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Flashcards in 5. Immunity & Disease Deck (39)
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1

Why do you need to know?

Affects all patients
Infections common
Some patients more susceptible to infection
Some medical conditions caused directly by the immune system

2

What is Immunity?

Protection or defence against infections…
BACTERIA
VIRUS
FUNGI
Toxins
Cancer

3

Immune System

Distinguishes self from non-self molecules

Activates multiple mechanisms to either eliminate or neutralise threat
2 main pathways
Innate
Adaptive

4

Defence against disease

Innate immunity
Adaptive immune reponse

5

Innate immunity

Defense mechansims present even before infection or activated in a non-specific way
Skin, mucous membranes
Phagocytic cells (neutrophils, macrophages), inflammation, fever

6

Adaptive immune reponse

Cell-mediated immunity
Humoral immunity

7

Non-specific defences

Non-specific defenses are designed to prevent infections by viruses and bacteria
These include:
Intact skin
Mucus and Cilia

8

Skin

Outer layer of keratin – mechanical barrier
Dead skin cells constantly sloughed off
hard for invading bacteria to colonize
Sweat and oils contain anti-microbial chemicals

9

Mucous membranes

Normal flow of mucus washes bacteria and viruses off of mucus membranes
Cilia (hair-like projections on cells) – respiratory tract
Acid – stomach, vagina
Enzymes – saliva, eye

10

Chemical barriers

Proteins
Complement - works with other defence mechanisms of the body
Interferons - inhibit the replication of many viruses

11

Cellular defences - phagocytosis (1)

Granulocytes
Neutrophils, eosinophils, basophils
Remove dead cells and micro-organisms
Attracted by an inflammatory response of damaged cells

12

Cellular defences - phagocytosis (2)

Monocytes
macrophages
In tissues which serve as filters for trapping microbes
Macrophages live longer than granulocytes
Attracted by different stimuli and usually arrive at sites of invasion later than granulocytes
Stimulate specific immune response (‘antigen-presenting’)

13

Non-specific responses to infection

-Macrophages release protein signals
interleukin-1 (IL-1) and interleukin-6 (IL-6)
-Fever
Most bacteria grow optimally at temp below body temp
-Pain, swelling, redness
Increasing capillary permeability, promoting blood flow, bringing more phagocytic cells
-Acute-phase proteins released from liver
Bind to bacteria and activate complement proteins

14

Specific (adaptive) immunity

Relies on antigens
specific substances found in foreign microbes
Lymphocytes
Can travel swiftly around the body when carried along in the blood or lymph
Approx 2 x 10^12 lymphocytes in human body
Approx 1 % are in the bloodstream
Rest in lymphatic system

15

Lymphocytes (1)

Produced in bone marrow
B-cells mature in bone marrow then concentrate in lymph nodes and spleen
T-cells mature in thymus
B and T-cells mature then circulate in the blood and lymph
Circulation ensures they come into contact with pathogens and each other

16

Lymphoid tissues

Adenoid
Tonsil
Thymus
Spleen
Appendix
Bone Marrow
Lymph Nodes
Peyers Patch (small intestine)
Lymphoid aggregates (large intestine)
Lymphatics

17

Lymphocytes (2)

B-cells
T-cells

18

B-cells

Secrete antibodies
Humoral immunity
Recognise pathogens outside cells

19

T-cells (1)

Do not recognise free antigen - only recognise antigen presented by major histocompatibility complex – class I (all cells) or class II (APC)
Directly attack invaders (cytotoxic, CD8+, MHC I)
Cell-mediated immunity
Recognise pathogens that have entered cells
Also help B-cells (helper cells, CD4+, MHC II)

20

T-cells (2)

Cytotoxic
Helper

21

Cytotoxic

Seek out and destroy any antigens in the system, and destroy microbes “tagged” by antibodies
Some cytotoxic T-cells can recognize and destroy cancer cells
Variable region on T-cell receptor

22

Helper

Stimulate B-cells
Activate cytotoxic - cells and macrophages to attack infected cells

23

How do T-cells recognise an invader?

Detect antigen – protein marker on cell surface
(Epitope = fragment of antigen)

If an antigen (“not self”) protein is encountered by a macrophage, it will bring the protein to a helper T-cell for identification.

If the helper T-cell recognizes the protein as “not self,” it will launch an immune response.

24

Signalling immune response

Helper T-cells (CD4+) stimulated by antigen  cytokines to stimulate B-cell division

HIV destroys helper T-cells so immune response diminished

25

B-cells (2)

Produce antibodies
Glycoproteins
Specific, hypervariable region
Different subtypes IgG, IgM, IgA, IgE, IgD
Opsonisation, bind and block (agglutinate), stimulate complement
Bind to antigen on cell or free  plasma cells  more antibody
Or become memory cells - remain ready to divide rapidly if an invasion occurs again

26

Immune System

Vital for survival but can be a double-edged sword
Immunodeficiency – prone to infections
Overactive immune system- hypersensitivity reactions
Failure to recognise self- autoimmune diseases

27

The Immune System - Deficient

Chemotherapy / Drugs
HIV
Splenectomy
Bone Marrow dysfunction

28

The Immune System - Hyperactive

Allergy (Hypersensitivity)
Auto-immunity
Overreaction to Pathogen

29

Immunodeficiency (1)

Drugs
Chemotherapy
Immunosuppressive Medication
Splenectomy
Bone Marrow Dysfunction

30

Immunodeficiency (2)
HIV – Human Immunodeficiency Virus

Retrovirus
- Infects CD4+ T cells
- causes AIDS (Acquired Immunodeficiency Syndrome)
Stages of progression : Infection, Latency, AIDS
AIDS - decline in CD4+ T-cells, opportunistic infections