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Chapter 19: Inflammation and the Immune Response

• Overview: Body has some defenses to prevent organisms


from gaining access to the internal environment, such as
intact skin and mucous membranes, normal skin flora, and
natural chemicals on the skin.

• Purpose of inflammation and immunity: to meet the need


for human protection by neutralizing, eliminating, or
destroying.

• HLAs (Human leukocyte antigens

o Present on all body cells

o Unique to each person

o Determine tissue type of a person

o Other names: Human transplantation antigens,


Human histocompatibility antigens, Major
histocompatibility antigens, Class I antigens

o Humans have 40 major HLAs

o Antigens present are determined by which MHC gene


alleles were inherited from the parents

o Key for recognition and self-tolerance! : Immune


system cells constantly come in contact with other
body cells. The immune cells compare the HLAs to
determine if the cell they have come in contact with
is “self” or “non-self”. If self, then the body leaves it
alone but if the cell is non-self then the body takes
action to get rid of it.

• Immune System/function changes during a person’s


lifetime according to the nutritional status, environmental
conditions, drugs, disease, age. Immune function is most
efficient when people are in their 20s and 30s.

• Organization of the Immune System

o Immune system cells come from the bone marrow.

o Stem cells are pluripotent meaning that each cell has


more than one potential outcome.
o Growth factors which are specific chemicals that
direct growth and determine what the stem cell will
be.

o White blood cells are the immune system cells.


Actions of the White blood cells are: recognition of
self, destruction of foreign invaders, cellular debris,
and healthy or abnormal self cells, production of
antibodies, complement activation, and production of
that stimulate increase formation of leukocytes in
bone marrow and increase specific leukocyte
activity.

o 3 processes that are needed for human protection


thru immunity are: Inflammation, antibody mediated
immunity, and cell mediated immunity.

• Inflammation

o It is a short term but an immediate reaction. It is also


a non-specific defense

o Infection is usually accompanied by inflammation,


however; inflammation can occur without an
infection.

o Cell Types involved in inflammation

 Neutrophils – 55% to 70% of total white blood


cells. Growth requires 12-14 days. More than
100 billion are released into circulation each
day. Life span of 12-18 hours. Take part in
phagocytosis but only mature ones. Small
energy supply. (ANC: the percentage and
number of mature neutrophils in the circulating
blood).

 Macrophages – Stored in the liver, spleen, and


intestinal tract. They are mature monocytes.
They have specific functions such as:
phagocytosis, repair, antigen processing, and
secretion of cytokines. Long life spans. Can
renew energy supplies.

 Basophils – 1% of total white blood cells. These


can cause manifestations of inflammation.
Contain chemicals: heparin, histamine,
serotonin, kinins, and leukotrienes. Vascular
leak syndrome (blood plasma to leak into the
interstitial space).

 Eosinophils – 1-2% of total white blood cells.


Act against parasitic larvae, and can limit the
inflammation reactions.

o Phagocytosis

 Exposure and invasion – leukocytes must first


be exposed to organisms/foreign bodies

 Attraction: occurs only when the white blood


cell comes into contact with the target

 Adherence: phagocytic cell first binds to the


surface of the target

 Recognition: when it recognizes the target cell


as non-self

 Cellular ingestion: when the target cell is


brought into the phagocytic cell (engulfs) and
forms a vacuoles

 Phagosome formation: granules break and


release enzymes that attack target cell

 Degradation: target is broken into smaller


pieces.

o Sequence of Inflammation Response

 5 cardinal manifestations of inflammation:


warmth, redness, swelling, pain, and decreased
function.

 Stage One: Changes in blood vessels,


hyperemia and edema, 24 to 72 hours, and the
macrophage is the major cell.

 Stage Two: Neutrophilia occurs. Exudate in the


form of pus. Limits the helpful effects of
inflammation and increases the risk for sepsis.

 Stage Three: Tissue repair and replacement.


White blood cells trigger new blood vessel
growth (angiogenesis) and scar tissue
formation.
• Antibody Mediated Immunity

o Purpose

 B cells are to become sensitized to a specific


antigen and produces antibodies against that
antigen.

 B cells have the most direct role in AMI.

 B cells start as stem cells in the bone marrow,


the primary lymphoid tissue. After they migrate
into secondary lymph tissues such as the
spleen, lymph nodes, tonsils, and mucosa.

o Antigen-Antibody Interactions

 Exposure or invasion: the antigen must first


enter the body

 Antigen-recognition: recognize the antigen as


“non-self”

 Lymphocyte sensitization: B cells recognize the


antigen and is now sensitized to his antigen

 Antibody production and release: antibodies


are produced against the antigen and search
out the antigen.

 Antibody-antigen: y shaped antibodies and the


specific antigen are bound together

 Sustained immunity: provides long lasting


immunity to a specific antigen resulted from B
cells

o Antibody Classification

 IgM – present upon the first exposure to the


antigen

 IgG – present upon re-exposure

o Acquiring antibody mediated immunity

 Natural active: occurs when antigen enters the


body with out human assistance and the body
responds by making antibodies (*Most effective
and longest lasting!!).

 Artificial active: protection that is developed by


a vaccination or immunization

 Natural passive – occurs when antibodies are


passed from the mother to fetus (placenta,
breast milk).

 Artificial passive – involves injecting a person


with antibodies that were produced in another
person.

• Cell Mediated Immunity

o Cell Types Involved in CMI

 Helper T cells – Easily recognize self versus


non-self cells. Helpers secrete lymphokines
that can enhance the activity of other white
blood cells. Increase bone marrow production
of stem cells and speed up their maturation.

 Suppressor T cells – Prevent hypersensitivity.


Help to inhibit the growth and activation of
immune system cells.

 Cytotoxic T cells – Destroy the cells by making


holes in the membrane causing it to lyse and
die.

 Natural killer cells – Most effective in


destroying unhealthy or abnormal self cells.

• Types of Rejection and Treatment

o Hyperacute rejection

 Begins immediately

 Occurs mostly in transplanted kidneys

 Patients at greatest risk are: Those who have


received donated organs of a different ABO
type, Have received multiple transfusions,
history of multiple pregnancies, and received a
previous transplantation.

 Process can not be stopped once it has started


and the rejected organ is removed as soon as
its diagnosed.

o Acute rejection

 Within one week to three months

 Necrosis leads to organ’s destruction

 Inflammation response and causes lysis of


organ cells.

 Does not automatically mean patient will lose


new organ

o Chronic Rejection

 No cure

 Decreased organ function

o Treatment of Transplant Rejection

 Immune suppression: Cyclosporine, Imuran,


Mycophenolate. * Treatment with these causes
an increased risk for infections and cancer
development

 Rescue therapy of ALG for acute rejection.

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