C3.2

Question 1

Innate Immune Responses

Pathogens?

Answer 1

A small organism/particle with the potential to cause disease.
* Most are bacteria and virsus, can be animals, protists and fungi.

Question 2

Innate Immune Responses

Innate Immune System?

Answer 2

Involves strategies to prevent and remove broad categories of pathogens that don’t change during the lifetime.
* Innante Immune responses are the same to different pathogens (not specialized to specfici invaders)
* We are born with it (don’r require exposure)
* Include both prevenative strategies and early figthing off of invaders.

Question 3

Innate Immune Responses

Mucous Membranes?

Answer 3

The thick stcky layer of mucous secreted by cells to trap pathogens in the mucous and prevent them from entering the bloodstrem.
* Areas of the body that by necessity aren’t covered in skin to faciliate gas exchange, eating and excreting.
* The mucous protects these points from pathogen entry.

Question 4

Innate Immune Responses

Cilia?

Answer 4

Hair-like extensions that can create a wave-like movement.
* Many areas of the body that have mucous membrances also have cilia.
* Their movement helps to trap pathogens into the mucous.
* (E.g.,) There’s cilia along our trachea to trap pathogens as they enter our airway.

Question 5

Innate Immune Responses

Platelets?

Answer 5

Cell fragments that are produced by bone marrow.
* Produced initially as a large cell but then broken into fragments (each of which IS a platelet)
* They have no nucleus and a lifespan of 8-10 says.
* They release clotting factors in response to danger to the skin to faciliate the production of a blood clot to minimize blood loss and infection risk.

Question 6

Innate Immune Responses

Prothrombin?

Answer 6

The inactive protein precursor to thrombin,always present in the blood plasma waiting for activation, requires conversion by other clotting factors.
* When converted by clotting factors after activatied by platelets, it becomes thrombin (active enzyme) which converts loose fibrinogen into fibrin (clot formation).
* Thrombin requires no activation for function, and is produced during blood clotting cascade.

Question 7

Innate Immune Responses

Fibrinogen?

Answer 7

Soluable proteins that are present in blood plasma that won’t form a clot in THAT form.
1. Once platelets begin the signalling pathway, the activated thrombin converts many firbinogen proteins to insoluable fibrin
2. The strands of protein that form the clot.

Question 8

Innate Immune Responses

Phagocytes?

Answer 8

A special form of white blood cell that can engulf invading materials by endocytosis (called phagocytosis when it is endocytosis by a phagocye).
* Enzymes in the lysosomes are then able to merge with the engulfed pathogen to break it down inside the phagocyte cell.

Question 9

Innate Immune Responses

Ameoboid Movement?

Answer 9

Involves purposeful cytoplasmic extensions (which can capture pathogens).
* Phagocytes move by amoeboid movement to produce the small movements needed to approach a pathogen.

Question 10

Innate Immune Responses

Epidermis vs Dermis

Answer 10

Dermis: The under layer of skin (living tissue).
* Includes sweat glands, capillaries (to deliver gases to cells), sensory receptors (capable of pain) and dermal cells.

Epidermies: Above, the layer of dead cells.:
* Them being dead is helpful as it prevents pathogens from entering living cells.

Question 11

Innate Immune Responses

Skin as the First Line of Defence

Answer 11

• The layer of non-living cells that function as our epidermis means that pathogens don’t come into contact with living cells (via which they can spread/damage with toxins)
• Pathogens can’t spread via skin, so as long as no cuts/ wash exposed areas (hands) we can prevent infection when exposed to pathogens.
• Areas of our body not covered by skin have mucous & cilia to protect them.

Question 12

Innate Immune Responses

The Protective Role of Cilia

Answer 12

• Cilia hairs can move in one direction and push pathogens into the muscous where they will die and be consumed by phagocytes.

Question 13

Innate Immune Responses

Steps for Blood Clot Formation

Answer 13

Formation of clots in essential to prevent bloods loss and to quickly close the opening for pathogens

1. When a damaged vessel is detected by platelets they release clotting factors.
2. They begin a signalling cascade of reactions that will convert prothrombin in the plasma intro throbmin.
3. This will link together firbrinogen molecules into long strangs of fibrin that can gather at the cut and form nets that trap red blood cells.

Question 14

Adaptive Immune Responses

Lymphocytes?

Answer 14

A specific type of white blood cell that are named such because they’re found in the lymphatic vessels and cluster in lymph nodes.
* The majority of them are either B-lymphocytes (B-cells) or T-lymphocytes (T-cells).
* Each lympohcyte generates an immune response to a specific pathogens and we accumulate more lymphocytes in response to pathogens with new antigens.

Question 15

Adaptive Immune Responses

Antibodies?

Answer 15

Large proteins that help to destroy pathogens.
* They have a Y-shape with a highly variable region that includes a specific binding site to the pathogen they are trying to fight.
* Antibodies bind to the pathogen, helping to make them recognizable to phagocytes and often causing them to cluster & prevent them from entering other cells.

Question 16

Adaptive Immune Responses

Binding Sites?

Answer 16

Located at the end of the Y shaped antibod is the pathogen specific binding site.
* Each type of antibod is produced in response to exposure to a pathogen & the ends of the antibody are compatible to the ANTIGEN of the pathogen.
* This allows the antibody to identity and bind to the pathogen, preventing spread of infection.

Question 17

Adaptive Immune Responses

Antigen?

Answer 17

A recognition molecule, often a glycolipid/glycoproteins on plasma membrances, or protein spikes on virus’s surface.
* They identify cells.
* We use them on our own cells to mark them as ours, so that our immune system doesn’t fight them.
* Pathogens have antigens specific and unique to themselves.
* Our body identifies pathogens by their antigens.
* We then make anitbodies with binding sites specific to that pathogen.

Question 18

Adaptive Immune Responses

Helper T-cells?

(A type of T-Lymphoctyes/Cells)

Answer 18

1. A pathogen is engulfed by a large phagocyte, called a macrophage.
2. It then presents the pathogen’s antigen on the surface of the macrophage.
3. Helper T-cells see this displayed antigen and those comptaible to that antigen type bind and are activated.
4. That activated helper T cell activates a specific lymphocyte (B or T cell).
5. These helper T-cells are the connection between innate and adaptive immune responses (crucial for adaptive immunity).

Question 19

Adaptive Immune Responses

Cytokines?

Answer 19

Small proteins that act as signalling molecules binding to receptors on the lymphocytes to activate them.
* An activated Helper T-cell (after binding to an anitgen displayed on macrophage) then needs to activate specific B and T cells to initiate the adaptive immune response.
* These cells have also encountered the antigen, but they rely on the helper T cell to activate them.
* To this, they use specific chemicals called cytokines.

Question 20

Adaptive Immune Responses

Plasma Cells?

Answer 20

Antibody producing cells that contain lots of rough ER and golgi to faciliate rapid antibody production once there are many copies of the these cells.
* After the B-cell has been activated, it won’t start producing anitbodies immediately as it can’t efficiently make enough to be efficient.
* It thus goes through mitosis for rapid cell proliferation to make large sets of B-cells.
* Some become memory cells, most are plasma cells.

Question 21

Adaptive Immune Responses

Memory Cells?

(Could be Memory T-cells, focusing on Memory B-cells.)

Answer 21

Memory B-cells surive and remain in the body with the informaiton of how to make antibodies to that speicifc pathogen.
* After the clone of speficic B-cells (or T-cells) are made, most of the cloned B-cells specialize into plasma B cells but few remain as memory B-cells.
* They remain inactive until exposed again to the pathogen, at which point they quickly generate large amount of antibodies.

Question 22

Adaptive Immune Responses

B vs T Lymphocytes?

Answer 22

Humoral Immunity: Involes B-cells and involves the production of antibodies to find and destroy antigens outside our cells.

Cell-mediated immunity: Uses T-cells to identity our own compromised cells and destory them (infected cells).
* There are multiple types of T cells - killer T cells are the ones that destory cells.
* Helper-T cells are involved in both humoral and cell mediated immunes responses (the only one you need to know).

Question 23

Adaptive Immune Responses

Antigens and Blood Transfusions

(Reasons for compatible blood transfusions)

Answer 23

The connection between antigens and antibodies also accounts for why blood types must be compatible for transfusions.
* Our Red Blood Cells have antigens on them (except for type O).
* We make antibodies to any antigens not on our own blood cells.
* If we get blood that has antigens that our own antibodies are matched with the antibodies cluster around the cell, causing clumping and damage.

Question 24

Adaptive Immune Responses

Helper T Cells

Answer 24

Many types of them, each which can only activate a specific type of B or T cell.
* They display the pathogen’s antigen on their surface, and after having encountered a marcophage who engulfed it and was presenting it to them.
* When that antigen presenting helper T-cell then encounters an activated B cell (activated by the same pathogen) it releases cytokines to initate the humoral immune response.

Question 25

# Adaptive Immune Responses Cell Cloning and the Adaptive Immune Response

Answer 25

* As we need to have many different B and T cells since they're each pathogen specific, we keep a small number of each. * It would take ages for them to produce enough antibodies, so upon activation, the relevant B cells undergo rapid cell proliferation via mitosis. * These cells are unspecialized B cells. * After there's a clonoy of them, some specialize itno memory cells that know how to make the anibody, & majority become plasma cells that begin mass producing antibodies.

Question 26

# Pathogens and Immunity Opportunistic Infections?

Answer 26

Infections caused by pathogens who aren't virulent enough to typically cause serious disease in humans as a healthy immune system is able to defeat them. * However, in humans with weak immune systems, these normally weak infections can become dangerous. * Opporunistic infections are life-threatening for individuals with advanced AIDS. * Examples include tuberculosis, pneumonia, salmonella and others.

Question 27

# Pathogens and Immunity Antibiotices?

Answer 27

Chemicals that seletvively block the specific biochemical pathways/physical structures that are unique to prokaryotes. * They kill bacteria while having no negative impact on eukaryotic cells. * Penecillin was the first to be discovered (naturally released by fungi to destroy competitive bactiera)

Question 28

# Pathogens and Immunity Zoonotic Diseases?

Answer 28

One which originated in an animal species then crosses species/spreads from that animal to now being pathogenic to humans. * Bacteria, viruses, protists, and fungi all have the potential to cross species and cause zoonotic disease. * Animal based food industries & domestification of animals has lead to an increase of zoonotic diseases.

Question 29

# Pathogens and Immunity Immunity?

Answer 29

Refers to having resistance to a pathogen - more specificially being **unlikely to develop serious symptons even if exposed to the pathogen.** * All aspects of the immune system contribute to immunity but generally the **term is used to refer to specific acquired immunity.** * This occurs as a **result of memory cells**, can also occur through vaccination/breastfeeding.

Question 30

# Pathogens and Immunity Primary Immune Response?

Answer 30

The first time we're exposed to a pathogen our immune response takes longer to build. * An adaptive response won't be initiated until after the macrophages have been recruited and an activated helper T and B cell come into contact. * This has a time lag during which people develop symptons/feel sick. * The degree of sickness varies depending on the pathogen (how quickly they spread & are detected in the body) * It's usually a full week after first exposure before we produce antibodies to fight the pathogen.

Question 31

# Pathogens and Immunity Secondary Immune Response?

Answer 31

The retaining of **memory cells** (that can generate specific antibodies) means the second (third, fourth...) time that we're exposed to a pathogen, we can **begin a specific immune response to the pathogen almost as soon as it's detected.** * The need for macrophage recruitment and B or T cell activation is removed --> **antibodies are made within 2-3 days of exposure** (often before symptons start) * The response is more aggressive with **higher numbers of antibodies** --> the defeat of the pathogen is **fast and effective**.

Question 32

# Pathogens and Immunity Herd Immunity?

Answer 32

The point where enough of the population is immune and the disease vanishes. * Immunity can be increased through vaccination, as they expose a weak, dead or partial pathogen to stimulate a primary immune response, after which any real-life exposure to the pathogen is attacked as a secondary immune response. * Once majority of the population is vaccinated against the pathogen, the ability for it to spread diminishes. * The percent needed for herd immunity can be from 55%-95%.

Question 33

# Pathogens and Immunity Spread of HIV

Answer 33

* HIV is only able to be trasmitted via blood or sexual fluids or breastmilk. * The most common forms of transmission are from sexual activity or intravenous drug use (transmitted through blood via shared needle) *Note that viruses aren't living, and can't stay in the enviornment*

Question 34

# Pathogens and Immunity HIV Infection and Helper T-cells

Answer 34

* Viruses can only invade specific cells who have cell membrane receptors that are compatible to their spikes. * For HIV, the host cells are helper T cells * As groups of helper T cells die, the invidiual loses immunity to whole groups of organisms, as well as the ability to form new accuired immune responses.

Question 35

# Pathogens and Immunity The Ineffectiveness of Antibiotics for Viral Infections

Answer 35

* Antibiotics either target prokaryotic cell walls (detecting peptidoglycan, a polymer only in bacteria) or prokaryotic metabolic processes (can attack ribosomes or specific DNA or RNA polymerases only in prokaryotes). * These medications/antibiotics then are entirely ineffective against viruses. * As firstly, viruses don't have cell walls, therefore antibiotics can't find them in the body or outside our cells. * Secondly, viruses don't carry out metabolic processes (they lack ribosomes or enzymes) * While antibiotics can effectively target bacteria, they have no ability to fight off viral infections.

Question 36

# Pathogens and Immunity The Origin of MRSA

Answer 36

MRSA stands for methicillin-resistant staphylococcus aureus. * Bacteria are living organism that evole to become more likely survive and reproduce. * Genetic mutations that cause bactertia to not be detected by/destroyed by antibiotics, kill sensistive bacteria and allow these resistant mutations to produce more rapidly. * Methicillian is any antibiotics (broad group) meaning these bacteria are resistant to almost all oral antibiotics.

Question 37

# Pathogens and Immunity Causes and Consequences of: Tuberculosis

Answer 37

* Zoonotic tuberculosis is a bacterial infection, originating from cattle, and humans usually obtain infections from dairy products. * Humans can get infected from airbone droplets, or other animals that have been infected by the cattle. * The man sympton is damage to lung tissue (breathing difficulties). Also causes growths in the lymph nodes.

Question 38

# Pathogens and Immunity Causes and Consequences of: Japanese Encephalitis

Answer 38

* Japanese Encephalitis is caused by a virus that's transmitted to humans by the bite of a very speific mosquito. * The mosquito must get the virus from a pig or wading bird then trasmit it to humans. * Humans don't pass it back to other mosquitos, so we're called 'dead end hosts' (unlike malaria). * Symptons include mild fever and headache, however can progress to coma and death.

Question 39

# Pathogens and Immunity Causes and Consequences: COVD-19

Answer 39

* All coronavirus infections are known to have a possible zoonotic transfer. * COVID has shown to be transferable from humans to other animals, found in many animal strains. * The origin is believed to be from bats and likely passed through an intermediate animal host before infecting people. * Symptons include cough, fever, loss and smell and taste.