17. Innate and Adaptive Immunity Flashcards Preview

3. TOB > 17. Innate and Adaptive Immunity > Flashcards

Flashcards in 17. Innate and Adaptive Immunity Deck (34):
1

What are humans and pathogens both made of, and why does that mean pathogens needs non self markers?

Proteins, carbohydrates and lipids. As they're both made of the same things, the immune system needs another way of differentiating between them, hence non-self.

2

What is the difference between pathogens and the host that allow the host's immune system to tell them apart?

The different proteins that allow the host and pathogen to survive and their respective niches.

3

What is damage to the host a result of?

The pathogen breaking through the barriers to gain access to the host.

4

What is an alert in the host a result of?

The damage caused to the barrier which allows entry of the pathogen.

5

What is the first barrier to infection?

Epithelia.

6

What type of epithelia is found at the following sites?
a. Blood vessel
b. Mesothelium
c. Trachea
d. Renal collecting tubule
e. Oviduct
f. Salivary gland duct
g. Skin
h. Vagina
i. Bladder
j. Gall bladder

a. Simple squamous
b. Simple squamous
c. Pseudostratified ciliated
d. Simple cuboidal
e. Simple columnar ciliated
f. Stratified cuboidal
g. Stratified squamous keratinised
h. Stratified squamous non-keratinised
i. Transitional
j. Simple columnar

7

How do epithelial cells act as a defence?

They form a selectively permeable barrier between outside and inside the host. They produce natural antibodies, possess motile cilia to keep the surface free of bacteria, they're rapidly renewable, they produce cytokines, chemokines (attract other cells) and mucins.

8

How does damage to endothelium trigger the innate and adaptive immune response?

The damage pathogens cause to the epithelia trying to break through activates the epithelia. The epithelial releases cytokines which permeabilise the endothelium so cell and fluid migrate. There is oponisation so it is phagocytosed more regularly. Phagocytosis raises an immune response.

9

What two responses do inflammatory mediators cause?

Increased permeability so fluid leakage from blood vessels allows antibodies to be released at the site of the infection.
Migration of macrophages, neutrophils and lymphocytes into the tissue so microbicidal activity is increased.

10

What five things happen in inflammation as an immunological response?

Calor, tumor, rubor, dolor and functio laesa.
Heat, swelling, redness, pain and loss of function.

11

Who championed cell-mediated immunity and when?

Elie Metchnikoff in 1893.

12

Who championed humour all immunity and when?

Paul Ehrlich in 1900.

13

Who saw the link between cell mediated and humour all immunity and when?

Sir Almroth Wright in the early 1900s.

14

What are three main roles of the innate immune response?

Inbuilt immunity to resist infection.
Native, natural immunity (from birth, not specific, not enhanced by second exposure, no memory, cellular and humour all components, poorly effective without adaptive immunity).
Involved in triggering and amplifying adaptive immune response.

15

Discuss the key features of adaptive immunity.

Established to adapt to infection. It's learnt from experience, confers pathogen-specific immunity, enhanced by a second exposure, has memory, uses cellular and humoural components, is poorly effective without innate immunity.

16

What is a distinction between less and more elaborate organisms in terms of their immune responses?

More developed organisms have an innate and adaptive immune response working together, less developed organisms just have an innate response.

17

What cells are involved in innate immunity? Give a function for each.

Macrophages - phagocytosis
Monocytes - presentation to lymphocytes
Neutrophil - phagocytosis
PMN - anti-bacterial
Eosinophil - anti-parasite and cause allergies
Basophil - may help in protecting mucosal surfaces and cause allergies
Mast cell - protection of mucosal surfaces and cause allergies
Natural killer cells.

18

Which innate immunity cell looks very red under the microscope?

Eosinophil.

19

What are pathogens?

Disease-causing organisms.

20

What are phagocytes?

Cells able to engulf and density bacteria, extracellular viruses and immune complexes.

21

What is phagocytosis?

Active engulfment of particles into a phagosome.

22

What do patients with neutrophil deficiencies suffer from?

Recurrent infections.

23

What is the role of macrophages?

Phagocytose microbial cells or damage/unwanted cells. They release cytokines for innate and adaptive immunity. They act as professional nation presenting cells in adaptive immunity.

24

What is opsonisation?

The coating of a microorganism by antibodies or complement to render it recognisable as foreign by phagocytes, thus enhancing phagocytosis.

25

What is the role of natural killer cells?

Part of the innate immune system, they recognise and kill abnormal cells, like tumour cells. They induce apoptosis in virus infected cells by pumping proteases through pores that they make in target cells.

26

What do people with natural killer cell deficiency suffer from?

Persistent viral infections.

27

Give the function of the following humoural components:
a. Transferrin and lactoferrin
b. Interferon
c. Lysozyme
d. Fibronectin
e. Complement
f. TNF-alpha

a. Deprive micro organisms of iron
b. Inhibit viral replication and activates other cells which kill pathogens
c. Breaks down bacterial cell wall of some gram positive bacteria
d. Coats bacteria and promotes their rapid phagocytosis
e. Components and their products cause destruction of microorganism directly or with the help of phagocytise cells
f. Suppressed viral replication and activates phagocytosis.

28

How is a pore in the pathogen membrane made?

C5b binds C6 and C7. C5b,6,7 complexes bind to the membrane via C7. C8 binds to the complex and inserts into the cell membrane. C9 molecules binds to the complex and polymerise. 10-16 molecules of C9 bind to form a pore in the membrane.

29

What can a deficiency in the following complement molecules lead to?
a. C1, C2 or C4
b. C3
c. C5-C9

a. Immune complex disease (type III)
b. Recurrent bacterial infections, pneumonia etc.
c. Recurrent Neisserial infections, N. meningitidis and N. gonorrhoeae.

30

Where do the T and B cells develop?

T - thymus
B - bone marrow

31

What happens when T and B cells are activated?

T cells become T helper cells that activate B cells, or cytotoxic T lymphocytes.
B cells become plasma cells that produce antibodies.

32

What are the three main ways in which an antibody protects the host from infection?

Neutralisation - prevents bacterial adherence to the host's cells.
Opsonisation - antibody promotes phagocytosis.
Complement activation - activates complement, which enhances opsonisation and loses some bacteria.

33

How does clonal selection solve the problem associated with clonal distribution?

Clonal selection raises the clonal frequency of cells with a particular antigen specificity rather than all cells. This means the particular lymphocytes have a high enough frequency to mount an effective response.

34

What are the five phases of an adaptive immune response?

Recognition phase - clonal selection and expansion
Activation phase - differentiation to effector cells
Effector phase - humoural and cell-mediated immunity, elimination of antigen
Decline homeostasis - T and B cell apoptosis
Memory - seeding of T and B cell memory.