Immunity

2. AQSA YASIN
USA

3. GENERAL FEATURES OF IMMUNITY
 Immunity
 General features of Immunity
HYPERSENSITIVITY REACTIONS
 General mechanism of hypersensitivity
reactions
 Types with clinical relevances
 Summary & comparison tables

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 Immunity refers to protection against infections.
The immune system is the collection of cells and molecules that are
responsible for defending the body against the countless pathogens
that individuals encounter.
Defects in the immune system render individuals easy prey to
infections and are the cause of immunodeficiency diseases
But the immune system is itself capable of causing tissue injury
and disease, which are often referred to as hypersensitivity
disorders.

6. The main features of the immune system are:
 The capacity to discriminate between its own and foreign
components
 The specificity of the response
 Memory
 Barriers (prevent entry)
 Innate immunity (general defense)
 Acquired immunity (specific defense)
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 WBCs called T lymphocytes (T cells) target and destroy infected
or cancerous cells
 WBCs calles B lymphocytes (B cells) and plasma cells produce
antibodies the target & destroy infected or cancerous cells
 WBCs calles neutrophils & macrophages engulf and destry
invaders and damaged cells

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 Specificity of the immune system is due to the fact that both
antibodies and lymphocytes only recognize one epitope or
antigenic determinant.
 The immune system can recognize thousands of millions of
different antigens, but a specific lymphocyte will be induced for
each determinant.
 There are as many lymphocytes stimulated as there are
determinants making up the antigen.

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 Occasionally, errors occur in the immune system when
distinguishing between the body’s own and foreign components
 Therefore, it could occur that the immune system does not
respond to a foreign particle. This phenomenon is known as
tolerance.
 On the other hand, in some circumstances the immune system
reacts against its own structures. These reactions are known as
autoimmunity.

12.  Hypersensitivity reactions are excessive
immune responses leading to damage in
the host.
These are inappropriate immune
responses to harmless foreign substances
resulting in pathological changes in the
host known as allergy or hypersensitivity
reactions.
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13. According to the Coombs and Gell classification, there are
four main types of hypersensitivity reaction.
 Type 1 : Anaphylactic and immediate reaction
 Type 2 : Antibody-mediated Hypersensitivity
 Type 3 : Immune-complex disease
 Type 4 : Delayed or cell-mediated immunity
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14.  A tissue reaction that occurs within minutes
after the interaction of antigen with IgE
antibody bound to the surface of mast cells
(sensitized mast cells).
 Initiated by entry of an Ag, which is called an
allergen (triggers allergy).
 Main cell : Th2 cells
 Main antibody : IgE
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16.  Initial exposure to the antigen causes the activation of Th2 cells,
and their release of IL-4 causes the B cells to switch their
production of IgM to IgE antibodies which are antigen-specific.
 Mast cell sensitization : The IgE antibodies bind to mast cells and
basophils, sensitising them to the antigen.
 Mast cell re-exposure to antigen & activation : When the
antigen enters the body again, it cross links the IgE bound to the
sensitised cells, causing the release of preformed mediators
including histamine, leukotrienes and prostaglandins.
 This leads to widespread vasodilation, bronchoconstriction, and
increased permeability of vascular endothelium.
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18.  Type 2 hypersensitivity reactions are antibody mediated
processes in which IgG or IgM antibodies bind to antigens on the
target cells’ surface. This subsequently leads to cell lysis, tissue
damage or loss of function.
 Main antibodies : IgG or IgM
 Antibody- Mediated cytotoxic reactions follow 3 mechanisms :
- Opsonization and phagocytosis
- Inflammation
- Antibody-mediated cellular dysfunction
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20.  Opsonization (cells coated with auto Ab), w/ or w/o complement
proteins --> become target cells of phagocytosis (phagocytes:
neutrophils & macrophages)
 Ab bound to Ag activates the complement system (recruiting
neutrophils & monocytes), triggering inflammation in tissues.
 Ab bound to host protein impair or dysregulate cellular functions
causing antibody-mediated cellular dysfunction.
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21.  Transfusion Reaction
 administration of inappropriate transfusions
 given blood not matching patient’s ABO type
Autoimmune hemolytic anemia
 Drug reactions
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22.  Immune complex disease
 An abnormal immune response is mediated
by the formation of antigen-antibody
aggregates called "immune complexes” (Ag-
Ab complexes).
 They can precipitate in various tissues such
as skin, joints, vessels, or glomeruli, and
trigger the classical complement pathway.
 Main Ab : IgG & IgM
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23. Formation of Immune Complexes.
The introduction of a protein antigen triggers an
immune response that results in the formation of
antibodies, typically about 1 week after the
injection of the protein.
These antibodies are secreted into the blood,
where they react with the antigen still present in
the circulation and form antigen-antibody
complexes
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24. Deposition of Immune Complexes.
In the next phase, the circulating antigen-
antibody complexes are deposited in various
tissues
Organs where blood is filtered at high pressure
to form other fluids, like urine and synovial fluid,
are sites
where immune complexes become concentrated
and deposit; hence, immune complex disease
often affects glomeruli and joints.
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25. Inflammation and Tissue Injury
Once deposited in tissues, immune complexes
initiate an acute inflammatory reaction via
complement activation and engagement of
leukocyte Fc receptors.
Typically, the antibodies are IgG or IgM.
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26.  RHEUMATOID ARTHRITIS (autoimmune and inflammato disease
causing painful inflammation and stiffness in affected joints of the
body)
 SERUM SICKNESS (atoimmune reactions following exposure to
medicines that contain proteins used to treat immune conditions)
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27.  Mediated by antigen-specific activated T-
cells.
 Main cell : T cells
 This reaction is also known as delayed-
type hypersensitivity due to its
characteristic longer time period to
appear following antigen exposure.
Type IV hypersensitivity reaction, is a
cell-mediated response to antigen
exposure.
Presensitized T cells initiate the immune
defense, leading to tissue damage.
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28. (A) CD4+ TH1 cells (and sometimes CD8+ T cells, not shown) respond to
tissue antigens by secreting cytokines that stimulate inflammation and
activate phagocytes, leading to tissue injury.
CD4+ TH17 cells contribute to inflammation by recruiting neutrophils
(and, to a lesser extent, monocytes).
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29. (B) In some diseases, CD8+ cytotoxic T lymphocytes (CTLs) directly kill
tissue cells expressing intracellular antigens (shown as orange bars inside
cells). APC, Antigen-presenting cell.
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30.  CONTACT DERMATITIS (redness, rash, & swelling caused by
direct contact with a substance like nickel, poison or household
cleaning products)
 DM TYPE I (insulin dependent + destruction of insulin making
beta cells)
 MULTIPLE SCLEROSIS (autoimmune disease affecting CNS)
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