Download Introduction to the immune system

Survey
yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project

Document related concepts

Monoclonal antibody wikipedia , lookup

T cell wikipedia , lookup

Lymphopoiesis wikipedia , lookup

Immune system wikipedia , lookup

Phagocyte wikipedia , lookup

Molecular mimicry wikipedia , lookup

Psychoneuroimmunology wikipedia , lookup

Adaptive immune system wikipedia , lookup

Cancer immunotherapy wikipedia , lookup

Immunomics wikipedia , lookup

Immunosuppressive drug wikipedia , lookup

Innate immune system wikipedia , lookup

Polyclonal B cell response wikipedia , lookup

Adoptive cell transfer wikipedia , lookup

Transcript
AHS C&T5
11/2/12
Role of the Immune System (IS)!
A network of cells and tissues that:!
1.  Defends the body against invading pathogens!
2.  Destroys abnormal/mutant cells within the body (e.g. control of cancer)!
3.  Removes ‘worn-out’ cells!
Immune System can also have harmful effects:!
1.  Allergies / autoimmune diseases!
2.  Tissue rejection.!
Infection-causing organisms (Pathogens)
PARASITE
Tapeworm
VIRUS
BACTERIA
Staphylococcus
aureus
(causes sepsis)
Polio
FUNGUS
Epidermophyton
floccosum
(Athlete’s foot)
Introduction to the immune system
•  Tissues
» Primary and secondary lymphoid organs
•  Cells
» Lymphocytes
» Granulocytes (Neutrophils, Eosinophils, Basophils)
» Monocytes/Macrophages
» Dendritic cells
» Natural killer cells
•  Soluble mediators
» Cytokines & chemokines
» Complement proteins
1
AHS C&T5
11/2/12
Lymphoid Tissues
CENTRAL (PRIMARY) LYMPHOID
TISSUES !
–  Bone marrow - site of B cell development
(and pre-T cell)!
–  Thymus – site of T cell development!
PERIPHERAL (SECONDARY) LYMPHOID
TISSUES!
–  Spleen!
–  Lymph nodes!
–  Gut-associated lymphoid tissue (GALT)
[Peyer’s Patches]!
–  Adenoids!
–  Appendix!
–  Tonsils!
White blood cells (WBCs)/Leucocytes
Mobile units of body’s immune defense system
2
AHS C&T5
11/2/12
Neutrophils!
•  Destroy bacteria by phagocytosis!
–  First defenders on scene of bacterial invasion!
–  Scavenge to clean up debris!
•  Most abundant leukocyte (60-70%)!
Eosinophils!
•  Increase in circulating eosinophils (eosinophilia) is associated
with!
–  Allergic conditions such as asthma and hay fever!
–  Internal parasite infestations, such as worms!
•  Attach to worm and secrete substances to kill it!
•  Make up 1-4% of Leukocytes!
Monocytes!
•  Emerge from bone marrow while still immature and circulate
for day or two before settling down in various tissues in body!
•  Mature and enlarge in resident tissue and become known as
macrophages (“large eaters”)!
–  Life span can range from several months to years!
•  Become professional phagocytes and can act as antigen
presenting cells!
•  Note: Dendritic cells are similar to monocytes but are more
efficient antigen presenting cells!
3
AHS C&T5
11/2/12
Organisation of the immune system
Nonspecific vs. Specific Immunity!
Nonspecific (Innate)!
Specific (Adaptive)!
(Lymphocytes)!
(Phagocytosis, Inflammation)!
Initial & immediate response against
invasion by any pathogens !
Comes into play after nonspecific
responses have begun.!
Main mechanisms!
1.  Physical barriers (skin, mucous
membranes)!
2.  Inflammation & Phagocytosis (by
neutrophils & macrophages)!
3.  Interferon, NK cells!
4.  Complement!
Responds to specific pathogens on 2nd
or later exposure!
Nonspecific— 2. Inflammatory Response!
Results
Destroys or inactivate invaders
Removes debris
Prepares for healing & repair.
Signs
Redness
Heat
Swelling
Pain
4
AHS C&T5
11/2/12
Nonspecific— 2. Phagocytosis
SEM macrophage engulfing bacteria
Stages of Phagocytosis
1.  Attachment
2.  Internalisation (0.1 s)
3.  Degradation
4.  Exocytosis
S&G 23.3!
Nonspecific— 3. Interferon, NK Cells
Interferon!
Natural Killer cells
α,β,γ
Cytokine released by virus-infected cells
Protects other cells from any virus
Attack virus-infected cells…
…Cause lysis via release of perforins
NK cells are also a major source of
interferonγ
Induces expression of enzymes that prevent
viral replication
Anti-cancer effects
Slows cell division
Enhances action of NK cells and
cytotoxic T cells
5
AHS C&T5
11/2/12
Nonspecific— 4. Complement System!
Consists of a number of small proteins that normally circulate as
inactive precursors in the blood. !
They account for about 5% of the globulin fraction of blood plasma!
Over 25 proteins and protein fragments make up the complement system.!
Activation of the complement cascade results in the formation of a
cell-killing membrane attack complex. !
Induces lysis of invading microorganisms!
Also complements the ability of other immune mechanisms to clear
pathogens [hence name!].!
Specific Immunity!
1. Specificity!
•  Lymphocytes (B and T cells) bind and respond to foreign
molecules known as antigens via antigen receptors!
2. Diversity!
•  The body possesses millions of lymphocytes that can
recognise and respond to millions of antigens (one each)!
3. Memory!
•  1st exposure to an antigen generates lymphocytes & longlived memory cells – next exposure to the same antigen,
memory cells react faster & with stronger response!
4. Self-Tolerance!
•  Lymphocytes can distinguish ‘self’ (our normal antigens) from
‘non-self’ (antigens from foreign material).!
6
AHS C&T5
11/2/12
Lymphocytes!
2 types of lymphocytes!
B lymphocytes (B-cells)!
Produce antibodies which circulate in blood!
Defend mainly against bacteria toxins and viruses present in body fluids!
Responsible for antibody-mediated or humoral immunity!
T lymphocytes (T-cells)!
Do not produce antibodies!
Directly destroy specific target cells by releasing chemicals that punch holes in
the victim cell (cell-mediated immunity)!
Target cells include body cells invaded by viruses and cancer cells!
Specific Immunity: 1. Specificity
Antigen receptors are present on B and T cells
Antibody-antigen interactions are specific
Specific Immunity: 4. Self-tolerance!
B or T cells that may detect and attack ‘self’ are usually destroyed in the bone marrow.
This process of self-tolerance fails in autoimmune diseases.
7
AHS C&T5
11/2/12
Specific Immunity: 2. Diversity & 3. Memory!
A single B or T cell has approx 100,000 specific antigen receptors – each cell can
detect just a few of the millions of possible antigens
CLONAL SELECTION
1.  Plasma cells!
•  Produce antibodies in blood!
•  Short-lived!
2.  Memory cells (clone)!
•  With same receptor!
•  Long-lived.!
Antigen fits B cell’s receptors…!
Proliferation and differentiation into:
Humoral immunity: How do antibodies function?
www.gcarlson.com!
Remember, antibodies are produced by B lymphocytes
5 classes: IgM IgD IgG IgE IgA
8
AHS C&T5
11/2/12
Cell mediated immunity
T Cells: Helper vs. Cytotoxic
HELPER T CELLS (~70% of T cells)!
• 
• 
• 
www.gcarlson.com!
Activated by MHC (Class II) on antigen-presenting cell (e.g. macrophage)!
Secrete cytokines that enhance the activity of cytotoxic T cells; enhance
phagocytosis!
Stimulate development of B cells into plasma cells (indirect action)!
CYTOTOXIC T CELLS!
• 
• 
Activated by MHC (Class I) on virus-infected cell!
Kill infected cells by lysis (direct action)!
Antigen presentation and Helper T-cell activation:
A central process in specific immunity
In an infected cell, Class I MHC molecules
present antigen at cell surface so cytotoxic T
cells can kill the infected cell
In a phagocytic immune cell, Class II MHC
molecules present antigen at cell surface
so Helper T cells can bind it and secrete
cytokines that will amplify the immune
response
9
AHS C&T5
11/2/12
Immune Disorders – Autoimmune Diseases!
If immune system does not recognise its ‘self’ (e.g. MHC),
it reacts against normal cells and tissues!
Immune Disorders - AIDS!
• 
• 
• 
• 
• 
AIDS is caused by Human Immunodeficiency Virus (HIV)!
HIV binds to the surface of helper T cells and its nucleic acids (RNA and DNA)
enter the T cell!
Inside the cell, HIV uses the cell to make copies of itself!
HIV slowly destroys helper T cells in the body!
(Helper T cells = 70% of all T cells)!
When T cell function is impaired, immune responses weaken and other diseases
develop (Opportunistic infections)!
10