Introduction

Clinical Immunology & Serology
A Laboratory Perspective, Third Edition
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.

Introduction

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Introduction

Uploaded by

Copyright:

Available Formats

Clinical Immunology & Serology

A Laboratory Perspective, Third Edition

Introduction and Natural

Copyright © 2010 F.A. Davis Company

Introduction and Natural Immunity

Copyright © 2010 F.A. Davis Company

Introduction and Natural Immunity

Copyright © 2010 F.A. Davis Company

Introduction and Natural Immunity

Introduction and Natural Immunity

Copyright © 2010 F.A. Davis Company

Introduction and Natural Immunity

Introduction and Natural Immunity

Copyright © 2010 F.A. Davis Company

Introduction and Natural Immunity

Copyright © 2010 F.A. Davis Company

Introduction and Natural Immunity

Introduction and Natural Immunity

Copyright © 2010 F.A. Davis Company

Introduction and Natural Immunity

Introduction and Natural Immunity

Introduction and Natural Immunity

Copyright © 2010 F.A. Davis Company

Introduction and Natural Immunity

Copyright © 2010 F.A. Davis Company

Introduction and Natural Immunity

Copyright © 2010 F.A. Davis Company

Introduction and Natural Immunity

Copyright © 2010 F.A. Davis Company

Introduction and Natural Immunity

Copyright © 2010 F.A. Davis Company

Introduction and Natural Immunity

Copyright © 2010 F.A. Davis Company

Introduction and Natural Immunity

Copyright © 2010 F.A. Davis Company

Introduction and Natural Immunity

Introduction and Natural Immunity; 1-7

Copyright © 2010 F.A. Davis Company

Introduction and Natural Immunity

Introduction and Natural Immunity

Introduction and Natural Immunity

Copyright © 2010 F.A. Davis Company

Introduction and Natural Immunity

Copyright © 2010 F.A. Davis Company

Introduction and Natural Immunity

Copyright © 2010 F.A. Davis Company

Introduction and Natural Immunity

Copyright © 2010 F.A. Davis Company

Introduction and Natural Immunity

Copyright © 2010 F.A. Davis Company

Introduction and Natural Immunity

Introduction and Natural Immunity

Copyright © 2010 F.A. Davis Company

Introduction and Natural Immunity

Introduction and Natural Immunity

You might also like