Presentation on theme: "I MMUNE S YSTEM B ASICS. H OW A V IRUS ATTACKS THE BODY. HTTP :// WWW. YOUTUBE. COM / WATCH ? V =R PJ 0 EM EGS H Q& FEATURE = RELATED HTTP :// WWW. YOUTUBE."— Presentation transcript:
I MMUNE S YSTEM B ASICS
H OW A V IRUS ATTACKS THE BODY. HTTP :// WWW. YOUTUBE. COM / WATCH ? V =R PJ 0 EM EGS H Q& FEATURE = RELATED HTTP :// WWW. YOUTUBE. COM / WATCH ? V =R PJ 0 EM EGS H Q& FEATURE = RELATED
P ATHOGENS 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:
HTTP :// WWW. YOUTUBE. COM / WATCH ? V =N ON 4M K YQ P YA& LIST =PL713E26869E18998B& INDEX =3 Pathogens will trigger the immune system to respond.
E XTERNAL DEFENSE Skin produces Sweat which contains lysozymes Oil – traps bacteria / fungi Mucus membranes of digestive and respiratory tract produce Mucus to trap foreign particles Cilia sweep the mucus to be cleared from body
N ON - SPECIFIC INTERNAL DEFENSE WHITE blood cells Monocytes and Neutrophils are able to cross capillary walls use PHAGOCYTOSIS to engulf foreign invaders Natural Killer cells Respond to chemical message from Neutrophils; sensing molecular changes in cells causes the release of cytotoxic proteins into “foreign cell”.
N ON - SPECIFIC INTERNAL DEFENSE Inflammatory Response Histamines 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)
N ON - SPECIFIC INTERNAL DEFENSE FEVER – triggered if pathogen is in bloodstream or infection is now systemic rather than localized. 102 – F is beneficial high temp in fighting viral infections and triggers release of interferon. Interferon literally interferes with viral replication.
S PECIFIC I NTERNAL R ESPONSE 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.
Leukocytes (White Blood Cells) lymphocytes T cellsB CellsNK Cells Other Types of WBC EosinophilsMacrophages W HITE B LOOD C ELLS
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.
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.
A NTIBODIES & A NTIGENS 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. Cell Class 1 MHC molecule Antigen Pathogen lymphokines 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.
A NTIBODIES – 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.
B- CELL RECEPTORS “Y” shaped proteins extend from cell membrane. 2 heavy chains 2 light chains that can be rearranged to match antigen.
T- CELL RECEPTORS 2 parallel protein chains - chain – chain These chains form the recognition site for each different antigen.
H OW ANTIGEN RECOGNITION BY L YMPHOCYTES 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
C ELL 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
C ELL MEDIATED IMMUNITY T-cells attack invaders directly Perforins released by cytoxic T-Cells create pores in infected cell resulting in ion/water inflow cell lysis Effective against intracellular parasites Infected cell Perforins T-Cell
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).
The ability to resist a pathogen Two forms of immunity; ◦ ACTIVE – direct exposure that creates immune response. ◦ PASSIVE – induced exposure through vaccination. W HAT IS IMMUNITY ?
I MMUNITY 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
Step three – macrophage activates Helper T-cells Helper T-cells set up the two prong attack of the immune response D EVELOPMENT OF PRIMARY IMMUNE RESPONSE - CONTINUED
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 D EVELOPMENT OF PRIMARY IMMUNE RESPONSE - CONTINUED antibodies
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 D EVELOPMENT OF PRIMARY IMMUNE RESPONSE - CONTINUED
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. D EVELOPMENT OF PRIMARY IMMUNE RESPONSE - CONTINUED
I MMUNE R ESPONSE 2- PRONG ATTACK TRIGGERED WHEN H ELPER T- CELLS ARE ALERTED 5b. Creation of Memory B-cell
I MMUNOLOGICAL M EMORY 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.
H OW 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.
I MMUNOLOGICAL M EMORY Heightened secondary response is due to long lived memory cells as a result of first exposure to antigen A.
I MMUNE R ESPONSE 2- PRONG ATTACK TRIGGERED WHEN H ELPER T- CELLS ARE ALERTED