I MMUNE S YSTEM B ASICS. H OW A V IRUS ATTACKS THE BODY. HTTP :// WWW. YOUTUBE. COM / WATCH ? V =R...

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IMMUNE SYSTEM BASICS

Transcript of I MMUNE S YSTEM B ASICS. H OW A V IRUS ATTACKS THE BODY. HTTP :// WWW. YOUTUBE. COM / WATCH ? V =R...

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IMMUNE SYSTEM BASICS

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HOW A VIRUS ATTACKS THE BODY.HTTP://WWW.YOUTUBE.COM/WATCH?V=RPJ0EMEGSHQ&FEATURE=RELATED

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PATHOGENS Any biological agent that causes illness

and/or disease to its host. Also known as a germs, simple as that!

Different types of pathogens include the following:

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3 MAIN DEFENSES

External Barriers

Non-specific Internal (aka INNATE)

Fever & Inflammatory response

Immune Response

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EXTERNAL DEFENSE

Skin produces Sweat which contains

lysozymes Oil – traps bacteria / fungi

Mucus membranes of digestive and respiratory tract produceMucus to trap foreign particlesCilia sweep the mucus to be

cleared from body

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NON-SPECIFIC INTERNAL DEFENSE

WHITE blood cellsMonocytes and Neutrophils

are able to cross capillary walls

use PHAGOCYTOSIS to engulf foreign invaders

Natural Killer cellsRespond to chemical message from Neutrophils; sensing molecular changes in cells causes the release of cytotoxic proteins into “foreign cell”.

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NON-SPECIFIC INTERNAL DEFENSE

Inflammatory ResponseHistamines make capillary walls

“leaky”RBC, WBC, platelets and fluid cross

capillary walls swelling, redness and warmth in

the injured area PUS formation – tissue debris,

microbes and WBC (dead and alive)

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NON-SPECIFIC INTERNAL DEFENSE

FEVER – triggered if pathogen is in bloodstream or infection is now systemic rather than localized.

102 – 1030 F is beneficial high temp in fighting viral infections and triggers release of interferon.

Interferon literally interferes with viral replication.

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SPECIFIC INTERNAL RESPONSE

aka IMMUNE RESPONSE Use Lymphocytes

B-Cells = humoral T-Cells = cell mediated

Thymus, lymph nodes and spleen house these cells until called into action by interleukins and cytokines.

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Leukocytes (White Blood Cells)

lymphocytes

T cells B CellsNK

Cells

WHITE BLOOD CELLS

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B CELLS B Plasma Cells- when the B

cell produces the antibody for a specific antigen, it begins to clone itself into B plasma cells, that produce more of that particular binding antibody.

These cells release immunoglobulin, or antibodies.

B plasma cells have a 5 to 7 day life-span; all its protein synthesis energy is going into the production of Antibodies, not self preservation.

B Memory Cells- These are the same as B plasma cells, except they remain inactive until the secondary immune response

Secondary immune response is considered anytime the body encounters a pathogen after the first time. Quicker response time.

Primary response is the first time the body encounters a specific pathogen, Lag period before B cells respond.

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T CELLS

T cells

Helper T cell (Th)

Memory T cell

Helper T cell

Killer T cell

Suppressor T cell

Killer T cell (Tk)

Suppressor T cells - in charge of slowing and stopping the immune response after the foreign substance is destroyed.

Helper T cells - secrete lymphokines that direct B cells into producing antibodies and also direct the Killer T cells as to which cell they get to eliminate.

Killer T cells - They find specifically coded infected cells, and then destroy them with cytotoxins. They may be directed by Helper T cells

Memory T cells - derived from Helper T cells, have the same properties as their parent cell, and circulates until the body encounters the pathogen its parent cells were designer for.

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ANTIBODIES & ANTIGENS

Antigens= a fragment of a protein or peptide from the pathogen, taken to the surface of the infected cell and bound in an MHC (major histocompatibility complex) molecule.

The class 1 MHC complex molecule and the foreign peptide form the antigen, which can be read by the receptors on Killer T cells.

CellClass 1 MHC molecule

Antigen

Pathogen

Antibodies are produced by B cells, when stimulated by lymphokines from helper T cells. The antibody attaches to the antigen, completing the signal, coding the infected cells for destruction.

Antibodies are constructed of DNA fragments, making them so unique and almost innumerable.

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ANTIBODIES – PROTEINS CREATED BY B-CELLS THAT “LOCK” DOWN FOREIGN ANTIGENS

Antibodies are shaped to match antigen binding sites called epitopes.

Epitopes are the accessible portion of the antigen – a single bacterial surface protein can have several different epitopes.

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B-CELL RECEPTORS

“Y” shaped proteins extend from cell membrane.

2 heavy chains 2 light chains that

can be rearranged to match antigen.

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T-CELL RECEPTORS

2 parallel protein chains a - chainb – chainThese chains form the recognition site for each different antigen.

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HOW ANTIGEN RECOGNITION BY LYMPHOCYTES WORKS

MHC – major histocompatibility complex Chemical signaling proteins

Class I MHC – found on ALL cells to tell self from non-self

Class II MHC – found on macrophages & B-cells display antigens to Helper T-cells

APC – antigen presenting complex Chemical signaling displays antigen

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CELL MEDIATED IMMUNITY

Helper T-Cells respond to chemical signals presented by macrophage.

Helper T-Cells stimulate cytokines and interleukin which triggers production of B-cells and cytotoxic T-cells.

Helper T cells function in both Humoral & Cell Mediated immunity.

Cell mediated =T-Cell

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CELL MEDIATED IMMUNITY

T-cells attack invaders directlyPerforins released by cytoxic T-Cells

create pores in infected cell resulting in ion/water inflow cell lysis

Effective against intracellular parasites

Infected cell

PerforinsT-Cell

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T-CELLS INTERACTION WITH ANTIGEN PRESENTING CELLS

In both interactions the MHC receptor allows a T-cell to bind which starts defense response.

In (a) an infected body cell alerts cytotoxic cells to destroy infected cell (short term).

In (b) a macrophage displays antigen which triggers immune response (long term).

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The ability to resist a pathogen Two forms of immunity;

◦ ACTIVE – direct exposure that creates immune response.

◦ PASSIVE – induced exposure through vaccination.

WHAT IS IMMUNITY?

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IMMUNITY INVOLVES PRODUCING A PRIMARY IMMUNE RESPONSE Step one – virus or bacteria infects body cell Step two – macrophage recognizes foreign

antigen of pathogen and engulfs it presenting antigen to alert SPECIFIC DEFENSE SYSTEM

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Step three – macrophage activates Helper T-cells Helper T-cells set up the two prong attack of the

immune response

DEVELOPMENT OF PRIMARY IMMUNE RESPONSE - CONTINUED

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Step four –Helper T-cells activate both plasma B-cells and Cytotoxic T-cells

Step five - B-cells form plasma cells which make antibodies to match foreign antigens of pathogen

DEVELOPMENT OF PRIMARY IMMUNE RESPONSE - CONTINUED

antibodies

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Step five part 2- memory B-cells are created to always remember foreign antigen.

Step six – Antibodies made by plasma B-cells

find & attach to pathogens antigens

DEVELOPMENT OF PRIMARY IMMUNE RESPONSE - CONTINUED

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Step seven - Antibodies mark pathogens for destruction.

Step eight - Cytotoxic T-cells locate and destroy infected cell by making a hole in the cell membrane.

DEVELOPMENT OF PRIMARY IMMUNE RESPONSE - CONTINUED

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IMMUNE RESPONSE 2-PRONG ATTACK TRIGGERED WHEN HELPER T-CELLS ARE ALERTED

5b. Creation of Memory B-cell

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IMMUNOLOGICAL MEMORY The reason why vaccines make sense, and we

eventually build a tolerance to certain diseases…

It’s because after every encounter with a pathogen, both the T cells and the B cells differentiate into an inactive form of their parent cell. They remain inactive until the second immune response for that specific pathogen.

Vaccination is an introduction of a dormant or dead pathogen, which allows our body to do its primary immune response without the risk of actual sickness.

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HOW DO VACCINES WORK?

Vaccine contains a dead or weakened pathogen or protein from pathogen.

Most vaccines are only effective against infections before you get them.

Vaccines can wear off overtime booster shots revive immunity.

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IMMUNOLOGICAL MEMORY

Heightened secondary response is due to long lived memory cells as a result of first exposure to antigen A.

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IMMUNE RESPONSE 2-PRONG ATTACK TRIGGERED WHEN HELPER T-CELLS ARE ALERTED