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Transcript
Human Anatomy and
Physiology
Immunology: Adaptive defenses
Overview


System must be primed before it can take
effect
1800 experiment



Inject a bacteria into an animal
It raises proteins (antibodies against the
infection
Serum containing antibodies protects other
animals not previously exposed
Overview

Characteristics of adaptive response




Specific recognition of pathogens
Response is systemic
Response has memory (mounts a stronger
attack on subsequent exposure)
Injecting lymphocytes also offered protection
Types of immunity

1. Humoral


Antibodies produced from lymphocytes present
in body as ‘humor’
2. Cellular

Lymphocytes themselves defend the body
Antigens


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Substances provoking an immune
response (i.e. any foreign cell)
Not normally present in body, therefore
‘nonself’
Self recognition


Major histocompatibility complex (MHC) class I
proteins - all cells except RBCs
MHC class II proteins (on APC cells)
Humoral immunity
Humoral immunity

Clonal selection- Steps




B-cells clone themselves upon encountering an antigen
(1° response, 3 - 6 days)
Resulting plasma cells secrete antibodies into plasma
Clone cells not differentiating into plasma cells become
memory cells
Re-infection produces a 2° response
B-cell cloning
Humoral responses
Antibody structure

Immunoglobulins (Ig)



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4 polypeptides 2H, 2 L (disulphide bonds)
Antibody monomer, T or Y shaped
2 antigen binding sites
C (constant) region
V (variable) region
Antibody classes


Classification based on C region in heavy chain
IgD, IgG, IgE, IgA, and IgM
monomer
dimer
pentamer
Antibody functions


Antibodies inactivate antigens and tag them for
destruction
Strategies




Neutralization
Agglutination
Precipitation
Complement
Humoral immunity


Active - natural vs. artificially
acquisition, memory B cells
 Long term protection
Passive - not challenged by
antigens, no memory B cells
 Short term protection. From
mother several months,
gamma globulin (gG) weeks.
Cells of adaptive immunity



1. Lymphocytes (B cells, T cells)
T cells (immunocompetent in thymus)
B cells (immunocompetent in bone marrow)
Cells of adaptive immunity

2. Antigen-presenting cells (APC)


Engulf antigens, present fragments to Tc-cells
to destroy
e.g. CT - dendritic cells, skin - Langerhans’
cells, lymph - macrophages
Cell-mediated immunity


2 types of T-cells, CD4
(TH) and CD8 (TC)
T-cells activate by
double recognition

V region binds to an
antigen, also recognize
self (MHC class I proteins)
Cell-mediated immunity

Helper T Cells

Bind to APC and help stimulate T cell and B cell
proliferation using interleukin-2 (hormone)
Clinical connections

1. Organ transplants


Immunosuppressive therapy



Tissue similarity so that Tc cells, NK cells and
antibodies do not attack the new organ
Anti-inflammatory drugs
Immunosuppressant drugs
2. Immunodeficiencies


Immune cells, phagocytes, complement behave
abnormally
AIDS/HIV - helper T cells destroyed
Clinical connections

3. Autoimmune diseases - loss of ability to
distinguish self from non-self. Body produces
antibodies against its own cells



MS: destroys white matter of brain and spinal cord
Type-1 diabetes: destroys pancreatic ß cells
4. Allergies


Anaphylaxis: basophils and mast cells become
oversensitized to allergens, resulting in histamine
release causing inflammation
Anaphylactic shock