Unit 1 Immune response
1. What of the following is considered the first responders of the innate immune systems?
Neutrophils-
2. Allergic contact dermatitis is an example type 4 of a Hypersensitivity reaction.
Allergic contact dermatitis is an example of a Type IV
hypersensitivity reaction mediated by T-cells. When the
individual comes in contact with the antigen (e.g. poison ivy),
an antigen complex is formed. On subsequent exposure to the
antigen, sensitized T-cells activate the inflammatory process
that causes the allergic contact dermatitis to appear
3. Hives (Urticaria ) are an example of a Hives (urticarial) are an
example of a Type 1 hypersensitivity reaction mediated by
the antibody, IgE, and mast cells.
4. Type 2 hypersensitivity reactions are mediated bt The Type 2
hypersensitivity reaction is mediated by IgG or IgM.
5. Anaphylaxis is a hypersensitivity reaction. Type 1
hypersensitivity reactions are mediated by IgE and mast cells.
An individual who is highly sensitized to the antigen may
experience anaphylaxis
6.
Type II Hypersensitivity Reaction
A Type II hypersensitivity reaction is tissue-specific and usually
occurs as a result of haptens that cause an IgG antibody or IgM
antibody-mediated response. The antibodies are specifically directed
to the antigen located on the cell membrane. A hapten is a small
molecule that can cause an immune response when it attaches to a
protein. Macrophages are the primary effector cells of Type II
responses. Typical examples of Type II reactions are drug allergies,
as well as allergies against infectious agents. The Type II response
begins with the antibody binding to the antigen and may cause the
following.
The cell to be destroyed by the antibody
Cell destruction through phagocytosis by macrophages
Damage to the cell by neutrophils triggering phagocytosis
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Natural killer cells release toxic substances that destroy the
target cell
Malfunction of the cell without destruction
Examples of type II reactions include drug allergies, hemolytic
anemia, blood transfusion mismatch with resulting transfusion
reaction and Rh hemolytic disease
Delayed hemolytic transfusion reaction
Type III Immune-Complex Reaction
The Type III hypersensitivity reaction is also an antigen-antibody
response. The major difference between Type II and Type III
responses is that in a Type II response, the antibody binds to the
antigen on the cell surface, but in Type III responses, the antibody
binds to the antigen in the blood or body fluids and then circulates
to the tissue. Type III reactions are not organ specific and use
neutrophils as the primary effector cell. In type III hypersensitivity
reactions immune-complex deposition (ICD) causes autoimmune
diseases, which is often a complication. As the disease progresses a
more accumulation of immune-complexes occurs, and when the
body becomes overloaded the complexes are deposited in the
tissues and cause inflammation as the mononuclear phagocytes,
erythrocytes, and complement system fail to remove immune
complexes from the blood. One of the classic Type III reactions is
serum sickness.
Serum Sickness
Immune complexes are formed in response o an antigen
(Amoxicillin) that has been taken into the body. These complexes
themselves into the vascular endothelium causing vasculitis and
tissue injury as a result of complement. The skin and joints are most
commonly affected. Fortunately, the condition is self-limiting.
Type IV Cell-Mediated, Delayed Reaction
The type IV hypersensitivity reactions are known as cell-mediated
responses and use lymphocytes and macrophages as primary
mediators. Unlike the first three types of responses, which are
humoral immune functions, a Type IV response is mediated by T-
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lymphocytes and does not use antibodies. A typical reaction from a
Type IV cell-mediated response would be a localized contact
dermatitis. When the individual comes in contact with the antigen, T-
cells are activated and move to the area of the antigen. The antigen
is taken up, processed, and presented to macrophages, leading to
epidermal reactions characterized by erythema, cellular infiltration
and vesicles. This process is illustrated in contact dermatitis on the
next page.
Contact Dermatitis is a classic type IV hypersensitivity reaction
that occurs after exposure to the skin. The symptoms typically
appear a few days later. This is an at-cell-mediated response that is
initiated when the individual comes into subsequent contact with
the antigen. It is possible that he has been exposed prior to the
appearance of the rash. On the current exposure, the t-cell
recognized the antigen and causes the classic immune reaction. The
macrophages begin phagocytosis which leads to the skin reaction of
erythema and the formation of vesicles. To reduce the itching and
rash, a high patency steroid topical cream can be prescribed.
Sometimes systemic steroids may be indicated if a large area of the
face or other body surfaces are involved.
Mast cell degranulation
IgE action on mast
I. Hay fever results in an inflammatory
cells
response
II. Tissue-specific 1-ABO 1-Complement damages
destruction or incompatibility RBC membrane and cells
impairment because lyse
5-Graves'
of:
disease 5-Autoantibodies specific
1. Antibody binding for thyroid tissue impair
followed by lysis receptor for TSH
via complement
2. Antibody binding
followed by
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macrophage
phagocytosis
3. Antibody binding
followed by
neutrophil
destruction
4. Antibody-
dependent cell
(NK)-mediated
cytotoxicity, or
5. Antireceptor
antibodies
Complex deposited in small
Antigen-Antibody peripheral vessels in cool
III Raynaud’s
complex deposited in temperatures leading to
. phenomenon
tissues vasoconstriction and
blocked circulation
Contact
Cytotoxic T cell- T cells attack tissue
IV. dermatitis (e.g.,
mediated directly (no antibody)
poison ivy)
The Type IV hypersensitivity reaction is mediated by T-cells
The symptoms are consistent with the life-threatening condition,
anaphylaxis after being exposed. to a bee sting.
Which of the following is the underlying pathology of hay fever?
Mast cell degranulation. Hay fever falls under a Type 1
hypersensitivity reaction where mast cell degranulation is the
underlying pathology that produces the symptoms.
ABO incompatibility- damage occurs Abo incompatibility. The
damage from ABO incompatibility occurs because of the effects of
complement on the RBC membrane that results in RBC lysis
Immunodeficiency
Secondary Immunodeficiency
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