3. Phagocytosis
Defined as the ingestion of extracellular particulate
material
Is actually one type of endocytosis
Can either be:
Receptor-mediated endocytosis
Pinocytosis
5. 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.
6. 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
7.
8.
9. 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)
10. 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.
12. Inflammation
Chemical mediators of inflammation:
Acute-Phase Reactants
Their concentration increases dramatically during inflammation
Protein Response
time (Hr)
Normal conc.
(mg/dL)
Increase Function
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
protein
? 0.15-1.0 ? Complement activation
13. 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
15. 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
17. 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.
18. 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.
19. 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
20.
21. 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
22. 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
23. 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
