Transcript No Slide Title - Pegasus @ UCF

The Immune System
I. Specific Immunity
A. Humoral Mediated:
(B-Cell immunity; Free Ig’s)
Antibodies react to bacteria by:
1. Binding directly with bacterial toxins to
neutralize them
2. Coat bacteria to enhance the
phagocytosis be non-specifics components
(monocytes, etc.,).
Immunoglobulin subclass: IgG, IgA, IgM,
IgD, & IgE
The Immune System
I. Specific Immunity
B. Cell Mediated:
( T-cell immunity; membrane receptors)
Viruses, parasites, fungi, etc., are reacted by:
1. Helper - T
2. Cytotoxic - Tcells
3. Macrophages
4. Tranfer factor
5. Cytokines (lymphokines/interleukins)
II. Non-specific Immunity
Table 15.2 Phagocytic Cells and
Their Locations
Phagocyte:
Neutrophis
Monocytes
Tissue macrophages
(histiocytes)
Kupffer cells
Alveclar macrophages
Microgia
Location:
Blood & all tissues
Blood & tissues
All tissues ( including
spleen, lymph nodes,
bone marrow)
Liver
Lungs
Central nervous system
Development of the Immune System
Yolk sac/Bone
Etrythrocytes
Granulocytes
Hematopoietic
stem cells
Monocytes
Megokaryocytes
Lymphoid
stem cells
Bone
B-lymphocytes
Plasma cells
Humoral Immunity
Thymus
T-lymphocytes
Sensitized
lymphocytes
Cellular Immunity
Immunology Review
Antigen
macrophage
Immune System
Transfer factor
Delayed hypersensitivity
T-cells
Cellular
thymus
Advanced
lymphcytes
B-cells
Humoral
Bone
(Gut associated
lymphoid tissue)
Plasma Cells
Immunoglobulins
(immediate
hypersensitivity)
Table 15.5 Immunology Review
Immunoglobulins
IgC most abundant Ig of internal body fluids,
particularly extravascular. Where they
combat micro-organisms and their toxins
IgA major Ig insero-mucus secretions where it
defends external body surfaces
IgM very effective agglutinator; produced early
in immune response - effective first line
of defense vs. bacteraemia
IgD present on lymphocytes surface of newborn
IgE raised in parasitic infections. Responsible for
symptions of atopic allergy
Table 15.5 Immunology Review
Immunoglobulins
Antibody model proposed by R.E. Porter with
two heavy and two light polypeptide chains
held by interchain disulphide bonds
light
X
Antigen
binding
sites
S
S
heavy
S
S
heavy
X
light
S
S
Birth
IgM
% Adult Level
100
IgG
50
IgA, IgD, IgE
0
-3
0
Infant
6
12
18
Mother
Age in months
Development of serum immunoglobulin levels
in the human.
The Complement System
Mechanism of Action
1. IgG & IgM-antigen complexes bind with C-1
to activate the enzyme system.
2. Activated C-1 converts C-4 into C-4a & C-4b.
3. C-4b binds to the antigen’s membrane (is
fixed) and causes theconversion of C-2 into C2a & C-2b.
4. C-2a attaches to C-4b and causes the cleaving
of C-3 into C-3a & C-3b. The C-3b attaches to
the complex while C-3a is secreted.
The Complement System
Mechanism of Action
5. Activated C-5 through C-9 become fixed to the
antigen & create large pores in the membranes
of the antigens allowing H20 influx. The cells
(bacterial) swell and burst.
6. C-3a & C-5a produce chemotaxic substances
which:
A) attract phagocytes
B) cause opsonization-stimulates phagocytes
C) cause release of histamine from mast cells
The Complement System
(continued)
Summary
1. Recognition: (C-1)
2. Activation: (C4, C2 + C3)
3. Attack: (C5 -C9)
Development of the T-cell System
Lymphocyte precursors originate in the yolk sac and
migrate into the fetus. The lymphoid stem cells then
migrate to the thymus under the influence of an
“attraction factor.” The cells then become
“programmed” and become immunocompetent.
PUTATIVE PROCESS:
1. Thymic hormones thyopoietin I & II transform the
stem cells into T-cells in the thymic cortex
2. Thymic hormone thymosin promotes the maturation of
T-cells in the thymic medulla & other lymphoid tissue.
3. Some of the T-cells enter the blood and travel to other
lymphoid tissues and establish colonies (germinal
centers) where they divide by clonal growth.
Helper T-cell
CD4
coreceptor
Antigen
presenting
cell
Killer T-cell
T-cell receptor
Foreign antigen
Class-2 MHC
molecule
Class-1 MHC
molecule
CD8
coreceptor
Target cell
Figure 15.18 Coreceptors on helper and killer T cells .
A foreign antigen is presented to T lymphocytes in association with
MHC Molecules. The CD4, on helper T cells and CD8 corecepters on
killer T cells, permit each type of T cell to interact only with a specific
class of MHC molecule
HIV life cycle: Viral Infection
Free
Virus
Attachment
Penetration
CD4
Viral RNA
Reverse
transcriptase
Proviral DNA
Reverse
Transcription
Cell Nucleus
Cellular DNA
Integration
HIV life cycle:
phase of viral expression
Free Virus
Budding
Packaging
Viral proteins
translation
Genomic RNA
splicing
Cell Nucleus
Viral RNA
Transcription
Proviral DNA
Acquired Immune Deficiency
Syndrome (AIDS)
Caused by Human Immunodeficiency Virus (HIV)
Classes:
1. Oncornaviruses (cause tumors, but not AIDS)
a. HTLV-1
b. HTLV-2
2. Cytopathic Virus (Lenti-viruses) cause AIDS
a. HIV-1 worldwide
b. HIV-2 less pathogenic (geographically
restricted)
Acquired Immune Deficiency
Syndrome (AIDS)
(continued)
Modes of transmissions:
1. Sexual contact with an HIV-infected
person
2. Transfusion of HIV contaminated blood
3. In utero from infected mother to baby
4. Injected drug use
5. Mucocutaneous exposure (one case from
kissing)
Acquired Immune Deficiency
Syndrome (AIDS)
(continued)
Risk of HIV Transmission:
A person is at risk of HIV infection
anytime s/he comes into contact with
the following fluids of an infected
individual:
Blood
Semen
Vaginal fluid
Breast milk
Table 1 Body Fluids to which Universal
Precautions Apply In Relationship to
“Bloodborne” Pathogens
Blood
Serum/plasma
Semen
Vaginal secretions
Cerebrospinal fluid
Vitreous fluid
Human Breast Milk
Synovial fluid
Pleural fluid
Pericardial fluid
Peritoneal fluid
Amniotic fluid
Wound exudates
Table 2 Body Fluids to which Universal
Precautions Apply If Containing Visible
Blood In Relationship to “Bloodborne”
Pathogens
Saliva
Feces
Vomitus
Urine
Nasal secretions
Sputum
Sweat
Tears
Table 3 Handling of Medical Devices /
Equipment for Reuse
Method of Reprocessing:
Use of Device:
Decontaminate only use intermediate
Contact with skin or low-level germicide or simple
wash with soap and water
Decontaminate, then preferably
Contact with
sterilize at a minimum do high level
mucous
disinfection by soaking 10 - 20
membrane
minutes in an EPA approved chemical
agent
Penetrate skin
Decontaminate and sterilize by cold
sterilization (12) or preferably by heat
steam or gas following the
recommendations of the sterilizer
Florida HIV Statistics as of 1/1/95
U.S.A. 1 in 250 est. to be HIV+
FLA. 1 in 100 est. to be HIV +
Dade 1 in 40 est. to be HIV+
Orlando 1 in 20 est. to be HIV+
HIV leading cause of death among women
aged 15 - 25 in USA
1 women infected every 1 -2 minutes
Worldwide
1 women dies due HIV every 2 minutes
AIDS/HIV Statistics as of 1/1/95
18,000 children have lost their mothers to HIV
# of teens contracting HIV doubles every 14 months
6,500,000 teenagers contract a STD in USA each year
30,000 HIV infected teens in USA 1/1/94
FLA is: #1 Heterosexual trasnsmission
#2 Injectable drug transmission
#2 Teenage & pediatric cases
#3 Total AIDS cases
AIDS/HIV Statistics as of 1/1/95
AIDS leading Counties
Cities
Dade
13,654
Miami
Broward
6,909
Ft. Lauderdale
Palm Beach
3,775
West Palm Beach
Hillsborough
2,585
Tampa
Duval
2,225
Jacksonville
Orange
2,249
Orlando
Total cases
43,242 Fla
401,749 USA
Characteristics of Lymphokines
B-cell: Ig helper effect
RNA or
Thymic hormone
Lymphokine
B-cell: No Ig Suppressor effect
T-cell: Blastogenesis
Lymphokine
Lymphokine
Macrophage:
Activiated marcophage
Macrophage migration inhibition
Chemotoxis
Other cells: Viral resistance
Cytotoxic inactivation