Immune System: Defense Against Disease

Topics 6.3 and 11.1Maria SaraoSamantha BryanEmily Waggoner

Vocabulary- It's important

Pathogen-An organism or virus that causes a diseaseAntigen-Any foreign macromolecule (either proteins,

polysaccharides or structures on the surface of bacteria) that triggers an immune response

Antibody-Antibodies are proteins that bind to particular antigens and

mark them for elimination from the bodyAntibiotics-Any substance that is able to kill or inhibit a microorganism

such as bacteria

Vocabulary Parte 2

Virus-An infective agent consisting of a protein coat

surrounding an RNA or DNA coreAre not cells and do not possess membranes or

organelles. They cannot manufacture their own proteins and

must invade living cells to take over their protein production “machinery”

Leucocytes-White blood cellsPhagocytic leucocytesSpecialized white blood cells that engulf foreign/invading

pathogens and destroy them•

Different Types of Leucocytes

Helpful Video:

https://www.khanacademy.org/science/biology/immunology/v/role-of-phagocytes-in-innate-or-nonspecific-immunity

Note: What is a MHC?• Polypeptides from pathogen attach to proteins from the

phagocyte (antigen presenting protein)• Polypeptide + antigen presenting protein = MHC II• MHC II's are recognized by helper-T cells• Helper-T cells have receptors that bind to MHC II's • This activates helper T-cells so that they can release

cytokines and alert other immunological cells of the pathogen

6.3.1: Define pathogen.

Pathogen- An organism or virus that causes a disease

• This includes bacteria, viruses, and other microorganisms that can cause disease.

• Synonym: germ

6.3.2: Explain why antibiotics are effective against bacteria but not against viruses.

• Antibiotics are chemicals that take advantage of the differences between prokaryotic and eukaryotic cells.• One type of antibiotic can selectively block protein synthesis in bacteria.• Another may inhibit the production of a new cell wall by bacteria, thus blocking their ability to grow and divide.• In both cases, our body cells will remain unaffected by the medicine.• Viruses are not affected because they use our own body cells' metabolism to replicate. • Therefore, any chemical that would inhibit this would also be damaging our own cells.

6.3.3: Outline the role of skin and mucous membranes in defense against pathogens.

• Skin and mucous membranes serve as external forms of defense against pathogens

• Skin is the physical barrier• Mucous membranes: mucous is lined in certain

areas of the body. -Trachea -Urethra -Nasal passages -Vagina

• When a pathogen enters the body, mucous surrounds the pathogen, the body senses the excess mucous, so coughing is induced to expel the pathogen.

6.3.4: Outline how phagocytic leucocytes ingest pathogens in the blood and in body tissues.

• A type of white blood cell• Float around the body in blood• Phagocyte surrounds the pathogen by

endocytosis• A vacuole containing the pathogen travels to a

lysosome• The membranes of the vacuole and lysosome

fuse• Digestive enzymes in the lysosome destroy the

pathogen• The pathogen “debris” is released by exocytosis

Phagocytic Leucocytes

* QUICK REMINDER: a macrophage is a type of phagocyte

Quick Review Video http://www.youtube.com/watch?v=KhqXxn5ay1U

6.3.5: Distinguish between antigens and antibodies.

Antibodies• Protein molecules produced in

response to a specific pathogen• Therefore, each antibody is different....• But all have are a "Y" shaped protein

Antigens• Foreign proteins embedded in

the outer surface of the pathogen (i.e. the capsid of a virus)• These trigger an immune response• Most pathogens have several different types of antigen and so may trigger the production of several different types of antibody

At the end of the forked end of the antibody, there is a binding site where the antibody attaches itself to the antigen, and thus the pathogen.

Explain Antibody Production 6.3.6/11.1.4

• Beta Cells produce antibodies in small amounts (in comparison to the infection).

• Antibodies are produced in response to a specific type of pathogen.

• Each antibody is y-shaped. At the end of each fork, there is a binding site, which is where the antibody attaches to the antigen.

Production of Antibodies Cont.d1. Before antibody production, a neutrophil releases chemicals to kill

the pathogen. If this isn’t successful, macrophages arrive.2. The macrophage attempts to ingest the pathogen.3. A protein floating in the blood (C3B) senses the pathogen and

attaches to the surface of the pathogen.4. If these methods don’t work and the pathogen invades a cell, the cell

sends out a stress signal.5. This signal brings a natural killer (NK) cell to kill the entire cell, in

hopes of stopping the pathogen.6. The other method is to prevent the pathogen from entering the cell in

the beginning, which is when antibodies are used.7. A specific B-lymphocyte is identified that can produce an antibody to

bind to the antigen.

Antibody Production Cont.d

8. The B-lymphocytes are cloned (divide repeatedly through mitosis) to rapidly increase the number of antibodies being produced.

9. Antibody production begins.10. The antibodies are released in the bloodstream, searching for the

correct antigen to bind to.11. This binding leads to the presence of T-helper cells to produce

chemicals to kill the pathogen.12 T-helper cells (another type of leucocyte that is specific to that

antigen) bind to the antigen presented by the macrophages and are activated/stimulated.

Antibody Production Cont.d

Basic Overviewhttp://www.youtube.com/watch?v=KpNFAEbLcvkhttp://www.youtube.com/watch?v=Nw27_jMWw10http://www.youtube.com/watch?v=Non4MkYQpY

Detailedhttp://www.youtube.com/watch?v=AmAa2g3fiI4

Review of HIV/AIDS:

• HIV stands for human immunodeficiency virus

• AIDS stands for acquired immunodeficiency syndrome.

• HIV is the virus that causes AIDS• Directly attacks T helper cells (T lymphocytes) • Piggybacks onto one of the T helper cells and then uses

that access into the cell to overtake the host cell and replicate.

• Once enough of the viruses have been replicated, the cell bursts and the virus infects other T cells.

6.3.7: Outline the effects of HIV on the immune system.

• HIV virus kills Helper T-cells• Helper T-Cells tell B-cells there is a

pathogeno no T cells, no recognition of other pathogens

• Immune system cannot mount an effective defense against invading pathogens

• Patients then succumb to secondary infections

6.3.8: Discuss the cause, transmission, and social implications of AIDS.

• AIDS = Acquired immunodeficiency syndrome• HIV = Human immunodeficiency virus

Cause- HIV infects helper-T cells, but can lie dormant in the host cell for many years

until a chemical signal activates it- Helper-T cells communicate which cells need to replicate and produce

antibodies- When Helper-T cells die, communication is lost and antibodies are not

produced- Therefore, the individual cannot fight off pathogens and develops AIDS- Since HIV mutates quickly it is hard to develop medication

6.3.8 continued

Transmission- HIV transmitted through bodily fluids (i.e. during sex, by reusing unsterile

needles, or breastmilk)- In the past blood for transfusions was not tested for HIV and other blood-

borne illnesses

Social Implications- AIDS used to be associated with homosexuals and drug abusers- Was called GRID (Gay-related immune deficiency)- Individuals with HIV are often discriminated against for things like

employment, access to insurance and education, etc.- Not all countries/areas have the education and medical technology to treat

prevent/treat HIV/AIDS- Infection rates can be increased if patients are grouped together in large

wards

The best way of prevention is to educated people on how to decrease their risk of exposure to HIV.

http://www.youtube.com/watch?v=hzQQiCPWSYA

11.1.1: Describe the process of blood clottingPlasma Proteins and platelets circulate in blood plasma.

Two Clotting Proteins: Remain inactive until receive a signal. -prothrombin -fibrinogen1. Damaged cells release chemicals which stimulate platelets to

adhere to the area.2. Other platelets begin adhering, eventually forming a barrier or plug.3. A signal is sent to bring prothrombin to the area.3. The damaging tissue and platelets also release clotting factors which

convert prothrombin into thrombin.

-Thrombin is produced to lead to the production of fibrinogen and eventually fibrin which makes up the clot.

11.1.2: Outline the principle of challenge and response, clonal selection and memory cells as the basis of immunity.Challenge and Response•When the body is challenged by a foreign pathogen it will respond with both a non-specific and specific immune reaction

•The body is capable of recognising invaders as they do not possess the molecular markers that designated all body cells as 'self' (MHC class I)

•Non-specific immune cells (macrophages) present the foreign antigens to lymphocytes as examples of 'non-self' (on MHC class II)

•These lymphocytes can then respond with the production of antibodies to destroy the foreign invaders

Clonal Selection•Each B lymphocyte has a specific antibody on its surface that is capable of recognising a specific antigen

•When antigens are presented to B cells (and TH cells) by macrophages, only the B cell with the appropriate antibody will become activated and clone

•The majority of B cell clones will differentiate into antibody-producing plasma cells, a minority will become memory B cells (BM cells)

•Because pathogens may contain several antigenic determinants, several B cell clones may become activated (polyclonal activation)

11.1.2 Continued Memory Cells

•a specific cell that is part of the immune system- obviously•starts in the bone marrow where lymphocytes are made•can be either a T cell or a B cell•function of these cells is characterized by the memory present in acquired immunity

o once a memory cell has been exposed to a pathogen, it will recognize it much quicker in the event that it encounters the same pathogen again

•There is a delay between initial exposure and the production of antibodies•When a B cell does divide and differentiate, a small proportion of clones will differentiate into memory cells

•Memory cells remain in the body for years (or even a lifetime)•Because the individual no longer presents with the symptoms of infection upon exposure, the individual is therefore immune

11.1.2- Continued

Clonal Selection-

11.1.3: Define active and passive immunity.

Active• Always leads to the production of

memory cells and thus provides for long-term immunity to a pathogen.• Memory cells are produced whenever the immune system is presented with an antigen and there is a full immune response.

Passive• When an organism acquires

antibodies from another• Only a short-term benefit to the receiver of antibodies because no memory cells• Examples- transfer of antibodies from mother to placenta, acquisition of antibodies from mother's colostrum, and injection of antibodies in antisera (i.e. antivenoms for treatment of poisonous snake or spider bites)

11.1.5: Describe the production of monoclonal antibodies and their use in diagnosis and treatment.

Definition- Monoclonal antibodies are monospecific antibodies that are the same because they are made by identical immune cells that are all clones of a unique parent cell, in contrast to polyclonal antibodies which are made from several different immune cells.

Production- 1. Antigens that correspond to a desired antibody are injected into an animal2. B-cells producing the desired antibody are harvested3. Tumor cells are obtained from another source (tumor cells grow and divide

endlessly)4. B-cells are fused with tumor cells, producing hybridoma cells that divide

endlessly, providing the desired antibodies5. The hybridoma cells are cultured and the antibodies they produce are

extracted and purified

11.1.5 Continued Use in Diagnosis- Malaria1. Monoclonal antibodies are made to bind to antigens in malarial parasites2. A test plate is covered with antibodies3. The sample is left on the plate long enough for malaria antigens (if present) to bind to

antibodies4. The sample is rinsed off

-Any bound antigens are detected using more monoclonal antibodies with attached color-changing enzyme

Use in Treatment- Rabies • Rabies usually causes death in humans before the immune system can control it.• Injecting monoclonal antibodies when a person gets infected will control the virus• At the same time, the person's body begins making its own antibodies• Triggers two-fold immune response• Passive through injection• Active through body’s production

11.1.6: Explain the principle of vaccination.

• You cannot be immune to a pathogen unless you're exposed to it at least once.• Vaccines act as the first exposure to a pathogen.• A vaccine is developed by weakening a pathogen an injecting it into the body.• A "weak" strain can be selected, or the pathogen can be heated or treated chemically.• Pathogen would still be recognized as foreign so a primary immune response would take place.• Memory cells would produce antibodies quickly if ever infected with strong pathogen.• Therefore, a vaccination doesn't prevent infection but the secondary immune response is quicker and more intense than the primary one.• Very mild or no obvious symptoms as a result

11.1.7 Discuss the benefits and dangers of vaccination.

Benefits:-Possible total elimination of a disease. Ex. Smallpox, hoping for polio

and measles-Decrease in the spread of epidemics-Costs are minimal in comparison to treatment- preventative medicine

is typically the most cost-effective approach-Each vaccinated person doesn’t have to experience the symptoms at

allDangers:-Before 1999, many vaccines contained thimerosal, containing mercury

which poisoned infants-The perception exists that multiple vaccines given to children in a

short period of time may overload their systems-Anecdotal evidence suggests that MMR vaccine may link to autism-Development of allergies