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Clinical Immunology & Serology
A Laboratory Perspective, Third Edition
Copyright © 2010 F.A. Davis CompanyCopyright © 2010 F.A. Davis Company
Introduction and Natural
Immunity
Chapter One

Copyright © 2010 F.A. Davis Company
Introduction and Natural Immunity
 Immunology can be defined as the study of
the reactions of a host when foreign
substances are introduced into the body.
 An antigen is a foreign substance that
induces such an immune response in a host.
 Immunity In a host is the condition of being
resistant to infection.

Humoral Immunity vs. Cellular Immunity
 Humoral immunity involves antibodies.
 Cellular immunity involves direct cell-to-cell
interaction.
 Both are essential for a healthy host.

 Natural or innate immunity is the ability of
the host to resist infection by means of
normally present body functions.
 No prior exposure is required; nonadaptive
or nonspecific and are the same for all
pathogens or foreign substances to which one
is exposed.
 The response does not change with
subsequent exposures.

 Acquired immunity is characterized by
specificity for each individual pathogen, or
microbial agent, and the ability to remember
a prior exposure, which results in an
increased immune response.
 Both natural and acquired immune
responses are required for a healthy host.

 The natural defense system can be
considered as being composed of two parts:
the external defense system and the internal
defense system.
 External system: Attempts to prevent entry of
pathogens.
 Internal system: Deals with pathogens that
gain entry.
 Both systems promote phagocytosis.

The external defense system includes
 Unbroken skin and mucous membranes
 Acidity in sweat, urine, vaginal fluid and
stomach
 Respiratory tract’s mucous secretions and cilia
 Flushing action (saliva, feces, urine)
 Exclusion by normal flora

The internal defense system
 Recognizes molecules unique to infectious
organisms
 Enhances phagocytosis
 Is enhanced by soluble factors called acute
phase reactants

 Acute phase reactants include
• Complement
• Fibrinogen
• C-reactive protein
 Acute phase reactants are stimulated by
cytokines.
 Cytokines are chemical messengers produced
by monocytes and macrophages during the
inflammatory response.

Cytokines include
 Interleukin-1b (IL-1b)
 Interleukin-6 (IL-6)
 Tumor necrosis factor alpha (TNF-a)

Cellular defense mechanisms include
 Actions of myeloid cells, including
• Neutrophils (See Figure 1-1)
• Basophils (See Figure 1-3)
• Eosinophils (See Figure 1-2)
• Monocytes & Macrophages (See Figure 1-5)
• Mast Cells (See Figure 1-4)
• Dendritic Cells

 Certain surface molecules are found on
human leukocytes and some nonleukocyte cell
types, and these are called Toll-like
receptors (TLRs).
 The highest concentration of these receptors
occurs on monocytes, macrophages, and
neutrophils.
 Each of these receptors recognizes a different
microbial product.

 See Figure 1-6
 Once a receptor binds to its particular
substance, or ligand, phagocytosis may be
stimulated, or the cell produces cytokines that
enhance inflammation and eventual
destruction of the microorganism.

Figure 1-1

Figure 1-6

Figure 1-2

Figure 1-3

Figure 1-4

Figure 1-5

Phagocytosis consists of four main steps
1. Physical contact between the white cell and
the foreign particle
2. Formation of a phagosome
3. Fusion with cytoplasmic granules to form a
phagolysosome
4. Digestion and release of debris to the outside

Introduction and Natural Immunity; 1-7
Figure 1-7

 Resting cells that engage in phagocytosis
normally derive their energy from anaerobic
glycolysis.
 However, when phagocytosis is triggered, the
respiratory burst produces greater energy
via oxidative metabolism.
 A radical known as O2
– (superoxide) is
formed. Superoxide is highly toxic but can be
rapidly converted to more lethal products

 By adding hydrogen ions, the enzyme
superoxide dismutase (SOD) converts
superoxide to hydrogen peroxide or the
hydroxyl radical OH.
 Its effect is potentiated by the formation of
hypochlorite ions.
 This is accomplished through the action of the
enzyme myeloperoxidase in the presence of
chloride ions.

 Hypochlorite ions are powerful oxidizing
agents.
 All of these substances contribute to killing
within the phagocyte.
 See Figure 1-8

Figure 1-8

 Opsonization enhances phagocytosis.
 Opsonins are serum proteins that attach to a
foreign substance and facilitate phagocytosis
by neutralizing repulsive forces on neighboring
cell membranes.
 Examples of opsonins include C-reactive
protein, complement components, and
antibodies.

Cellular defense mechanisms include the
action of
 Lymphocytes
 Macrophages
 Mast cells
 Dendritic cells

 Inflammation: Both cellular and humoral
mechanisms are involved.
 The four cardinal signs / clinical symptoms of
inflammation are
• Redness
• Swelling
• Heat
• Pain

Major events associated with the process of
inflammation are
 Increased blood supply to the infected area
(due to vasodilation)
 Increased capillary permeability
 Migration of white blood cells, mainly
neutrophils to the injured area (diapedesis)
 Migration of macrophages to the injured area
 (chemotaxis)

Figure 1-9

 Neutrophils are the primary cell involved in
the acute inflammatory response.
 Neutrophil emigration may last 24 to 48 hours
and is proportional to the level of chemotactic
factors present in the area.
 Migration of macrophages from surrounding
tissue and from blood monocytes occurs
several hours later and peaks at 16 to 48
hours.

 Macrophages attempt to clear the involved
area through phagocytosis, and in most cases
the healing process is completed with a return
of normal tissue structure.
 Tissue damage and loss of function may result
from chronic inflammation.
 C-Reactive Protein (CRP) is the most widely
monitored of the acute phase reactants and is
the best indicator of acute inflammation.

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