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The University of Asia Pacific
An immune disorder is a dysfunction of
the immune system. These disorders can be
characterized in several different ways:
• By the component(s) of the immune system
• By whether the immune system is overactive
• By whether the condition is congenital or
A state of altered reactivity in which the body
reacts with an exaggerated immune response to
what is perceived as a foreign substance.
Immune response that results in tissue injury or
other physiological changes are called
hypersensitivity (allergic) reactions”.
Hypersensitivity reactions are classified into four types:
• Type I: Anaphylactic hypersensitivity
• Type II: Cytotoxic hypersensitivity
• Type III: Immune complex hypersensitivity
• Type IV: Cell mediated hypersensitivity
TYPES OF HYPERSENSITIVITY
• It is an immediate reaction beginning within minutes of
exposure to an antigen.
• It is mediated by antibodies.
• It requires previous exposure to specific antigen.
• It usually affects on skin, lungs and gastrointestinal tract.
– Allergic rhinitis
– Systemic anaphylaxis.
– Atopic dermatitis
TYPE I: ANAPHYLACTIC
Anaphylactic (type I)
• It occurs when the system mistakenly identifies a
normal constituent of the body as foreign.
• This reaction may be a result of cross-reacting
antibody, possibly leading to cell and tissue damage
• It involves activation of complement by IgG or IgM
antibody binding to an antigenic cell.
• Myasthenia gravis
TYPE II: CYTOTOXIC
Pathogenesis of type II hypersensitivity
Cytotoxic (type Il)
• It involves in the formation of immune complexes when
antigen binds to antibodies.
• These type III complexes deposit in tissues or vascular
endothelium and leads to injury with the help of
vasoactive amines and the increase number of circulating
• The joints and kidneys are particularly susceptible.
• Systemic lupus erythematous
• Rheumatoid arthritis
• Serum sickness
TYPE III: IMMUNE COMPLEX
IMMUNE COMPLEX (TYPE III) HYPERSENSITIVITY
Pathogenesis of type III hypersensitivity
• Also known as cellular hypersensitivity
• It occurs 24-72 hrs after exposure to an allergen
• The reaction is mediated by sensitized T cells and
• The reaction results In tissue damage by releasing
lymphokines, macrophages and lysozymes.
• Contact dermatitis
• Tuberculin test.
TYPE IV: CELL MEDIATED
CELL MEDIATED (TYPE IV) HYPERSENSITIVITY
Pathogenesis of type IV hypersensitivity
It is also called as Hay Fever
Definition: It is an inflammation of the nasal mucosa
by an allergen.
PATHOGENESIS: ALLERGIC RHINITIS
Inhalation of an antigen (sensitization)
Nasal mucosa reacts (histamine is mediator)
Slowing of ciliary action, edema formation and
Tissue edema and increase capillary permeability
• Nasal congestion
• Clear to greenish rhinorrhea
• Intermittent sneezing and nasal itching
• Fatigue, loss of sleep and poor coordination.
• Oral anti histamines (blocks the action of histamine)
• Nasal decongestant
• Mast cell stabilizers.
• Analgesics and antipyretics.
ATOPIC DERMATITIS (ECZEMA)
Inflammation of the skin
• Familial tendency
• It is highest in infants and children
• 1% population is suffering from this disease
• Aggravated in low humidity and in winter.
Allergen /Sensitizing antigen
Affect the skin (changes in lipid content, sebaceous gland activity and
Reduced water-binding capacity of the skin
Higher trans epidermal water loss and decreased water content
Itching, rubbing leads to infection
Clinical manifestations: Atopic dermatitis
• Red oozing crusting rash (in childhood)
• Dry thick brownish – grey and scaly skin (later
• Lesion are mostly found on hand, foot, back of
the knees, neck, face, eyelids and elbow bands.
Medical Management: Atopic dermatitis
It is an immediate life threatening systemic reaction that can occur on
exposure to particular substances
It is an immediate (type I hypersensitivity) immunologic reaction, results from
This reaction affects many tissues and organs.
Death may occur due to respiratory tract spasm and constriction or collapse.
• Food ( peanuts, fish, milk, eggs, wheat and chocolate).
• Medications (penicillin, NSAID’s)
• Insects stings (bees, ants)
Interaction of foreign antigen with IgE antibodies
Release of histamine
Activation of platelets, eosinophils and neutrophils
smooth muscle spasm, bronchospasm, mucosal edema and
Mild Moderate Severe
Occurs within first
2hrs of exposure
Peripheral tingling Flushing Bronchospasm
Itching Laryngeal edema
Fullness in mouth
Bronchospasm Severe Dyspnea,
Nasal congestion Edema of larynx Hypotension
Dyspnea Cardiac arrest and
coma may follow.
Clinical manifestations: Anaphylaxis
Medical management: Anaphylaxis
1. If cardiac arrest then cardiopulmonary resuscitation
2. Antihistamine to prevent recurrence reaction
3. Start intravenous fluids to maintain hemodynamics.
4. Give aminophylline for bronchospasm
• Transplant rejection occurs
when transplanted tissue is rejected by the
recipient's immune system, which destroys
the transplanted tissue.
• Transplantation can be:
homologous (alogenic) - human tissue
heterologous - animal tissue (pig skin, ovine
• hyperacute (Ab mediated) - widespread
arteriolitis, arteritis, ischemic necrosis
• acute (cell mediated) -
vasculitis, tubulitis, edema (days-months)
• chronic - vascular changes -
sclerosis, intimal fibrosis (months-years)
• GVHD happens when particular types of white
blood cell (T cells) in the donated bone marrow
or stem cells attack host body cells. This happens
because the donated cells (the graft) see the
body cells (the host) as foreign and attack them.
• It is difficult to say who will develop GVHD after a
transplant. We don’t know exactly, but
somewhere between 1 and 4 out of every 5
people (20 to 80%) having a donor transplant will
develop some degree of GVHD. Some people
have a very mild form which doesn’t last long.
For others, GVHD can be severe. It may even be
life threatening in a few cases. Some people
may have GVHD over many months, or even
GRAFT VERSUS HOST DISEASE
• GVHD happens because the transplant affects your immune
system. The donor's bone marrow or stem cells will contain some T
cells. T cells are a type of white blood cell that help us fight
infections. T cells attack and destroy cells they see as
foreign, and potentially harmful, such as bacteria and viruses.
Normally T cells don’t attack our own body cells, because they
recognize proteins on the cells called HLA (human leukocyte
antigens). We inherit our HLA from our parents. Apart from
identical twins HLA is unique to each person.
• Before a bone marrow or stem cell transplant, you and your
donor have blood tests to check how closely your HLA matches.
This test is called tissue typing. If you and your donor have very
similar HLA this lowers the chance of GVHD. The more differences
there are between your HLA and your donor's, the more likely you
are to get GVHD.
• After a transplant your bone marrow starts making new blood
cells from the donor stem cells. These new blood cells have the
donor's HLA pattern. They recognize the HLA pattern on your
body cells as different (foreign) and may begin to attack some of
them. The GVHD may affect different areas of your body. Most
commonly it affects the
• Digestive system (including the bowel and stomach)
HOW GVHD DEVELOPS