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Immune System - Body Defenses


Inflammatory Response
Innate Immunity)
Acquired Immunity
T cells
Innate Immunity
Acquired (Adaptive) Immune Response
Innate Immunity
Immune System Functions/Defense
Inflammatory Response
Adaptive (Acquired) Immune Response
Bone marrow – Origin of blood cells
Cell-Mediated Immunity – T Cells
Major Histocompatibility Complex
Antibody Structure
Antigen-Specific Responses
B Cell Antibody Production
Immunological Memory
Allergic Response/Inflammation Reaction


Inflammatory Response

The immune system protects your body against foreign pathogens such as bacteria and viruses. The immune system has 3 lines of defense against foreign pathogens:

1. Physical and Chemical Barriers (Innate Immunity)

2. Nonspecific Resistance (Innate Immunity)

3. Specific Resistance (Acquired Immunity)


Physical and Chemical Barriers (Innate Immunity)

Physical and chemical barriers form the first line of defense when your body is invaded.

Physical Barriers

  • Your skin has thick layer of dead cells in the epidermis which provide protection
  • Your mucous membranes trap microbes.

Chemical Barriers

  • Lysozyme, an enzyme produced in tears, acts as an antibiotic (kills bacteria)
  • Gastric juice in the stomach destroys bacteria because the gastric juice is highly acidic (pH 2-3).

Nonspecific Resistance (Innate Immunity)

The second line of defense is nonspecific resistance that destroys invaders in a generalized way without targeting specific individuals:

  • Phagocytic cells ingest and destroy all microbes that pass into body tissues. For example macrophages are cells derived from monocytes (a type of white blood cell). Macrophages leave the bloodstream and enter body tissues to patrol for pathogens. When the macrophage encounters a microbe, this is what happens:
    1. The microbe attaches to the phagocyte.
    2. The phagocyte's plasma membrane extends and surrounds the microbe and takes the microbe into the cell in a vesicle.
    3. The vesicle merges with a lysosome, which contains digestive enzymes.
    4. The digestive enzymes begin to break down the microbe. The phagocyte uses any nutrients it can and leaves the rest as indigestible material and antigenic fragments within the vesicle.
    5. The phagocyte makes protein markers, and they enter the vesicle.
    6. The indigestible material is removed by exocytosis.
    7. The antigenic fragments bind to the protein marker and are displayed on the plasma membrane surface. The macrophage then secretes interleukin-1 which activates the T cells to secrete interleukin 2, as described below under specific resistance .
  • Inflammation is a localized tissue response that occurs when your tissues are damaged and in response to other stimuli. Inflammation brings more white blood cells to the site where the microbes have invaded. The inflammatory response produces swelling, redness, heat, pain
  • Fever inhibits bacterial growth and increases the rate of tissue repair during an infection.

Specific Resistance (Acquired Immunity)

The third line of defense is specific resistance. This system relies on antigens, which are specific substances found in foreign microbes.

Most antigens are proteins that serve as the stimulus to produce an immune response. The term "antigen" comes from ANTI-body GENerating substances.

Here are the steps in an immune response:

  1. When an antigen is detected by a macrophage (as describe above under phagocytosis), this causes the T-cells to become activated.

    The activation of T-cells by a specific antigen is called cell-mediated immunity. The body contains millions of different T-cells, each able to respond to one specific antigen.

  2. The T-cells secrete interleukin 2. Interleukin 2 causes the proliferation of certain cytotoxic T cells and B cells.
  3. From here, the immune response follows 2 paths: one path uses cytotoxic T cells and the other uses B cells.

Cytotoxic T Cell Pathway

  • The cytotoxic T cells are capable of recognizing antigens on the surface of infected body cells.
  • The cytotoxic T cells bind to the infected cells and secrete cytotoxins that induce apoptosis (cell suicide) in the infected cell and perforins that cause perforations in the infected cells.
  • Both of these mechanisms destroys the pathogen in the infected body cell.


Click here for an animation on cytotoxic T cells. The animation is followed by practice questions. Click here for even more practice questions.


T Cell Pathway

  • T-cells can either directly destroy the microbes or use chemical secretions to destroy them.
  • At the same time, T cells stimulate B cells to divide, forming plasma cells that are able to produce antibodies and memory B cells.
  • If the same antigen enters the body later, the memory B cells divide to make more plasma cells and memory cells that can protect against future attacks by the same antigen.
  • When the T cells activate (stimulate) the B cells to divide into plasma cells, this is called antibody-mediated immunity.


Click here for an animation on the immune response. The animation is followed by practice questions.



Antibodies (also called immunoglobulins or Ig's) are Y-shaped proteins that circulate through the blood stream and bind to specific antigens, thereby attacking microbes.

The antibodies are transported through the blood and the lymph to the pathogen invasion site.

The body contains millions of different B cells, each able to respond to one specific antigen.

There are 4 classes of antibodies (listed from most common to least common):






Each antibody is made of four polypeptide (protein) chains: 2 heavy chains and 2 light chains. Both heavy chains are identical to each other and both light chains are identical to each other. Each contains a constant region and a variable region. The constant region forms the main part of the molecule while the variable regions forms the antigen-binding site.Each antibody has 2 antigen-binding sites.

Antibodies work in different ways:

1. Neutralizing an Antigen

The antibody can bind to an antigen, forming an antigen-antibody complex. This forms a shield around the antigen, preventing its normal function. This is how toxins from bacteria can be neutralized or how a cell can prevent a viral antigen from binding to a body cell thereby preventing infection.

2. Activating Complement:

Complement is a group of plasma proteins made by the liver that normally are inactive in the body. An antigen-antibody complex triggers a series of reactions that activates these proteins. Some of the activated proteins can cluster together to form a pore or channel that inserts into a microbe's plasma membrane.This lyses (ruptures) the cell. Other complement proteins can cause chemotaxis and inflammation, both of which increase the number of white blood cells at the site of invasion.

3. Precipitating Antigens

Sometimes the antibodies can bind to the same free antigen to cross-link them. This causes the antigen to precipitate out of solution, making it easier for phagocytic cells to ingest them by phagocytosis (as describe above).

Also, the antigens within the cells walls of the bacteria can cross-link, causes the bacteria to clump together in a process called agglutination, again making it easier for phagocytic cells to ingest them by phagocytosis.

4. Facilitating Phagocytosis

The antigen-antibody complex signals phagocytic cells to attack. The complex also binds to the surface of macrophages to further facilitate phagocytosis.


There are 3 major types of T cells:

1. Cytotoxic T cells

These cells secrete cytotoxin which triggers destruction of the pathogen's DNA or perforin which is a protein that creates holes in the pathogens plasma membrane. The holes cause the pathogen to lyse (rupture).

2. Helper T cells

These cells secrete interleukin 2 (I-2) which stimulates cell division of T cells and B cells. In other words, these cells recruit even more cells to help fight the pathogen.

3. Memory T cells

These cells remain dormant after the initial exposure to an antigen. If the same antigen presents itself again, even if it is years later, the memory cells are stimulated to convert themselves into cytotoxic T cells and help fight the pathogen.



Innate Immunity

Innate immunity provides broad defenses against infection

Present before any exposure to pathogens and is effective from the time of birth

Involves nonspecific responses to pathogens

A pathogen that successfully breaks through an animal’s external defenses encounters several innate cellular and   chemical mechanisms that impede its attack on the body

Non-selective and no lag time – immediate response, no previous exposure required

Protects against infections, toxins

Works with specific (acquired) immune response

Physical barriers, secretion, chemical toxins

Phagocytosis - macrophages neutrophils engulf and digest recognized "foreign" cells – molecules

Inflammatory response - localized tissue response to injury producing swelling, redness, heat, pain

Complement system – activated proteins that destroy pathogen plasma membranes

Natural Killer cells – special class of lymphocyte-like cells that destroy virus infected cells and cancer cells

Interferon  - proteins that non-specifically defend against viral infection


Acquired (Adaptive) Immune Response

Depends on B and T lymphocytes

Specific immune response directed attack against pathogens (antigen)

Lag time

Previous Antigen exposure required

Protects against pathogens and cancer cells


    Antibody-mediated: B cells

    Cell-mediated: T cells

Click here for an animation that summarizes the immune response. The animation is followed by practice questions.



Innate Immunity / External Defenses

  1. Epidermis - provides a physical barrier, periodic shedding removes microbes              
  2. Mucous membranes and mucus - traps microbes and foreign particles
  3. Hair - within the nose filters air containing microbes, dust, pollutants
  4. Cilia - lines the upper respiratory tract traps and propels inhaled debris to throat
  5. Lacrimal apparatus - produces tears that cleanse the eye
  6. Saliva - dilutes the number of microorganisms and washes the teeth and mouth
  7. Urine - flush microbes out of the urethra
  8. Defecation and vomiting - expel microorganisms.


Chemical Factors

1. Skin acidity - inhibit bacterial growth
2. Sebum -unsaturated fatty acids provide a protective film and inhibit growth
3. Lysozyme- found in perspiration, tears, saliva  can breakdown the cell wall of certain bacterial
4. Hyaluronic acid - gelatinous substance that slows the spread of noxious agents
5. Gastric Juice - strong acid that destroys ingested microbes and most toxins

Immune System Functions

  1. Scavenge dead, dying body cells
  2. Destroy abnormal (cancerous)
  3. Protect from pathogens & foreign molecules: parasites, bacteria, viruses

Steps in Immune Defense

  During an immune response, cells detect invader/foreign cells, communicate alarm & recruit immune cells, suppress or destroy invader


  • Macrophages and neutrophils respond to invasion by foreign pathogens, engulf and digest recognized "foreign" cells
  • molecules, remove cellular debris
  • Monocyte - macrophage system – free and fixed
  • Macrophages – Neutrophils and eosinophils
  • Margination – stick to the inner endothelial lining of capillaries of affected tissue 
  • Move by diapedesis – move through capillary walls, exhibit chemotaxis

Phagocytes release chemical mediators

  • Kinins -  stimulate complement system (plasma proteins), chemot0xins, pain
  • Clotting factors – walling off invasion
  • Lysosomal enzymes – destroy invaders


  • Fastest response of all WBC to bacteria and parasites
  • Direct actions against bacteria
  • Release lysozymes which destroy/digest bacteria
  • Release defensive proteins that act like antibiotics
  • Release strong oxidants (bleach-like, strong chemicals ) that destroy bacteria


  • Leave capillaries to enter tissue fluid
  • Attack  parasitic worms
  • Phagocytize antibody-antigen complexes


  • Take longer to get to site of infection, but arrive in larger numbers
  • Become free (roaming) macrophages, once they leave the capillaries
  • Destroy microbes and clean up dead tissue following an infection



Phagocytosis Mechanisms

  • Chemotaxis- attraction to certain chemical mediators, released at the site of damage, chemotaxins induce phagocytes to injury
  • Opsonization- identify (mark) pathogen, coated with chemical mediators, most important opsonins
  • Toll-like receptors (TLR’s)- phagocytic cells studded with plasma membrane receptor proteins, bind with pathogen markers, recognition function - allows phagocytes to “see” and distinguish from self-cells



Inflammatory Response

Effects of inflammation include: temporary repair of injury, slowing the spread of pathogens, mobilization of local, regional, and systemic defenses

Macrophages, Mast Cells release histamine
- Localized vasodilation  

    1. Capillary permeability - increased gaps in capillaries bring more WBC's & plasma proteins
    2. Swelling, redness, heat and pain are incidental

- Phagocytes release chemical mediators

    1. Kinins -  stimulate complement system (plasma proteins), chemotaxinsClotting factors – walling off invasion
    2. Remove pathogens, debris


Natural Killer Cells

  • Patrol the body and attack virus-infected body cells and cancer cells
  • Recognize cell surface markers on foreign cells
  • Destroy cells with foreign antigens
  • Rotation of the Golgi toward the target cell and production of perforins
  • Release of perforins by exocytosis
  • Interaction of perforins causing cell lysis+

Antimicrobial Proteins - Complement System

  • System of inactive proteins produced by liver circulating in blood and on cell membranes
  • Cascade of plasma complement proteins (C) activated by antibodies or antigens causing cascade of chemical reactions
  • Direct effect is lysis of microorganisms by destroying target cell membranes
  • Indirect effects include: chemotaxis, opsonization, inflammation: recruit phagocytes, B & T lymphocytes


  • Complement system –System of inactive proteins produced by liver circulating in blood and on cell membranes, activated by antibodies or antigens causing cascade of chemical reactions, direct effect is lysis of microorganisms via membrane attack complex that destroy pathogen plasma membranes
  • Indirect effects include:
     - Chemotaxis
     - Opsonization
     - Inflammation: recruit phagocytes, B & T lymphocytes


  • proteins that non-specifically defend against viral infection, produced by virus-infected cells, binds to membranes of adjacent, uninfected cells, triggers production of chemicals that interfere with viral replication
  • Enhances macrophage, natural killer, and cytotoxic T cell & B cell activity 
  • Slows cell division and suppresses tumor growth
  • Three major types of interferons are:
    • Alpha– produced by leukocytes and attract/stimulate NK cells
    • Beta– secreted by fibroblasts causing slow inflammation
    • Gamma – secreted by T cells and NK cells stimulate macrophage activity

Adaptive (Acquired) Immune Response - 3rd line of defense
Depends on B and T lymphocytes - specific immune response directed attack against pathogens (antigen)
Lag time ~ two weeks, previous Antigen exposure required
Protects against pathogens and cancer cells

Two Components:

Antibody-mediated: B cells

Cell-mediated: T cells

Properties of Acquired Immunity
Specificity – activated by and responds to a specific antigen
Versatility – is ready to confront any antigen at any time
Memory – “remembers” any antigen it has encountered
Tolerance – responds to foreign substances but ignores normal tissues


Lymphocytes - B and T cells originate in red bone marrow, move to lymphatic tissue from processing sites and continually circulate

Primary lymphatic organs - lymphocytes mature into functional cells (red bone marrow B cells and thymus T cells)
Secondary lymphatic organs site of immune response – lymph nodes


Bone marrow – origin of blood cells

Thymus site of maturing T Lymphocytes

Lymph nodes Exchange Lymphocyte w/ lymph (remove, store, produce, add). Resident macrophages remove microbes and debris from lymph. Lymphocytes produce antibodies and sensitized T cells released in lymph

Spleen – Exchange Lymphocytes with blood, residents produce antibodies and sensitized T cells released in blood, (worn RBCs)

- An antigen is any foreign molecule that is specifically recognized by lymphocytes and elicits a response from them
- A lymphocyte actually recognizes and binds to just a small, accessible portion of the antigen called an epitope or antigenic determinant

    1. Antigenic determinants - Specific regions of a given antigen recognized by a lymphocyte
    2. Antigenic receptors -Surface of lymphocyte that combines with antigenic determinant

Cell-Mediated Immunity – T Cells
- Antigens that stimulate this response are mainly intracellular (cell to cell).
- Requires constant presence of antigen to remain effective
- Involves cytokines:  Chemical messengers of immune cells.
- Over 100 have been identified.
- Stimulate and/or regulate immune responses.

    1. Interleukins:  Communication between WBCs.
    2. Interferons:  Protect against viral infections.
    3. Chemotaxins:  Attract WBCs to infected areas.

Major types of T cells
- Cytotoxic T cells (TC) – attack foreign cells
- Helper T cells (TH) – activate other T cells and B cells
- Suppressor T cells (TS) – inhibit the activation of T and B cells
- Memory T cells – function during a second exposure to antigen

Cell-Mediated Immunity – T Cells
-T cells bind to small fragments of antigens that are bound to normal cell-surface proteins called MHC molecules
- MHC molecules are encoded by a family of genes called the major histocompatibility complex
- Infected cells produce MHC molecules which bind to antigen fragments and then are transported to the cell surface in a process called antigen presentation
- A nearby T cell can then detect the antigen fragment displayed on the cell’s surface
- Depending on their source peptide antigens are handled by different classes of MHC molecules
- Antigen activates effector T cells and produces memory T cells and cytotoxic T cells that lyse virus-infected cells, tumor cells, and tissue transplants

Antigen Recognition
- Lymphocytes respond to antigens bound to either class I or class II MHC proteins
- T cell membranes contain CD markers
- CD3 markers present on all T cells
- CD8 markers on cytotoxic and suppressor T cells
- CD4 markers on helper T cells

Major Histocompatibility Complex

- T cell activation involves recognition of antigens combined with major histocompatability (MHC) glycoproteins on the surface of cells.
- Class I molecules display antigens on surface of nucleated cells, resulting in destruction of cells
- Class II molecules display antigens on surface of antigen-presenting cells, resulting in activation of immune cells

Class I MCH molecules are found on almost all nucleated cells of the body display peptide antigens to cytotoxic T cells.

Click here for an animation on cytotoxic T cells. The animation is followed by practice questions. For even more practice questions on cytotoxic T cells, click here.

Class II MHC molecules are located mainly on dendritic cells, macrophages, and B cells display antigens to helper T cells.


1. A fragment of foreign protein (antigen) inside the cell associates with an MHC molecule and is transported
to the cell surface.

2. The combination of MHC molecule and antigen is recognized by a T cell, alerting it to the infection.

Antigen Presenting Cells

- Macrophages & Dendritic Cells engulf foreign antigens by phagocytosis, proteins broken down into peptides
- Peptides go to ER and Golgi where they are attached to new MHC self antigen molecules
- New self antigen and its antigen fragment are added to the cell membrane and presented to lymphocytes


T Cells Only Recognize Antigen Associated with MHC Molecules on Cell Surfaces


Types of T cells:

T Helper (TH) Cells
-  Primary role in immune response.
-  Most are CD4 (identifier - acts as an accessory molecule, forming part of larger structures such as the T-cell receptor)
- Recognize antigen on the surface of antigen presenting cells (e.g.: macrophage).
- Secrete Interleukin II (T-cell growth factor), interferon and cytokines which stimulate B-cells and natural killer cells
 - Activate macrophages
 - Induce formation of cytotoxic T cells
 - Stimulate B cells to produce antibodies.


Cytotoxic T (Tc) Cells: Destroy target cells
 - Killer Ts or CD8
 - Recognize antigens on the surface of all cells: kill host cells that are infected with viruses or bacteria. Also recognize and kill cancer cells, and transplanted tissue.
 - Release protein called perforin which forms a pore in target cell, causing lysis of infected cells.
 - Produce cytokines, which promote phagocytosis and inflammation
 - Undergo apoptosis when stimulating antigen is gone.

Memory T-Cells

 - Can survive a long time and give lifelong immunity from infection
 - Can stimulate memory B-cells to produce antibodies
 - Can trigger production of killer T cells
- Thymosin - hormone important in T cell lineage, enhances capabilities of existing T cells and the proliferation of new T cells in lymphoid tissues - decreases after age 30-40


Antibody-Mediated (Humoral) Immunity
Involves production of antibodies against foreign antigens.
- Antibodies are produced by a subset of lymphocytes called B cells.
- Mature in Bone marrow - lymphatic tissue, especially spleen and lymph nodes
- B cells that are stimulated will actively secrete antibodies and are called plasma cells.
- Antibodies (immunoglobulins, Ig) are found in extracellular fluids (blood plasma, lymph, mucus, etc.) and the surface of B cells.
- Defense against bacteria, bacterial toxins, and viruses that circulate freely in body fluids, before they enter cells.
- Also cause certain reactions against transplanted tissue.

- 1000s of different B cells, each recognizes a different antigen on the surface of a macrophage.
- Each antigen stimulates production of a single specific antibody B cells (along with T cells) come in contact with antigen.
- They are stimulated (by T cells) to produce many clones, plasma cells, which make antibodies.
- Memory B cells – secondary response = faster, more sensitive


Antibody Structure

- Antibodies or Immunoglobulins (Ig)

- Classes: IgG, IgM, IgA, IgE, IgD

- Structure:
Variable region -  combines with antigenic determinant of antigen
Constant region -responsible for activities

Antibodies (immunoglobulins, Ig) are proteins that recognize specific antigens and bind to them. They are found in extracellular fluids (blood plasma, lymph, mucus, etc.) and the surface of B cells.

Defense against bacteria, bacterial toxins, and viruses that circulate freely in body fluids, before they enter cells.
Also cause certain reactions against transplanted tissue.

Antigenic determinants - specific regions of a given antigen recognized by a lymphocyte
Antigenic receptors are found on surface of lymphocyte that combines with antigenic determinant to form Antigen-Antibody Complex

Antibodies affinity: A measure of binding strength.

Consequences of Antibody Binding
 - Agglutination: Antibodies cause antigens (microbes) to clump together.
 - Hemagglutination:  Agglutination of red blood cells.  Used to determine ABO blood types - like Antibodies & antigens will agglutinate.
 - Opsonization  - Phagocytosis
 - Activates Complement System/Inflammatory Response
 - Antigen-Specific Responses
Activate T lymphocytes: direct attack
Activate B lymphocytes to become: memory cells: secondary  immune response to that antigen, plasma cells that produce more antibodies to attack that antigen

Antigen-Specific Responses
- Activate T lymphocytes: direct attack
- Activate B lymphocytes to become:
Memory cells: secondary immune response to that antigen
Plasma cells: antibodies – attack that antigen

Classes of Immunoglobulins
Percentage serum antibodies:  80%, location: Blood, lymph, intestine
Enhances phagocytosis, neutralizes toxins and viruses, protects fetus and newborn.

Percentage serum antibodies:  5-10%, location: Blood, lymph, B cell surface (monomer)
First antibodies produced during an infection. Effective against microbes and agglutinating antigens.

Percentage serum antibodies:  10-15%, location: Secretions (tears, saliva, intestine, milk), blood and lymph.
Localized protection of mucosal surfaces.  Provides immunity to infant digestive tract.

Percentage serum antibodies:  0.2%, location: B-cell surface, blood, and lymph
In serum function is unknown.  On B cell surface, initiate immune response

Percentage serum antibodies:  0.002%, location: Bound to mast cells and basophils throughout body.  Blood.
Allergic reactions.  Possibly lysis of worms.

B Cell Antibody Production
- B cells develop from stem cells in the bone marrow of adults (liver of fetuses).
- After maturation B cells migrate to lymphoid organs (lymph node or spleen). 
- Clonal Selection:  When a B cell encounters an antigen it recognizes, it is stimulated and divides into many clones called plasma cells, which actively secrete antibodies.
- Each B cell produces antibodies that will recognize only one antigenic determinant.


Immunological Memory:
Primary Response - After initial exposure to antigen, no antibodies are found in serum for several days. A gradual increase number of Abs, first of IgM and then of IgG is observed.  Most B cells become plasma cells, but some B cells become long living memory cells. Gradual decline of antibodies follows.

Secondary Response - Subsequent exposure to the same antigen displays a faster/more intense response due to the existence of memory cells, which rapidly produce plasma cells upon antigen stimulation


Clonal Selection

...B cells (and T cells) that encounter stimulating antigen will proliferate into a large group of cells.
- Why don’t we produce antibodies against our own antigens?  We have developed tolerance to them.
- Tolerance: To prevent the immune system from responding to self-antigens
- Clonal Deletion:  B and T cells that react against self antigens are normally destroyed during fetal development
- Preventing activation of lymphocytes – activate suppressor T cells, control the immune system when the antigen / pathogen has been destroyed

Apoptosis- programmed cell death (“Falling away”).

- Human body makes 100 million lymphocytes every day.  If an equivalent number doesn’t die, will develop leukemia.
- B cells that do not encounter stimulating antigen will self-destruct and send signals to phagocytes to dispose of their remains.
- Many virus infected cells will undergo apoptosis, to help prevent spread of the infection.

Autoimmune Diseases: Failure of “Self-Tolerance”

- Some diabetes mellitus – attack beta cells
 - Multiple sclerosis – attack on myelin nerve sheath
 - Rheumatoid arthritis – attack joint cartilage
 - Myasthenia gravis – ACh-receptors at endplate attacked



Allergic Response - Inflammation Reaction to Non-pathogen

 - First exposure: sensitization and activation clone B cells that form antibodies and memory cells
 - Re-exposure: many antibodies produced, activated Ts intensify inflammatory response



- Body defends itself with barriers, chemicals & immune responses
- WBCs and relatives conduct direct cellular attack: phagocytosis, activated NK & cytotoxic T cells and produce attack proteins (i.e.  antibodies, complement, & membrane attack complex)
- Cytokines, communicate cell activation, recruitment, swelling, pain, & fever in the inflammation response
- Defense against bacteria is mostly innate while viral defense relies more on acquired immune responses

- Autoimmune diseases are a failure of self-tolerance

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This material is based upon work supported by the Nursing, Allied Health and Other Health-related Educational Grant Program, a grant program funded with proceeds of the State’s Tobacco Lawsuit Settlement and administered by the Texas Higher Education Coordinating Board.