Download IMMUNE SYSTEM

Dr. Vince Scialli
BSC 1086
IMMUNE SYSTEM
Rev. 12/28/06
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
Immune System ~ Chapter 22 ~ 6/28/2017
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Dr. Vince Scialli
BSC 1086
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
Monocytes
Neutrophils
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
Immune System ~ Chapter 22 ~ 6/28/2017
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Dr. Vince Scialli
BSC 1086
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
Immune System ~ Chapter 22 ~ 6/28/2017
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Dr. Vince Scialli
BSC 1086
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
Immune System ~ Chapter 22 ~ 6/28/2017
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Dr. Vince Scialli
BSC 1086
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 WBC’s
Monocytes enter tissue & become enlarged
Free Macrophages ~ wander through tissue
Fixed Macrophages ~ stationary
Kupffer cells & Microglia
Immune System ~ Chapter 22 ~ 6/28/2017
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Dr. Vince Scialli
BSC 1086
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 body’s ability to defend against invaders
Two MOST important:
Immune System ~ Chapter 22 ~ 6/28/2017
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Interferon & Complement
Dr. Vince Scialli
BSC 1086
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 WBC’s to area
Lyses microorganisms~ destroys microorganism
Immune System ~ Chapter 22 ~ 6/28/2017
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Dr. Vince Scialli
BSC 1086
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
Immune System ~ Chapter 22 ~ 6/28/2017
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Dr. Vince Scialli
BSC 1086
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
Immune System ~ Chapter 22 ~ 6/28/2017
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Dr. Vince Scialli
BSC 1086
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
Immune System ~ Chapter 22 ~ 6/28/2017
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Dr. Vince Scialli
BSC 1086
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
Immune System ~ Chapter 22 ~ 6/28/2017
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Dr. Vince Scialli
BSC 1086
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
Immune System ~ Chapter 22 ~ 6/28/2017
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Dr. Vince Scialli
BSC 1086
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
Immune System ~ Chapter 22 ~ 6/28/2017
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Dr. Vince Scialli
BSC 1086
CELLS OF THE IMMUNE SYSTEM
T - LYMPHOCYTES ~ T-cells
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
Migrate to blood, lymph nodes, spleen & other organs of
lymphatic system in ready position ~ memory
Immune System ~ Chapter 22 ~ 6/28/2017
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Dr. Vince Scialli
BSC 1086
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
Poison ivy
Animal dander
Detergents
Penicillin
Cosmetics
Pollens
Grasses & Weeds
Household Products Foods
Thus . . . allergic in some individuals & not in others
Immune System ~ Chapter 22 ~ 6/28/2017
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Dr. Vince Scialli
BSC 1086
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
EG:
Immune System ~ Chapter 22 ~ 6/28/2017
Interferons, interleukins, etc.
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Dr. Vince Scialli
BSC 1086
Antigen Presentation
T-cells MUST be activated by exposure to antigen
Antigen-Presenting Cells ~ Macrophages ~ APC’s
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
Blood Transfusion ~ ABO blood type
Tissue or Organ Transplants
Could be recognized as foreign in “autoimmune disease”
Immune System ~ Chapter 22 ~ 6/28/2017
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Dr. Vince Scialli
BSC 1086
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
Memory T-Cells ~ “the ready position”
Trigger differentiation into cytotoxic T-cells upon
repeated exposure to same foreign antigen
Immune System ~ Chapter 22 ~ 6/28/2017
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Dr. Vince Scialli
BSC 1086
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 WBC’s 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
HIV (Aids Virus) ~ inhibits Helper T-Cells
Causes massive immunodeficiency
Immune System ~ Chapter 22 ~ 6/28/2017
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Dr. Vince Scialli
BSC 1086
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
Slow destruction of tumor cells
Stimulation of macrophages
Immune System ~ Chapter 22 ~ 6/28/2017
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Dr. Vince Scialli
BSC 1086
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
Immune System ~ Chapter 22 ~ 6/28/2017
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Dr. Vince Scialli
BSC 1086
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 light (variable) & two heavy chains (constant)
Specialized Binding Sites ~ very specific
Antigen Binding Sites
Complement Binding Sites
Macrophage Binding Sites
Immune System ~ Chapter 22 ~ 6/28/2017
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Dr. Vince Scialli
BSC 1086
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
Developed from vaccines or vaccination
PASSIVE IMMUNITY ~ immediate but temporary ~ NO
ANTIBODIES
PRODUCED
Antibodies received directly from an “external” source
Antibodies in mother’s milk or in serum infusion
Tetanus Anti-toxin antibodies
Snake Anti-venom antibodies
Immune System ~ Chapter 22 ~ 6/28/2017
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Dr. Vince Scialli
BSC 1086
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”
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
Immune System ~ Chapter 22 ~ 6/28/2017
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Dr. Vince Scialli
BSC 1086
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
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
Immune System ~ Chapter 22 ~ 6/28/2017
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Dr. Vince Scialli
BSC 1086
Antibody Classification
Heavy chain structure determines way antibody is secreted &
how it is distributed in body
Heavy Chain = Constant Segment
Five major classes
IgG – MOST common in serum ~ 80%
IgA – local immunity antibody ~ in glandular secretions
IgM – early protecting antibody ~ first antibodies
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
Immune System ~ Chapter 22 ~ 6/28/2017
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Dr. Vince Scialli
BSC 1086
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 antigenantibody interaction
Antibodies bind to antigenic determinant target sites
on pathogen
Results in complement fixation & activation
Chemicals released attracts macrophages &
enhances inflammatory response & lysis
Complement coated invaders attracted to Blymphocytes
Immune System ~ Chapter 22 ~ 6/28/2017
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Dr. Vince Scialli
BSC 1086
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 antigenantibody 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
Skin Allergy – contact dermatitis
Immune System ~ Chapter 22 ~ 6/28/2017
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Dr. Vince Scialli
BSC 1086
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
Rheumatoid arthritis
Multiple Sclerosis
Immune System ~ Chapter 22 ~ 6/28/2017
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