Dr.

Vince Scialli
BSC 1086
Rev. 7-18-08

IMMUNOLOGY
NON-SPECIFIC
DEFENSES

LECTURE 4

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Rev. 5-15-08 IMMUNE SYSTEM

Specialized body defense system

Made up of billions of cells ~ MOSTLY lymphocytes

Provides specific resistance to disease ~ IMMUNITY

1. Microorganisms ~ pathogens & parasites

Bacteria
Viruses
Fungi
Parasites

2. Foreign tissue cells & Foreign Proteins Allergens

Blood transfusions
Tissue transplants

3. Cancer Cells

Types of Immune Protection

1. Innate ~ Natural ~ Local Non-specific Body Defenses

Intact surface membranes ~ barriers to entry

Specialized cells & chemicals ~ mucous, NK

phagocytes

2. Acquired ~ Adaptive ~ Specific Defense System

Antibodies

Immune Modulators ~ interferons & cytokines

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NON-SPECIFIC BODY DEFENSES

Barriers to entry ~ Prevents foreign invasion & infection

Mechanisms of Protection

1. Surface Membrane Barriers ~ first line of defense

Prevent Pathogens from entering the body

Skin ~ Hair
Dermal Secretions ~ sweat, sebum
Mucous Membranes

2. Internal Cellular & Chemical Defenses ~ second line

Phagocytes ~ remove foreign debris

Macrophages Neutrophils
Monocytes Eosinophils

Natural Killer Cells ~ surveillance ~ T-cells

Interferons ~ increase resistance against virus

Complement ~ destroys invader cell walls

Attract Phagocytes

Stimulate Inflammation

Inflammatory Response ~ many effects

Fever ~ mobilizes defenses

Accelerates Repairs ~ Inhibits pathogens

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SURFACE MEMBRANE BARRIERS

First Line of Defense - Nonspecific defenses

Provide mechanical barrier for entry of pathogens

Produce chemical substances ~ enhance defense effects

SKIN ~ microorganisms CANNOT penetrate intact skin

Keratinized Epithelial Cells

Keratin ~ resistant to toxins & enzymes produced

by bacteria

Sebum from sebaceous glands

Toxic to bacteria

pH of skin ~ 3 to 5 (acid) ~ Inhibits bacterial growth

Most bacteria need alkaline media

MUCOUS MEMBRANES ~ mucosa

Protective membranes ~ contain goblet cells

Line body passageways exposed to outside

Digestive Tract

Respiratory Tract

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PROTECTIVE MECHANISMS

Digestive Tract

Mucous ~ produced by mucous membranes in

intestine traps bacteria

Saliva ~ from salivary glands ~ in oral cavity

Contains Lysozyme ~ destroy bacteria

Lacrimal secretion ~ tears contains Lysozyme

Other Digestive Secretions ~ kills bacteria

HCl in Stomach . . . Proteolytic Enzymes in Intestine

Respiratory Tract

Mucous ~ produced by mucous membranes in

trachea & nose traps bacteria

Cilia ~ of upper respiratory tract & trachea trap dust

& bacteria ~ cough into mouth and swallow

Fine mucous-coated hairs ~ inside nose traps

particles when inhaled ~ stimulates sneezing reflex

Urogenital System

Normal urine is slightly acid ~ pH < 7.0

Prevents bacterial growth ~ urinary acidifiers

Vaginal secretions are very acid ~ inhibits bacteria

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CELLULAR & CHEMICAL DEFENSES

Second Line of Defense ~ Nonspecific defenses

PHAGOCYTES

Engulf & destroy pathogens & foreign debris ~ pac-man

Attack invaders that cross epithelial barriers ~ clean up

Enhanced by complement or antibodies which attach to

bacteria & provide binding surface for phagocyte

Microphage ~ small ~ usually circulate in blood

Leave blood ~ move into damaged tissue

Neutrophils ~ abundant WBC ~ become phagocytic

Attack bacteria and other foreign

Eosinophils ~ Weak phagocytes ~ attack Parasitic

Mast Cell ~ phagocytic cell ~ releases histamine

Macrophage ~ large ~ most important type of phagocyte

Derived from monocytes ~ large WBCs

Monocytes enter tissue & become enlarged

Free Macrophages ~ wander through tissue

Fixed Macrophages ~ stationary

Kupffer cells & Microglia

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CELLULAR & CHEMICAL DEFENSES

Natural Killer Cells ~ NK Cells

Immune Surveillance Cells ~ Police ~ Army

Constant monitoring of normal tissue by NK cells

Recognize & destroy abnormal or foreign cells

Large granular lymphocytes in blood & lymph

T-lymphocytes ~ from thymus

Non-specific ~ kill viruses, bacteria & malignant cells

Help fight cancer

Early Protection ~ Act before immune system is activated

Action is NON-phagocytic

First ~ Disrupt the membranes of those cells

they attack

Second- release cytolytic chemicals ~ Perforin

Cause breakdown of cytoplasm of cell foreign

or abnormal cell being attacked ~ lysis

Antimicrobial Proteins

Enhance bodys ability to defend against invaders

Two MOST important: Interferon & Complement

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Interferon ~ produced by virus infected cells

Anti-viral ~ anti-microbial protein

Cytokine ~ Produced by lymphocytes, macrophages,

virus infected cells & other immune cells

Prevents viruses from multiplying in other normal

adjacent body cells

Activates macrophages . . . Stimulates natural killer cells

Complement

Anti-microbial circulating protein

Complement Activation ~ Complement Fixation

Activated after binding to antibody-covered

antigens complex

FIXES on bacteria surfaces & makes bacteria more

susceptible to body defenses

Marks bacteria for phagocytosis

Intensifies inflammatory & immune response

Enhances phagocytosis by phagocytes

Stimulates mast cells & basophils to release

histamine & heparin

Attracts neutrophils & other WBCs to area

Lyses microorganisms~ destroys microorganism

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CELLULAR & CHEMICAL DEFENSES

Inflammation ~ Inflammatory Response

Tissue response to injury or breakdown

Response triggered in an area where injury occurs

Trauma
Heat or Burn
Irritating Chemicals
Infection ~ viral, bacteria, parasitic, fungi

Signs or symptoms of inflammation

Four Cardinal Signs

Swelling
Redness ~ hyperemia
Pain
Heat

Impairment of Function (5th sign) ~ sometimes

Functions of Inflammation

1. Prevents spread of damaging agents

2. Disposal of cellular debris & pathogens

3. Helps to prepare for repair & regeneration

4. MUST occur prior to the healing process

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INFLAMMATORY PROCESS ~ Overview

1. Vasodilation & Increased Vascular Permeability

Chemical Mediators ~ released from tissue

Histamine & Heparin

Kinins ~ plasma proteins

Prostaglandins ~ attract platelets & swelling

Complement ~ marks invaders

Lymphokines ~ cytokines

Exudate formation ~ Pus or Purulent Exudate

Local edema

Pus ~ Purulent Exudate

Pain

2. Phagocyte Mobilization ~ army moves in

Leukocytosis ~ increased WBC count

Margination ~ neutrophil pavementing in vessels

Diapedesis ~ neutrophil emigration into tissue

Chemotaxis ~ macrophages remove cellular debris

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READ ABOUT INFLAMMATION DETAIL IN NOTES . . .

NOT COVERED IN LECTURE

INTERNAL CELLULAR & CHEMICAL DEFENSES

FEVER

Increased body temperature common during pathogenic

infection > 99.2 oF

Pyrogens ~ produced by macrophages & leukocytes

following pathogenic exposure

Stimulate febrile response ~ increase temperature

Effects of Fever ~ Good & Bad

Increase metabolic rate of tissue cells

Faster immune response & tissue repair

Inhibit some viruses & bacteria

NOT very comfortable

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IMMUNOLOGY
SPECIFIC
DEFENSES

LECTURE 5 & 6

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IMMUNE SYSTEM

Specific Body Immunity ~ Adaptive Immunity ~ Acquired

Third Line of Defense . . . A Very Specific Defense

Immune system recognizes something as foreign

Body responds to immobilize, neutralize or remove

foreign substances

Properties of Acquired Immunity

1. Specificity ~ NOT general ~ NOT local

Immunity recognizes & is directed against a

particular foreign substance

Antigen ~ foreign substance ~ NOT SELF

2. Versitle & Systemic

Not restricted to location of infection ~ systemic

Can respond to millions of different antigens

Tolerance ~ NO normal response to self

3. Memory

After initial exposure to an antigen . . .

Sensitization ~ it remembers

Immune system responds stronger the second time around

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FORMS OF IMMUNITY

Innate Immunity

Genetically Determined at Birth ~ species specific

NO prior exposure to foreign substance needed

Acquired Immunity

Produced by PRIOR EXPOSURE

Develop own or receive antibodies to foreign substance

Acquired Passively ~ Passive Immunity

Produced by transfer of antibodies from another

person or another source

Induced ~ Receive antibodies directly

Tetanus anti-toxin . . . Snake anti-venom

Natural ~ Receive antibodies from mother ~ milk

Acquired Actively ~ Active Immunity

Make OWN antibodies in response to antigens

Induced ~ Develops from artificial exposure

Vaccines

Acquired ~ from exposure to environment

Natural exposure/recovery
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MECHANISMS OF ACQUIRED IMMUNITY

Cell Mediated Immunity ~ occurs within cells

From t-cells ~ T-lymphocytes

Defends against abnormal pathogens or antigens

within cells

Humoral Immunity ~ occurs outside cells

Antibody Mediated Immunity ~ classical

Defends against abnormal pathogens or antigens in

body fluids outside cells

Antibodies produced by B-lymphocyte plasma cell

Antibodies circulate freely in blood

Circulating antibodies bind to a pathogen or toxins

produced by pathogen -----> neutralization

Neutralization ~ marks foreign substance for

destruction, removal by phagocytes, or complement

Specific Body Defense Involves the Immune Response

Cell-mediated Immunity

Antibody Mediated Immunity

Long Term Immunity ~ memory

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CELLS OF THE IMMUNE SYSTEM

T - LYMPHOCYTES ~ T-cells ~ Controls Immune System

From hemocytoblasts stem cells in bone marrow

Migrate to thymus & mature

Develop immunocompetence in thymus

Sub-populations: Cytotoxic T-cells ~ NK cells

T-helper cells
T-suppressor cells
Memory cells

Recognize foreign antigens & respond

Non-antibody producing ~ stimulate cell-mediated

immunity

Activated by macrophages ~ cytokines

Migrate to blood, lymph nodes, spleen & other organs of

lymphatic system in ready position ~ memory

B - LYMPHOCYTES ~ B-cells
From hemocytoblasts stem cells in bone marrow

Important in humoral immunity ~ antibody mediated

Sub-populations: Plasma Cells ~ become antibodies

Memory cells

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Migrate to blood, lymph nodes, spleen & other organs of

lymphatic system in ready position ~ memory

ANTIGENS ~ Ag

Substances recognized as foreign by body ~ NOT SELF

Usually large complex molecules

Proteins ~ strongest & MOST COMMON antigens

SOME Lipids . . . Nucleic Acids . . . Polysaccharides

Provoke immune response specific to foreign substance

Antigenic Determinant ~ portion recognized as foreign

Complete Antigens

Immunogenic ~ Protective & Neutralizing ~ GOOD

Stimulate a proliferation of specific B-lymphocytes to

produce specific antibodies ~ lock & key fit

Reactive ~ Anaphylaxis & Hypersensitivity ~ BAD

React with specific lymphocytes & IgE antibodies

Partial Antigens ~ Haptens >>> ALLERGY

Small foreign particles NOT immunogenic by themselves

Become immunogenic antigens & reactive when linked to

other body proteins in some people

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Poison ivy Animal dander Detergents

Penicillin Cosmetics Pollens
Grasses & Weeds Household Products Foods
Thus . . . allergic in some individuals & not in others
MACROPHAGES ~ antigen presenting cells

Arise from Monocytes

Distributed throughout lymphoid organs

Engulf foreign particles ~ phagocytosis

Antigen Presenting Cells ~ APC

Present antigenic determinants on surfaces of

pathogen recognized as foreign

Present to T-cells

Stimulates engulfment by macrophage

Secrete Cytokines

Chemicals which mediate cellular immunity

Activate T-cells to become phagocytic

Enhance Inflammatory response

Stimulate B & T-cell proliferation

Stimulate immature helper T-cells

Secrete bactericidal chemicals ~ kill bacteria

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EG: Interferons, interleukins, etc.

Antigen Presentation

T-cells MUST be activated by exposure to antigen

Antigen-Presenting Cells ~ Macrophages ~ APCs

Macrophages respond to activated T-cells

Release lysosomes ~ lyse foreign invader

Presents marked antigen on surface for destruction

MHC Proteins ~ Self Antigens ~ produced by SELF

MHC = major histo-compatability complex

Proteins on our own cells ~ Mark Self as NOT foreign

Only identical twins have same MHC proteins

If cells infected by foreign invader . . .

MHC proteins sense foreign proteins ~ warning flag

MHC proteins become marked by foreign protein

Body MUST get rid of marked MHC complex

before it causes harm

Self MHC Antigens are antigenic to other persons

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Blood Transfusion ~ ABO blood type

Tissue or Organ Transplants

Could be recognized as foreign in autoimmune disease

CELL MEDIATED IMMUNITY

Defends against abnormal cells & pathogens inside cells

Involves T-lymphocytes ~T-cells

Needed where humoral immunity is ineffective or slow

When pathogens attack quickly & replicate

Target cells infected with viruses, bacteria, parasites &

cancerous cells ~ all have abnormal foreign protein (not self)

Types of T- lymphocytes ~ T-cells ~ many & diverse

Cytotoxic ~ Killer T-Cells ~ NK Cells

Kill invaded, damaged or cancerous cells ~ perforin

Helper T Cells ~ the master switch

Promote development of other T-cells

Also stimulate B-cells to produce antibodies

Suppressor T Cells ~ the regulator

Release chemicals which inhibit T & B-cells

End immune response ~ turn off

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Memory T-Cells ~ the ready position

Trigger differentiation into cytotoxic T-cells upon

repeated exposure to same foreign antigen

CELL MEDIATED IMMUNITY

Antigen engulfed by Macrophage ~ becomes APC

Activates immature Helper T-cells

Antigen displayed on surface of infected cell ~ marked MHC

Activates immature Cytotoxic T-cells

Helper T Cells ~ the master switch

Become primed & activated by APC & MHC

APC ~ antigen presenting cells ~ macrophages

MHC ~ major histocompatability complex ~ marked

Release cytokines & lymphokines that attract other

types of WBCs to infection site

Interferons & Interleukins

Stimulate proliferation of mature B & T cells ~ MAJOR

T- cells ~ cell mediated immunity

B-cells ~ humoral immunity & antibody production

Enhance nonspecific defense system & inflammation

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HIV (Aids Virus) ~ inhibits Helper T-Cells

Causes massive immunodeficiency

Cytotoxic T-cells ~ NK cells ~ the weapon

Only T-cell that can attack & kill other cells

Attack & lyse invading foreign protein ~ MHC marked

Release PERFORIN ~ kills target cell

Roam through body via blood and lymph ~ mobile

Search for MHC cells displaying foreign antigens

Target infected cells (virus & bacteria), foreign cells, &

cancer cells

NK Cell Lethal Hit Mechanism

1. Killer T-cell docks to target cell ~ APC ~ Macrophage

2. PERFORIN is released from T-cell & inserted into

target cell plasma membrane

3. Killer T- cell detaches

4. PERFORIN molecules cause cell membrane lysis

5. Other lethal mechanisms:

DNA fragmentation in target cells

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Slow destruction of tumor cells

Stimulation of macrophages

Memory T-Cells

Remain in reserve to differentiate into cytotoxic T-cells

Differentiation occurs immediately after a second attack

Overwhelms attacking organism before it can become

established

Memory B-Cells

Remain in reserve to differentiate into plasma cells

Differentiation occurs immediately after a second attack

Very rapid antibody response occurs

Overwhelms attacking organism & neutralizes it before it

can become established

Suppressor T-Cells ~ the regulator

Regulatory cells which inhibit activity of B & T-cells

Stop immune response after foreign antigens have

been destroyed

Suppression occurs slowly

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HUMORAL IMMUNE RESPONSE ~ Antibodies

Antibody Mediated Immunity ~ Humoral Immunity

Very specific antibody response to an antigen challenge

Formation of Antigen-Antibody Complex

ANTIGEN ~ Antigenic Determinates

Portion of antigen recognized as foreign

Could be many antigenic determinates on an antigen

Determines the immunogenicity of antigens

Stimulates production of Antibodies

ANTIBODIES ~ Immunoglobulins ~ Ig

Proteins produced by B-lymphocytes & plasma cells

Attach to antigenic determinants on antigen

Antibody Structure

Four chains arranged in a Y or T shape

Two short light & two long heavy chains

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Tips are Variable . . . Heavy Chains are Constant

Specialized Binding Sites ~ very specific

For Antigens . . . Complement . . . Macrophage

ACTIVE IMMUNITY ~ body response to antigen challenge

1. Naturally Acquired ~ antibodies self produced

Exposure to bacteria, viruses or other pathogens

2. Artificially Acquired ~ antibodies self produced

Induced from vaccines or vaccination

PASSIVE IMMUNITY ~ immediate but temporary ~ NO

ANTIBODIES
PRODUCED

Antibodies received directly from an external source

Antibodies in mothers milk or in serum infusion

Tetanus Anti-toxin antibodies

Snake Anti-venom antibodies

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Antigen-Antibody Complex Formation ~ STEPS

1. Antigen Challenge ~ Primary Challenge

First encounter between B-lymphocytes & invading

foreign substance ~ the antigen

B-cell lymphocytes ~ recognize antigen challenge

B-lymphocyte multiplies into army of sensitized B-cells

Sensitization ~ B-cell Activation

Occurs in spleen, lymph nodes or lymphoid tissue

2. Primary Response ~ a humoral antibody response

Differentiate into a specific antibody against the antigen

B-cells become Plasma Cells ~ Takes 3 - 6 days LAG

Secrete specific antibodies ~ last for 4 - 5 days

B-cells become Memory B - cells for future attacks

READY in case of a second invasion by antigen

3. Future Antigen Challenge ~ Secondary Challenge

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The next time same antigen invades body by exposure

4. Secondary Response ~ Anamnestic Response

Memory B - cells mount an immediate humoral response

if specific antigen is ever encountered again
SECONDARY RESPONSE ~ Anamnestic Response

Results in MANY MORE antibodies produced VERY RAPIDLY

Overwhelms secondary foreign invader

Memory B-cells provide body with IMMUNE MEMORY

Memory can last a life time ~ but decreases with age

Secondary response involves an encounter of memory B-cells

with a previous recognized antigen

Anamnistic Antibody Response is . . .

1. Faster ~ immediate

Response occurs in only 2 - 3 days ~ NOT 5 - 7 days

2. Stronger

Plasma level antibodies rise to much HIGHER levels

than the primary response

3. Longer

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Plasma antibody levels REMAIN HIGH for weeks to

months ~ not 4 - 5 days

4. More Effective

Antibodies bind with greater affinity to antigen as

compared to primary response

Overwhelms the invading antigen or attacker

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Antibody Classification

Heavy chain structure determines way antibody is secreted &

how it is distributed in body

Heavy Chain = Constant Segment

Five major classes

IgM early protecting antibody ~ first antibodies

IgA local immunity antibody ~ in glandular secretions

IgG MOST common in serum ~ 80%

IgD B-cell activation

IgE antibodies of allergic reactions ~ histamine

Mechanism of Antibody Action

Antibodies function to inactivate & tag foreign invaders

1. Neutralization

Simple mechanism

Antibody blocks binding sites on virus or bacteria or

on toxins secreted by pathogenic organisms

Prevents toxins from binding to receptor sites on

tissue cells

Antigen-antibody complex engulfed & phagocytized

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2. Agglutination ~ ABO Blood

Antibodies bind to more than one antigen ~

clumping

Antigen-antibody complex become cross linked

forming matrix or lattice

Matrix engulfed & phagocytized

3. Precipitation

Antibodies cause soluble antigenic molecules to

become cross-linked with other soluble antigenic
molecules

Antigen-antibody complexes settle out of solution as

precipitates

Precipitates engulfed & phagocytized

4. Complement Fixation and Activation

MOST COMMON of primary mechanism of antigen-

antibody interaction

Antibodies bind to antigenic determinant target sites

on pathogen

Results in complement fixation & activation

Chemicals released attracts macrophages &

enhances inflammatory response & lysis

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Complement coated invaders attracted to B-

lymphocytes
IMMUNE SYSTEM IMBALANCES

Hypersensitivities & Allergy ~ COMMON

Intense reaction to allergen AFTER an initial sensitivity

Initial exposure ----> release of very reactive IgE antibody

Second encounter with antigen results in antigen-

antibody reaction with MOSTLY IgE

Common foreign antigens: Bee sting

Fire ants
Poison ivy
Animal dander

Symptoms caused by Histamine release from mast cells

& basophils

Vasodilation of blood vessels

Constriction of bronchioles

Immediate hypersensitivity ~ anaphylaxis

IgE induced

Anaphylactic Shock ~ serious

Sub-acute hypersensitivity ~ less severe

IgM or IgG induced

Delayed hypersensitivity ~ cell mediated response ~ slow

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Skin Allergy contact dermatitis

Organ Transplants

Graft Rejection of foreign organ transplant is COMMON

Due to cell mediated response ~ cytotoxic T-cells attack

foreign graft

Organs from others recognized as foreign ~ NOT SELF

Must immunosuppress first ~ with cortisone

Infections are major complications

Immunodeficiencies

Involves many syndromes AIDS

Body destroys its own Helper t-cells

Body CANNOT mount humoral or cell mediated response

Overwhelming infections fatal if not treated (antibiotics)

Autoimmune Diseases

Body recognizes itself as foreign ~ NOT SELF

Mounts an immune response against self antigens ~ MHC

Auto-antibodies ~ antibodies against self

Examples: Graves Disease ~ anti-TSH antibody

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Rheumatoid arthritis

Multiple Sclerosis

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