsonisation

A

Marking of a pathogen/antigen with antibody for it to be ingested

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Macrophages

A

Wen monocytes leave blood stream n enter tissue, become macrophages

Macrophages engulf pathogens/bad stuff

Can do antigen presenting

Release cytokines (eg TNF and IL-1) - signal local endothelial cells to increase adhesion molecules n increase gap bw cells

Hav receptors for Fc portion of antibodies- so can easily eat stuff that has already been oponisedm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Natural killer cells

A

Kills virus infected cells/cancer cells/phagocytes with phagocytosed microbes inside (ie kills OUR OWN cells, not pathogen)

Dont need activation (cos dont hav antigen-specific receptor)

Has granular cytoplasm - cytotoxic granules induce apoptosis in target cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Fibrosis

A

Formation of excess fibrous connective tissue

In response to injury, this is called scarring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Epithelioid

A

Macrophage that has retained a very big size cos it has done a lot of eating

In chronic inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Granulation tissue

A

New connective tissue with tiny blood vessels on surface of wound during healing process

In chronic inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Abscess

A

Accumulation of pus in swelling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Granuloma

Pl. granulomata

A

‘Nodular collection or epithelioid histiocytes’

Basically: nodular collection of big macrophages

Epithelioid histocytes=macrophages that look like epithelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Chronic inflammation

A
Macroscopic appearance;
Chronic ulcer
Abscess cavity
Hollow viscus(organ) with thickened walls
Granulomatous inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Chronic inflammation

A
Microscopic appearance:
Lymphocytes
Plasma cells
Macrophages
Granulation tissue n fibrosis
Necrosis
Granuloma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Granulomatous inflammation

A

Subtype of chronic inflammation

Caused by VERYFEW diseases

Characterised by formation of granulomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Antibodies: light chain

A

Have lambda or kappa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

IgM

Heavy chain: mu

A

1st antibody to b made in response to antigen

Interacts with complement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

IgA

Heavy chain: alpha

A

Found in secretions eg milk, bile, saliva

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

IgD

Heavy chain: delta

A

Minor class of antibodies

Functions mainly as receptor

Rarely secreted

Only found on surface of B cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

IgE

Heavy chain: epsilon

A

Involved in allergic response as it binds to mast cells

Cross linkin of antibodies on surface of mast cell = mast cells degranulation n release of histamines

Defence agaisnt HELMINTHS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
IgG Heavy chain: gamma
``` Most common antibody Interacts with complement Can cross placenta Made slightly later in the infection Is produced faster n in larger amouts jn secondary infections ```
25
Fab fragment | On antibody
Binds to antigen
26
Fc fragment | On antibody
Mediates effector functions
27
Clonal selection theory | 4 principles
1. Each lymphocyte only has 1 type of receptor 2. Binding of antigen with high affinity will activate lymphocyte 3. Differentiated effector cells will have identical receptors to parent cells 4. Lymphocytes with receptors for self molecules r deleted early on.
28
T cells 'movement'
Born in bone marrow Mature in thymus THEN move to 2ndary lymphoid organs: spleen + lymph nodes
29
Class I MHC
Found on surface of all nucleated cells xept RBC Presents antigen synthesised within cell eg virus infected cell CD8 T cells respond
30
Class II MHC
Found on B cells n Antigen Presenting cells (APC Presents anitgens that enter cell from outside eg bacterial toxins CD4 T cells respond
31
MHC restriction
Process where T cell recognise MHC Note: T cells can OnLy be activated wen antigen is presented to it in MHc groove by an antigen presenting cell APC ( ie cant be activated by naked antigen Vs B cell - can b activated by naked antigen or antigen from APC
32
MHC I markers
Contain antigen synthesised within cell Present to CD8 (killer) T cell Which kills the cell Killer T cells ONLY see antigen wen it is in the MHC I groove
33
MHC II markers
Contain antigen that enters cell from outside Presents this to CD4 (helper) T cell To help B cells make antibodies Helper T cells ONLY see antigen when it is in the MHC II groove
34
Toll-like receptors
Recognise PAMPs On dendrites Part of innate response
35
Active immunity
There is ANTIGENIC STIMULATION leading to CLONAL EXPANSION, ANTIBODY SYNTHESIS and making of MEMORY CELLS. Ie we r making the antibodies Eg recovery from naturally occuring infection; vaccination 'Immunity that is learned'
36
Passive immunity
Transfer of immunity by antibodies (immune serum) Ie antibodies r given to us Eg transferral of immunity to foetus/infant through placenta/breast milk 'Immunity that is given'
37
Chronic inflammation: cells
Lymphocytes (both T n B) Macrophages Epithelioid histiocytes (in granulomatous inflammation) Multinucleate giant cells
38
Interferon
Secreted by some virus infected cells Act on uninfected cells by makin them more resistant to the virus
39
Cytokines
Group of proteins (eg chemokines, interferons, interleukins) that do CELL SIGNALLING bw immune cells and do things like activate macrophages, neutrophils etc
40
NLR, RLR
Intracellular receptors( ie PRRs) that recognise PAMPs
41
Signs of acute inflammation
``` Redness (vasodilation) Heat (increased blood volume + endogenous pyrogens) Swelling Pain Loss of f(x) ```
42
Pyrexia
Fever
43
Wen splinter punctures epidermis (acute inflammtion.....)
``` 2-Bac start to multiply 3-Injured cells release histamines (causing vasodilation) 4-Neutrophhils/macrophages come in 5-Bac engulfed by phagocytosis Also hav other WBC comes in ```
44
Mutualism
2 independent organisms livin togez, Both benefits Eg natural flora n us
45
Commensalism
2 independent organisms livin togez, They benefit, and dont affect us (ie we dont get harmed/damaged ) Eg natural flora n us
46
Parasitism
2 independent organisms livin togez, | Parasite benefits, we get harmed
47
Immunodeficiencies 3 types
1. Genetic (primary) immunodeficiency ( due 2 mutations in immune response genes) 2. Secondary immunodeficiencies (Inabiltiy to generate immune resp Due 2 malnutrition, drugs, cancer, post-infection) 3. Acquirer immunodeficiencies (eg HIV)
48
DiGeorge syndrome | Genetic immunodeficiency)
Due to pLack of thymus- no Tcells- highly suscep to infection Aka CATCH-22
49
SCID | Genetic immunodeficiency)
Severe combined immune deficiency Impaired production of both T n B cells due to genetic mutations
50
Autoimmune diseases
Wen immune system reacts to self antigens, causing tissue damage
51
Monoclonal antibodies | Mabs
Antibodies specific for one antigen cos Made by identical immune cells that were CLONES from a unique parent cell Used in immunotherapy
52
Anergic
Lack to response to antigen/allergen by immune cells
53
Tolerance
Failure of immune system to react to self It is a LEARNED process (occurs via clonal abortion)
54
Anti-nonself clones | In clonal abortion/deletion
Need to b KEPT
55
Anti-self clones | In clonal abortion/deletion
Nedd to b DELETED
56
Rheumatoid arthritis | Autoimmune disease
Systemic (all around body) inflammatory disorder targetin synovial joints
57
SLE | Autoimmune disease
Systemic LUPUS Erythematosus Characteristic butterfly rash on face Generalised tissue damage n inflammation due to antibodies Can affect any organ
58
MS | Autoimmune disease
Multiple Sclerosis Myelin sheath is damaged, affectin neural transmission
59
Myasthenia Gravis | Autoimmune disease
Antibodies block nicotinic receptors at the post-synaptic NMJ
60
Type 1 diabetes | Autoimmune disease
Cytotoxic cell destruction of beta cells of pancreas (islets of langerhans) = no secretion of insulin
61
Thyrotoxicosis | Autoimmune disease
Antibodies stimulate thyroid so thyroid goes overactive
62
Complement functions
Chemotaxis (recruitment of phagocytic cells) Oponisation Cell lysis via MAC
63
Complement die by
Mild heat treatment | 56 degrees for 30 mins
64
Chronic Granulomatous disease | (Genetic immunodeficiency
Phagocytes ingest bac but cant do anythin about it cos Problem wit NADPH oxidase Treat wit antibiotics
65
Selective IgA deficiency | Genetic immunodeficiency)
Ppl wit this lack IgA So no IgA in secretions like mucus So eg bac trapped by cilia but not neutralised Can get pneumonia, bronchitis - anythin to do wit trappin
66
HIV | (Acquired immunodeficiency
Befor enter cell, must bind to 2 things on our t CD4 cells: CCR5 Chemokine receptor CD4 receptor HIV has 3 enzymes: Reverse transcriptase(converts rna 2 dna) Integrase (integrates their DNA into our DNA) Proteases (chops up their proteins to be in active form, ready to b shipped off)