Immune System Flashcards

1
Q

What does the Immune System do?

A

Protects our body from internal and external attacks

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2
Q

Define Antigen

What are self and non-self antigens

A

Antigens are the cellular identity tag that says who and what that cell is

  1. Self Antigens - belonging to us
  2. Non-self Antigen - do not belong to us - ATTACK
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3
Q

What is innate immunity and adaptive immunity?

A

Innate immunity (non specific immunity): INITIAL DEFENCE. Mechanisms that are built into our body that are ready for action.

Adaptive Immunity (specific immunity):  DEVELOP LATER. Body adapts.
--> Develop because lymphocytes activate to work against foreign cells
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4
Q

Lines of Defence

What are the 3 lines of defence in order from external to internal? how do they work?

A
  1. Set of barriers between internal and external environment (SKIN)
  2. Innate inflammatory responses . (MACROPHAGES –> PHAGOCYTOSIS, where they consume and digest foreign cells)
  3. Adaptive Immune Response. (PRODUCES ANTIBODIES)
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5
Q

INNATE IMMUNITY

FIRST LINE OF RESPONSE
Define…

  1. Species Resistance
  2. Mechanical barrier
A
  1. Genetic characteristic common to a particular species provide defence against certain pathogen
  2. Mechanical Barrier: Internal environment of humans are protected by continuous mechanical barrier (skin) as well as mucus membranes
  3. Chemical Barriers: skin and mucous membranes make chemical barriers that include, SEBUM, MUCUS ENZYMES AND HYDROCHLORIC ACID
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6
Q

INFLAMMATORY RESPONSE

  1. Define when this would kick in and how it works
  2. A lot of mediators of inflammation have Chemotactic Factors, what does this mean?
  3. What is Diapedesis?

4.

A
  1. If bacteria breaks through first line of response, second line kicks in. Tissue damage triggers the release of inflammatory mediators including mast cells. Mast cells release HISTAMINE. Other cells release CYTOKINES AND PROSTOGLANDINS.

–> They work to dilate blood vessels and increase permeability in order to help phagocytic white blood cells get to the battle field.

  1. Mediators of inflammation (mast cells) release CHEMOTACTIC factors (A FLAG FOR HELP). These chemicals that attract white blood cells to the area in a process called CHEMOTAXIS
  2. Example: mast cells wave chemotactic flag –> neutrophils get called to the scene –> they exit the capillary through DIAPEDESIS (the process of which cells can pass through un injured wall)
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7
Q

SECOND LINE OF DEFENCE
PHAGOCYTOSIS I AND II

  1. How does phagocytosis I work?
  2. What are common phagocytes?
A
  1. Phagocytosis: ingestion and destruction of foreign cells in the body
    Function of phagocyte: approaches micro-organism –> sees that it is not normal –> releases pseudopods that encase it in a sac in its belly (called a phagosome) –> comes into contact with lysosomes inside its belly, they fuze with the phagosome and gets the name PHAGOLYSOSOME –> then it gets destroyed
    • Neutrophil: first cell to arrive at the site of injury (by diapedesis) –> neutrophils are involved in the formation of pus
  • Antigen presenting cells: once this phagocyte eats the foreign cell it wears the proteins of it as a coat
  • Macrophage: Large eater. Important antigen presenting cells
  • Dendritic cell: found in skin and mucus. it has many branches.

***Phagocytosis is both INNATE and ADAPTIVE immunity

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8
Q

FEVER

A

bacterial infections produce SIRS. (systemic inflammatory response syndrome)

Pyrogens trigger fever response.
They do this by promoting prostaglandin production. Prostaglandins reset the body’s temp to really hot to burn off the pathogen. Advil will reverse this temperature.

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9
Q

INNATE DEFENCE

Describe how Natural Killer cells attack foreign cells and how they know not to attack our normal cells.

A

Group of lymphocytes that kills tumour cells and viruses.

They recognize these cells by using killer activating receptor and a killer inhibiting receptor
they are two prongs that come off of it. It will attach to normal cells of the body, but a normal cell has an MHC molecule that’s like naw man don’t attack me. So it doesn’t.

Only abnormal and foreign cells fail to bind to the killer inhibiting receptor and are killed.

They use lysis to kill.

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10
Q

INNATE IMMUNITY
PROTECTIVE PROTIENS

Describe how interferons and complimentary proteins work.

A

If cells are invaded on our body they can respond rapidly by using a cell called INTERFERON.
It will signal other cells to tell them to enter PROTECTIVE STATE

Complement: Enzymes that produce a cascade of reactions that cause lysis of foreign cells. They essentially compliment in the immune response.

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11
Q

ADAPTIVE IMMUNITY
Specific immunity.

  1. Where do B and T cells mature?
  2. How does the B cell become activated?
  3. Once activated what do they split into?
    - -> These cells can further divide when they come in contact with what?
A

Two different classes called lymphocytes. Two classes are B or T cells.

  1. lymphocytes originate in bone marrow.
    -T cells: travel to the THYMUS to mature. (t for thymus)
    -B cells: mature in the bone
    Then it travels to the lymph-nodes and SPLEEN.

Activation of these cells requires 2 signals.

  1. B cell immunity is also called humeral immunity. At this point they are referred to as naive B cells. (after 1st developmental stage)
    - synthesis antibody molecules and WEAR on cell surface.
    Once they release the bone marrow (still niave) they travel to spleen, liver and lymph-nodes. To be activated though they need to encounter a specific antigen that bins to the B cells surface, then it is ACTIVATED. then it clones into maybe a plasma cell or a memory B cell.
  2. Plasma cells synthesis and secrete many antibodies.
    Memory B cells will rapidly divide if they are exposed to the initial antigen that triggered their formation in order to produce more plasma and more memory cells.
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12
Q

ANTIBODY STRUCTURE

A

Antibodies: protein from immunoglobulin family. Large molecules composed of 4 polypeptide chains. 2 heavy, 2 light. Folded to form Y shape.

Immunoglobulins contain variable regions–> where sequence of amino acid vary in different antibody molecules. This differentiates them. These regions take on different shapes in order to bind to different antigens.

Different niave B cells can then bind to different microbial antigens

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13
Q

Clonal Selection Theory

What are the 2 major key points to this theory?

A
  1. Body contains enormous number of diverse clones of cells. Each committed to synthesis specific antibody
  2. When antigen enters the human body, it selects the clone who’s cells are committed to synthesizing its specific antibody, and stimulates them to proliferate (increase in number)

**Think of the B cells

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14
Q

Describe the Primary and Secondary Response to antigens

A

Primary Response: initial encounter will produce primary response. Antigen is dealt with through igM (the first one in the graph)

Secondary Response: memory B cells are waiting around for exposure. Antigen comes again and trigger the waiting memory cells. They produce more memory and plasma cells. So this later encounter (SECONDARY STIMULUS) it is FASTER AND GRANDER. igG

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15
Q

Natural vs. Artificial Immunity

Passive and Active

A

Natural Immunity: exists in active or passive form
Active form: person is exposed to something and actively produce antibodies.
Passive form: antibodies are given to you passively. Example: mother is breastfeeding, gives baby antibodies instead of baby acquiring them on their own.

Artificial Immunity:
ARTIFICAIL IS NOT ACQUIRED NATURALLY
Active: vaccine
Passive: Example: reach in garbage and get pricked by needle. Instead of waiting for body to produce antibodies, DOCTORS WILL INJECT antibodies.

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16
Q

Antibody Functions

A

Produce antibody mediated immunity, Type of immunity also called humeral immunity (humeral refers to fluid)

Antibody may inactivate the antigen if it recognizes it as (not-self)

it may cause a agglutination to make the antigens more accessible to phagocytes

May also cause complement cascade: inflammation, chemotaxis and lysis.

antibodies can attach to mast cells which initiate the release of inflammatory chemicals

17
Q

T CELLS:

A
  1. Develop on red bone marrow (same as bone marrow)
    Mature in Thymus
    –> migrate to lymph-nodes and spleen
  2. When antigen encounters naive T cell the antigen will bind to T cell receptors on its surface. This will cause activation of T cell leading to rapid division into specific T cells called effector t cells and memory T cells.
  3. Effector T cells release cytokines: cytokines are proteins involves in cell signalling
  4. Memory T cells: REMAIN IN RED BONE MARROW until they produce additional effector T cells when needed

T CELL ACTIVATION
T cells can only react to foreign antigens that have already been phagocytosed by antigen presenting cell (APC’s)
–> Forms an immunological synapse

  1. Cytoxic T cells: (KILLER CELLS) contact killing of target cell
    - -> defence against cancer
    - -> Perforin

MEMORY CELLS REMAIN TO PREARE BABY