The Immune System

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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

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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.,). - PowerPoint PPT Presentation

Transcript of The Immune System

Page 1: The Immune System

The Immune SystemI. 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

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The Immune SystemI. Specific Immunity

B. Cell Mediated:( T-cell immunity; membrane receptors)Viruses, parasites, fungi, etc., are reacted by:1. Helper - T2. Cytotoxic - Tcells3. Macrophages4. Tranfer factor

5. Cytokines (lymphokines/interleukins)II. Non-specific Immunity

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Table 15.2 Phagocytic Cells and Their LocationsPhagocyte:NeutrophisMonocytesTissue macrophages (histiocytes)

Kupffer cellsAlveclar macrophagesMicrogia

Location:Blood & all tissuesBlood & tissuesAll tissues ( including spleen, lymph nodes, bone marrow)LiverLungsCentral nervous system

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Development of the Immune System

Hematopoietic stem cells

Yolk sac/Bone

Lymphoid stem cells

T-lymphocytes

Thymus

Sensitized lymphocytes Cellular Immunity

Bone

B-lymphocytes

Plasma cells Humoral Immunity

EtrythrocytesGranulocytes

MonocytesMegokaryocytes

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Immunology ReviewAntigen

macrophage

Immunoglobulins(immediate hypersensitivity)

Plasma Cells

Transfer factorDelayed hypersensitivity

Advanced lymphcytes

Immune System

T-cellsCellularthymus

B-cellsHumoralBone(Gut associated lymphoid tissue)

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Table 15.5 Immunology ReviewImmunoglobulins

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 newbornIgE raised in parasitic infections. Responsible for

symptions of atopic allergy

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Table 15.5 Immunology ReviewImmunoglobulins

Antibody model proposed by R.E. Porter withtwo heavy and two light polypeptide chains held by interchain disulphide bonds

X

X

SS

SS

light

light

heavy

heavy

Antigenbindingsites

SS

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Birth

Mother -3 0 6 12 18

Infant

IgM

IgG

IgA, IgD, IgE

% A

dult

Lev

el

0

50

100

Age in monthsDevelopment of serum immunoglobulin levelsin the human.

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The Complement SystemMechanism 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 C-2a & 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.

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The Complement SystemMechanism 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

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The Complement System(continued)

Summary1. Recognition: (C-1)2. Activation: (C4, C2 + C3)3. Attack: (C5 -C9)

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Development of the T-cell SystemLymphocyte 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 cortex2. 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.

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T-cell receptor

Helper T-cellKiller T-cell

Foreign antigenCD4coreceptor

Antigen presenting

cell

Target cell

Class-2 MHCmolecule

Class-1 MHCmolecule

CD8coreceptor

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 specificclass of MHC molecule

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HIV life cycle: Viral Infection

CD4

Viral RNAReverse transcriptase Reverse

Transcription

AttachmentPenetration

Integration

Proviral DNA

Cellular DNA

Cell Nucleus

Free Virus

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HIV life cycle:phase of viral expression

Viral proteins

Transcription

Budding

Packagingtranslation

Proviral DNA

Viral RNA

Free Virus

Cell Nucleus

Genomic RNAsplicing

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Acquired Immune Deficiency Syndrome (AIDS)

Caused by Human Immunodeficiency Virus (HIV)Classes: 1. Oncornaviruses (cause tumors, but not AIDS) a. HTLV-1

b. HTLV-22. Cytopathic Virus (Lenti-viruses) cause AIDS

a. HIV-1 worldwideb. HIV-2 less pathogenic (geographically restricted)

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Acquired Immune Deficiency Syndrome (AIDS)

(continued)Modes of transmissions:1. Sexual contact with an HIV-infected

person2. Transfusion of HIV contaminated blood3. In utero from infected mother to baby4. Injected drug use5. Mucocutaneous exposure (one case from

kissing)

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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:

BloodSemenVaginal fluidBreast milk

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Table 1 Body Fluids to which Universal Precautions Apply In Relationship to

“Bloodborne” Pathogens

BloodSerum/plasmaSemenVaginal secretionsCerebrospinal fluidVitreous fluidHuman Breast Milk

Synovial fluidPleural fluidPericardial fluidPeritoneal fluidAmniotic fluidWound exudates

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Table 2 Body Fluids to which Universal Precautions Apply If Containing Visible Blood In Relationship to “Bloodborne” Pathogens

SalivaFeces Vomitus Urine Nasal secretions Sputum Sweat Tears

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Table 3 Handling of Medical Devices /Equipment for Reuse

Use of Device:Contact with skin

Contact with mucous membrane

Penetrate skin

Method of Reprocessing:Decontaminate only use intermediate or low-level germicide or simple wash with soap and waterDecontaminate, then preferably sterilize at a minimum do high level disinfection by soaking 10 - 20 minutes in an EPA approved chemical agentDecontaminate and sterilize by cold sterilization (12) or preferably by heat steam or gas following the recommendations of the sterilizer

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Florida HIV Statistics as of 1/1/95U.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 USA1 women infected every 1 -2 minutes Worldwide1 women dies due HIV every 2 minutes

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AIDS/HIV Statistics as of 1/1/9518,000 children have lost their mothers to HIV# of teens contracting HIV doubles every 14 months6,500,000 teenagers contract a STD in USA each year30,000 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

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AIDS/HIV Statistics as of 1/1/95AIDS leading Counties CitiesDade 13,654 MiamiBroward 6,909 Ft. LauderdalePalm Beach 3,775 West Palm BeachHillsborough 2,585 TampaDuval 2,225 JacksonvilleOrange 2,249 OrlandoTotal cases 43,242 Fla 401,749 USA

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RNA or Thymic hormone

Lymphokine

Lymphokine

Lymphokine

Characteristics of LymphokinesB-cell: Ig helper effect

B-cell: No Ig Suppressor effect

T-cell: Blastogenesis

Activiated marcophageMacrophage migration inhibition Chemotoxis

Other cells: Viral resistance Cytotoxic inactivation

Macrophage: