Introduction to Immunology

The innate components one by one

CPMS
Physiologic Factors
 Temperature
 Ph
 Soluble Chemicals
 Lysozyme
 Interferon
 Complement
Phagocytosis
 Defined as the ingestion of extracellular particulate
material
 Is actually one type of endocytosis
 Can either be:
 Receptor-mediated endocytosis
 Pinocytosis
Process of Phagocytosis
 Initiation
 Chemotaxis
 Engulfment
 Digestion
 Process of Phagocytosis
 Initiation
 Initiated by Tissue Damage by trauma or microorganism multiplication.
 Activated phagocytes has increased surface receptors that allow
adherence

 Chemotaxis
 Physical contact occurs as neutrophils roll along until they encounter the
site of injury or infection. They adhere to receptors on the endothelial cell
wall of the blood vessels and penetrate through to the tissue by means of
diapedesis. This process is aided by chemotaxis, whereby cells are
attracted to the site of inflammation.
 Process of Phagocytosis
 Engulfment & Digestion
 1. Physical contact between the phagocyte and the particle
 2. Formation of a phagosome
 3. Fusion with cytoplasmic granules to form a phagolysosome
 4. Digestion and release of debris to the outside
 Inflammation
 The overall reaction of the body to injury or invasion by an infectious agent is
known as inflammation.
 Both humoral and cellular components play a role in this response
 Has Five (5) cardinal signs:
 Rubor (Redness)
 Tumor (Swelling)
 Calor (Heat)
 Dolor (Pain)
 Functio Laesa (Loss of function)
 Inflammation
 Major events of the inflammatory response:
 Vasodilation
 an increase in the diameter of blood vessels proximal to the site occurs as the
vessels that carry blood away from the affected area constrict, resulting in
engorgement of the capillary network. This is responsible for Rubor and Calor.
 Increase in capillary permeability
 facilitates an influx of fluid and cells from the engorged capillaries into the tissue.
This is responsible for Tumor and Dolor.
 Influx of phagocytes
 They go to the tissue from the vessel through margination, chemotaxis, and
diapedesis. The release of lytic enzymes contribute to the death of nearby cells
(Functio laesa), digested material, and fluids. This components forms pus.
Inflammation
 Inflammation
 Chemical mediators of inflammation:
 Acute-Phase Reactants
 Their concentration increases dramatically during inflammation
Protein Response Normal conc. Increase Function
time (Hr) (mg/dL)
CRP 6-10 0.5 1000x Opsonization, complement activation
Serum Amyloid A 24 3.0 1000x Removal of cholesterol
Alpha1-Antitrypsin 24 200-400 2-5x Protease inhibitor
Fibrinogen 24 110-400 2-5x Clot formation
Haptoglobin 24 40-200 2-10x Binds hemoglobin
Ceruloplasmin 48-72 20-40 2x Binds copper, oxidizes iron
C3 48-72 60-140 2x Opsonization, cell lysis
Mannose-Binding ? 0.15-1.0 ? Complement activation
protein
Inflammation
 Chemical mediators:
 Histamine
 binds to receptors on nearby capillaries and venules, causing
vasodilation and increased permeability.

 Kinins
 Tissue injury activates these peptides, which then cause vasodilation
and increased permeability of capillaries.
 Example: Bradykinin: Stimulates pain receptors in the skin
Inflammation
 Repair and Regeneration
 Capillaries grow on broken blood vessels or those with fibrin
 New connective tissue called Fibroblasts replaces the fibrin
clot as it dissolves
Other components
 Complement system
 group of serum proteins that circulate in an inactive state.
When activated, they result in cell lysis
 The Phagocytes (Neutrophil & Moncyte/Macrophages)
 Other cells (Basophils, Eosinophils, Mast cells)
 Others
The Adaptive Immunity
An overview
 Adaptive immunity
 Adaptive immunity is capable of recognizing and selectively eliminating specific
foreign microorganisms and molecules. Unlike innate immune responses,
adaptive immune responses are not the same in all members of a species but
are reactions to specific antigenic challenges.
 The attributes of the adaptive system are:
 Antigenic Specificity
 Diversity
 Memory
 Self/Nonself recognition

 Remember, innate and adaptive immunity are not independent of each other;
they help each during immune response.
Cellular components of the adaptive immunity

 B-Lymphocytes
 Contains an antigen receptor molecule in their surfaces called the Antibody
 Once an antigen binds these receptors, B-cells begin to proliferate as Memory or
Plasma cells.
 Memory cells live longer and express the same receptors as their parent B-cell
 Plasma cells have little membrane antibody because they release them.
Cellular components of the adaptive immunity

 T cells
 Contains the T-cell receptor, receptors which can only recognize antigens that
are bound with cell-membrane proteins called Major Histocompatibility
Complex (MHC) molecules through antigen presentation
 Two major types: T helper (TH) and T cytotoxic (TC) cells.
 T Helper cells release cytokines when activated
 T Cytotoxic cells help in immune regulation and may control the proliferation of
foreign cells in the body
 Cellular components of the adaptive immunity

 Antigen Presenting cells

 They regulate the T-cell response
 Has MHC-II molecules and
delivers signal to T-helper cells
 Are able to internalize antigens
and present them to T-cells
Humoral Immunity
 ANTIBODIES
 They are the effector cells of the humoral immunity
 They do these by binding and neutralizing antigens
 Once an antibody binds or coats an antigen, the ability to clear
these foreign material is well-facilitated cleared at a faster rate
Immune dysfunction and Deficiencies
 Sometimes the immune system fails to protect the host adequately or
misdirects its activities to cause discomfort, debilitating disease, or even
death.
 The following are some consequences of immune dysfunction:
 Allergy
 Graft rejection and Graft-versus-host disease
 Autoimmune diseases
 Immunodeficiency