Week 2- Immune System Flashcards

(55 cards)

1
Q

Describe innate immunity (3)

A

First line of defence against invading pathogens
Fast acting
Non-specific, no memory
Doesn’t improve after exposure to antigen
Always present
Activates adaptive immune system

Components:
Physical barriers, chemical barriers , cellular components (macrophages, neutrophils and dendritic cells, NK, mast cells)
Soluble factors like cytokines

Steps:
Pathogen recognition
Release of mediators like cytokines and chemo lines are released to recruit immune cells to site of infection and promote inflammation

Phagocytosis
Inflammatory rep isn’t where vasodilation occurs
Destruction of pathogen
Links to adaptive immunity

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

List physical barriers

A

Skin and mucous membrane

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

List chemical barriers

A

Gastric acid
Lysosome
Lactoferin
Nitric acid

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

List cell barriers

A

Phagocyte and natural killer

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

List protein defence barriers

A

Complement, acute phase proteins and interferons

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

List mechanical removals

A

Sneezing
Coughing
Secretions
Urine
Perisatalsis
Ciliary escalator
Respiratory mucosa

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

List colonisation resistance barrier

A

Skin
Gut micro biome

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

List types of host defence mechanisms

A

Physical barrier
Chemical barriers
Cell
Protein
Mechanical removal
Colonisation resistance

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

List certain factors which reduce the effectiveness of this protection

A

• Breach of physical barrier (i.e. trauma, burns, eczema)

• Loss of chemical barriers (i.e. drugs which inhibit gastric secretion)

• Suppression of the cough reflex (i.e. opiates, neurological disease)

• Failure of respiratory mucus clearance (i.e. smoking, asthma, cystic fibrosis)

• Failure of washing mechanism (i.e. urinary stasis)

• Loss of colonization resistance (i.e. broad spectrum antibiotic use

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

List factors that influence the level of innate immunity

A

Age
• Very old or very young are more susceptible to infectious disease

Hormones
• Endocrine disorders such as Diabetes Mellitus, hypothyroidism and adrenal dysfunctions create
enhanced susceptibility to infection.
• Increased corticosteroid - decreased anti-inflammatory effect.

Nutrition
• Immune response is reduced in malnourished patient

Medications
Detox immune system

Diet

Stress

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

In recombination, what protein is called upon to alter dna

A

Major histamine compatibility

MCH2

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

Why does recombinbantion occur

A

In order for an antigen to be presented on the phagosomes cell surface

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

Why do monocytes undergo exocytosis

A

Monocytes are not antigen presenting cells

Instead they transport the pathogen out of the cell by vesicle docking at plasma membrane, fusing with the cel membrane and are released outside the cell in apoptic bodies

Once exocytosis is undergpon, an antigen is also released from the cell

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

What are apoptotic bodies

A

A controlled for of cell death
Small fragments contain cellular components and are packaged by cuytosplasm of ‘monocyte’ type cell to ensure safely packaged cells.

Doesn’t cause inflammatory response of cause damage

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

List the 4 functions of complement system

A
  1. Lysis of infectious organisms
  2. Activation of inflammation
  3. Opsonisation
  4. Immune clearance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Once antigens are presented/ floating where do they move to

A

Lymph nodes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Once antigens are presented/ floating where do they move to

A

Lymph nodes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

In lymph nodes what occurs to the antigen involving a B-cell

A

B-cell rejectors on a b-cell binds to the antigen.
Recombination occurs
The MCH2 molecule presents the antigen

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

In lymph nodes what occurs with the antigen and a t-cell

A

Antigen contacts t-cell receptor which activates cd4. T-cell locks on to the antigen on the macrophage’s presented antigen.

T-cell needs to be activated to stimulate the b-cell
Cell turns from naive to mature and active via interlukin cell 2,4,5,6. Undergoes colonial expansion by creating other b-cells presenting this antigen (Memory cells)

Differentiation occurs where some cells are plasma cells and some are antibodies, memory cells.

T-cells create t helper cells

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

Describe t-cytotoxic cells

A

Activated when there is a virus, cancer or infection

It has CD8 as detection

It releases preferin which creates gaps in these cell walls.

Releases granuloysin which can induce apoptosis in target cells.
Destroying intracellular pathogens such as bacteria or paracytes with infected cells,

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

In t-cell what is released to activate the b-cell

A

Interleukins 2,4,5,6

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

CD4 role

A

CD4= helper t-cells.
Recognsises antigens presented by MHC2 which further helps activate B-cells to produce antibodies
Stimulates cytoxic t-cells and macrophages to destroy infected or cancerous cells

Release cytokines to amplify immune repose

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

CD8 role

A

A receptor Found on cytoxic t-cells
Kil infected or abnormal cells

24
Q

What is innate immunity

A

Genetically determine

No prior exposure or antibody production involved

25
What is acquired immunity
Produced by prior exposure or antibody production
26
Describe innate immunity
Bacteria with antigen on surface releases endotoxins Endotoxins act on mast cell nucleus to release inflammatory cytokines Stimulating P-selectin on endothelial cells to initiate extravasation Transmigration, margination, adhesion, diapedeasis and positive chemotaxis occurs The inflammatory cytokines act on endothelial cells causing them to contract and increase permeability (swelling) Smooth muscle cells are acted on and they relax leading to vasodilation and heat and redness Neutrophils undergo exocytosis of free antigens. Apoptosis Macrophages undergo phagocytosis forming a phagolysosome MCH2 recombination and attach to specific antigen and present on cell membrane Macrophage turns into antigen presenting cell Complimentary pathway is activated Classical Alternative Lectin Allowing chemoattract more neutrophils and macrophages to the area Opsonisation(pathogens are marked for destruction) Cell lysis Inflammation enhances by activation of mast cells Interferential Alpha, beta, gamma stimulate neighbouring cells / macrophage toi increase in size and number
27
Describe adaptive immunity
Viral or cancer infected cell exposes viral protein on self antigen Cytoxic t clell bind to viral protein on viral cell with a CD8 receptor Cytoxic T cell releases performing Granzymes we hitch move through pores and activate pro-apoptosis genes
28
Describe adaptive immunity
Viral or cancer infected cell exposes viral protein on self antigen Cytoxic t clell bind to viral protein on viral cell with a CD8 receptor Cytoxic T cell releases performing Granzymes we hitch move through pores and activate pro-apoptosis genes
29
Name complimentary pathway steps
Classical 2. Alternative 3. Lectin
30
Name the cells which stimulate neighbours cels and macrophages to increase in size and number
Interferential alpha, beta, game
31
Describe the process of humoral response
Free antigen binds to b lymph MCH2 and b cell receptor form an antigen presenting cell Macrophage binds to t-h cell via CD4 protein and tcell receptor Differentiation of th cell into Th1 Th2 (IL 2,4,5) IL 4 + 5 send chemical messages to b lymph to stimulate cell proliferation = clinal expansion B cell differentiation into memory b cells for long term protection Plasma cells which secrete antibodies which cause neutralisation or opsonisation
32
What is opsonisation
Where pathogens are marked for destruction by immune cells via tagging
33
What is the role of P-selectin
Cell adhesion molecule found on the surface of endothelial cells. When there is inflammation or damage, it appears on the blood vessel wall, helping wbc stick and roll along the surface of the vessel. This allows slowing of the cells so they can exit the bloodstream and reach the affected tissue.
34
What activates pain in inflammatory response
Plasma leaks out of the blood via intracellular clefts which causes swelling in this space pressure of excess fluid stimulates nociceptors causing pain Bradykinins activate nociceptors causing pain
35
Function of inflammatory mediators, name them
Histamines, leukotrienes, prostoglandins, bradykinins bind to smooth muscle causing them to vasodilate leading to hyperaemia (redness and heat)> speeding up metabolism to attract more wbc to area
36
Mast cell function
WBC When allergens enter body, mast cells release histamines and other chemicals from their granules, Degranulation occurs. This helps to increase blood flow to affected area Attract other immune cells to the site Promote healing
37
How many granules are on the cytoplasm of the mast cell
50-200
38
Leukotrienes function
Promote mucus production Blood vessel leafiness Narrowing of airways Can worse’s respiratory inflammation and asthma
39
Why do inflammatory mediates send chemicals signals- positive chemotaxis
To attract macrophages to gram negative bacteria
40
What do macrophages secrete
Interlukin 1 and 8 Tumour necrotic factor alpha
41
Functions of interlukin
Recruit inflammotary cells to site Attract and activate neutrophils buy activating protein by endo9thelial cell which facilitates diapedesis
42
What is clonal expansion
Immune cell t/b cell recognsises a specific antigen and undergoes rapid division producing many identical copies.
43
Cellular vs humerol response
C= targets and destroys infected/ abnormal cells. H= targets pathogens in body fluid C= key cels are t-cells ct cells, ht cells H= b cells, plasma cells C= targets intracellular pathogens H=targets extracellular pathogens C=mechanism is cytoxic T cells destroy infected cells H= b cels produce antibodies that neutralise or mark pathogens
44
What is the role of the compliment system
Proteins and immune cells in our body have a specific shape which is complimentary to other pathogens. When they bind, it formes a complimentary complex. It ensures that the correct cell is destructed, complimatry memory cells to be made to ensure upon re infection it will be able to fight it off faster, pathogen destruction and promote inflammation. Without this, any cells could bind to one another ands the correct immune response would jot be undergone. It bridges the innate and adaptive immune response increasing the effectiveness of immune response
45
Innate vs adaptive
Innate is non-specific and targets all pathogens whereas adaptive is highly specific Innate immunity response is immediate within minutes to hours. Adaptive is delayed and days to weeks Innate there is no memory as same response is repeated to exposure whereas adaptive has memory so is faster, stronger response Duration of innate is short term defence, adaptive is long lasting Key cells innate is phagocytes (macrophages, neutrophils), natural killer. Adaptive is B-cells, t-cells
46
Name 3 cells involved in immune response and their roles
Macrophages engulf and digest pathogens and are antigen presenting allowing T cells to be activated in adaptive immune repsonse TH cells- release cytokines that activate other immune cells like B cells to produc antibodies and CT cells to kill infected cells B cells for humoral immune response. Differentiate to plasma when activates which produce antibodies to neutralise pathogen or marking them for destruction by other immune cells
47
Name 3 antigen presenting cells
Macrophage-phagocyte Dendritic cells- activate T cells B-cells-present to ht cells
48
Identify and describe the role of t-cells in the inflammatory response
Th cells release cytokines IL-2,4,6 which activate other immune cells like macrophages, b cells and cytoxic T cells Cytoxic T cells kill infected or abnormal cells by releasing perferin and granzymes which leads to cell death and pro-inflammatory signals that attract other immune cells to the site of infection or injury. T-cells suppress excess inflammation. They release anti-inflammatory cytokines to prevent tissue damage
49
Describe extravasation anfd its 5 stages
Margination. Neutrophil loosely binds to endothelial cells lining blood vessel. Mediated by p-selectin Rolling, weak interactions between selectins allow it to roll along the serfuce to slow them down Adhesion neutrophil adhere to wall facilitated by inter grins Transmigration. Neutrophil squeeze between endothelial cells into surrounding tissue Diapedesis- follow chemical signals via positive chemotaxis to site of infalammation
50
Describe the humeral response
B cell receptors bind to angiotensin receptors However they require activation Helper T cells with CD4 receptors provide activation signals by releaseing cytokines after interacting with this antigen. It involves MHC2 molecules to bind antigen to b cell Activated B cells undergo rapid division to produce clones of themselves Plasma cells (antibodies) Memory B cells Plasma release antibodies into blood stream and lymph fluid. They can neutralise, opsonise, agglutinate these antigens as well as activate the compliment system. Vaccines stimulate humeral response Leading to productive of memory b cells and antibodies Autoimmune disease, allergic reaction and immunodeficiencuieds can affect the humeral response
51
Describe the cell mediated humeral response
Defends against intracellular pathogens like virus and bacteria and cancer cells Macropgeas and dendritic cells ingest pathogens and present their receptors. Naive T cells are activated upon binding it antigfen complex They mature, Activated T cells proliferate and differentiate into effector T cells and memory T cells Cytoxic T cells kill infected cells performing and granny ears Helper T cells secrete cytokines interlukin 2,4,5,6 to activate B cells for humeral repose Recruit other immune cells Most effector T cells undergo apoptosis
52
Describe adaptive immunity
Second line of defence Highly specific Long lasting, memory Specific Delayed response Components: Humoral immunity Defends against extracellular pathogens (e.g., bacteria, toxins, viruses in the bloodstream). Mediated by B cells and antibodies. 2. Cell-Mediated Immunity Defends against intracellular pathogens (e.g., viruses inside cells) and abnormal cells (e.g., cancer cells). Mediated by T cells. Main molecules: Lymphocytes: B cells: Responsible for antibody production in humoral immunity. T cells: Responsible for cellular responses in cell-mediated immunity. Helper T cells (CD4+): Coordinate immune responses by releasing cytokines. Cytotoxic T cells (CD8+): Kill infected or abnormal cells directly. Antigen-Presenting Cells (APCs): Includes dendritic cells, macrophages, and B cells.
53
Compare and contrast addaptive and innate immunity
I= Immediate. Min-hours A= delayed. Days-weeks I=non-spec A=highly spec I= no memory. Same response A=has memory. Stronger and faster upon re exposure I=limited diversity. A=highly diverse can recognise millions of antigens I=short-lived. Active whilst pathogen is present A=long lasting. Sustained immunity through memory cells I=Majorly cells= phagocytes like macrophages, neutrophils, NK, Dendritic cells A= lymphocytes, b cells and T cells I= effector molecule is compliment proteins, cytokines and interferons, A=antibodies produced by B cells Cytokines, interlukin from T cell I=effective against extracellular pathogens A=effective against extracellular and intracellular pathogens I= Limited mechanisms for self-recognition A=highly developed mechanisms to distinguish self from non-self I= First line of defense: Prevents pathogens from spreading A=Second line of defense: Clears infection and builds long term immunity
54
Cigarette smoke is an irritant which can lead to inflammation in the lungs, resulting in excessive sputum production. Name the cellular adaptation that occurs in the cells of the airway. In your answer, identify the specific tissue type that normally lines the airways and the tissue type that occurs because of cellular adaptation to chronic exposure to cigarette smoke.
The tissue which normally lines the airways is cilia which performs a cilia escalator to remove pathogens and bacteria using mucus. Smoke can damage the cilia, altering the tissue structure, undergoing metaplasia. Metaplasia is reversible reaction forming more resilient cells which can withstand mechanical stress and chemical irritation. These cells are less functional and affect the ciliary escalator These cells are called tratified squamous epithelium. Leading to build up of mucus and inflammation. Goblet cells often become hyperplastic (increase in number) as well, further increasing mucus production in response to irritation.
55
Functions of cells in humeral response
Macrophages: Engulf and digest pathogens and debris. Neutrophils: Rapidly recruited to infection sites; phagocytose and kill pathogens. Dendritic Cells: Capture pathogens and present antigens to adaptive immune cells (link between innate and adaptive immunity). Macrophages: Engulf and digest pathogens and debris. Neutrophils: Rapidly recruited to infection sites; phagocytose and kill pathogens. Dendritic Cells: Capture pathogens and present antigens to adaptive immune cells (link between innate and adaptive immunity).