vce bio acquiring immunity

3rd LOD, lymphatic system, antibodies, cells of adaptive immunity, b & t cells, clonal selection & expansion, natural & artificial and active & passive immunity, allergens & treatments

adaptive immunity & its features

aka acquired, specific. Developed by being exposed to diff pathogens.

• activates when innate immune system fails to fight off infection

• this immunity is slower

DIFFS TO INNATE

• adaptive is long lasting, has memory of prior infections, only happens after infection, not born with

3 features

1. SPECIFICITY

   • adapimm is specific to one antigen by the antibodies produced

2. TOLERANCE

   • self tolerant, immune cells dont respond to self antigens (if they do = autoimmune disease)

3. MEMORY

   • remember previous antigens → immunological memory. Helps with fast response in future → memory cells

lymphatic system

network of lymphatic vessels with lymph and connects to lymph organs. ROLE → filter blood of pathogens before returning it in circulatory system.

• lymph fluid contains WBC

LYMPHATIC ORGANS

1. primary → where matures

   • bone marrow (B cell, stem cells), thymus (T cell)

2. secondary → where its activated by meeting complementary antigen

   • lymph node, spleen (flat organ filtering blood has t & b cells)

lymph nodes

• throughout body, pathogens get trap and then filtered. Site where foreign antigens meet and activate b&t cells

• on blood vessels and lymphatic vessels for b & t cells to access

• lymph nodes swell up cause of b &t cell inc

adaptive immunity 2 ways

1. humoral immunity

   • EXTRAcellular pathogens

   • involves antibodies that bind to pathogens tagging it for other cells to destroy

2. cell-mediated immunity

   • INTRAcellular pathogens

   • involves T cells like cytotoxic t cells for infected body cells.

   • indirect via t helper cells, direct via cytotoxic t cells

whatre antibodies

immunoglobulins, directly identify & bind to extracellular pathogens neutralising and tagging it for destruction. Its proteins w quart structure

• made by b plasma cells

• has 2 binding sites to bind to antigens on pathogen surface

4 ways antibodies work

neutralisation

• antibodies bind to surface antigen and coat pathogen to neutralise it. It blocks the receptors so it cant bind to healthy cells

• can bind to venoms & toxins to stop its effect.

agglutination

• antibodies attach to pathogen and form network → immbolises pathogen = unable to move = easier for pathogen to be engulfed, reduces spread

opsonisation

• antibodies coat surface of pathogen, make it more susceptible to elimination phagocytosis

complement protein activation MACs

• antibodies bind to surface antigen and activate complement proteins. Complement proteins make MACs (membrane attack complex) making pore and cause lysis.

structure of antibodies

• 2 light chains, 2 heavy chains, y shaped

constant region

• dont change, complement proteins bind to it

• its the light & heavy chains

variable region → complementary

• diff for every antibodies. Diff shape determines what antigen binds to the antibody

• antigen binding site → FAB fragment antigen binding.

• when antigen & antibody bind = antibody antigen complex

class of antibodies

1. igG → main antibody. Can cross placenta. Its in blood

2. igM → first antibody to appear in infection giving defence until igG formed

3. igE → stimulates histamine release and causes allergies

4. igA → attaches to mucous membranes of airways

5. igD → surface receptor of b cells

cells of adaptive immune system + test

lymphocytes WBC → t and b cells

T cells → cell mediated → intracellular

B cells → humoral → extracellular

test

• b&t made in bone marrow, b develop in bone marrow, t develop in thymus

• b&t have many copies of one surface receptor that recognise & bind to one specific antigen

• the b&t cells exposed to self antigens and if it doesnt recognise self antigens = apoptosis

• cells that dont respond to nonself antigen also destroyed

  • ensures cells are self tolerant

• go to secondary lymph organs and become naive and activated by complementary antigens when needed

B CELLS

b cell

• part of humoral immune response. Defend against extracellular pathogens, toxins, venoms. Made & mature in bone marrow

plasma b cell

• clones of activated b cells, makes antibodies

b memory cell

• clones of activated b cells thatre inactive = lasting immunity allow for quicker response next time body exposed to same antigen.

• when activated it activated into effector B plasma cells and makes antibodies to destroy pathogen.

T CELLS

cytotoxic t cells

• destroy infected body cells by intracellular pathogens.

  • cytot cells have receptors for non self specific to antigen

  • infected cells show foreign antigen, cytot cell bind to it and release perforin → makes pores, then release granzyme and initiate apoptosis

t memory cells

• long term after infection, gives long term immunity. Converts to effector t cells when exposed to specific antigen

t helper cells

• activates b & t cells. Activated when dendritic cell presents antigen on its mhc 2 marker to t helper cell

  • activate cytotoxic t cells, release cytokines attract b&t cells

  • activate b cells → plasma cells

  • activate macrophages

t regulator cells

• regulate immune response. Shuts down immune response, can supress action of lymphocytes & phagocytes. For body to not overreact to stimulus.

clonal selection and expansion - B CELLS

1. bone marrow produces stem cells → differentiates into b cells

2. b cells mature in bone marrow → move to lymph node

3. dendritic cell engulf pathogen (phagocytosis) and present antigen on mhc 2 marker → move to nearby lymph node

4. dendritic cell presents it to t helper cell activating it → t helper cell releases cytokines → stimulates b cell that already encountered same antigen

5. b cell activated and divides (mitosis) and differentiates into:

   • plasma cells to make antibodies specific to antigen

   • memory cells for fast response to future exposure of same antigen

clonal selection and expansion - T CELLS

1. bone marrow produces stem cells → differentiates into t cells

2. t cell mature in thymus → move to lymph nodes

3. dendritic cell engulf pathogen (phagocytosis) and present antigen on mhc 2 marker → move to nearby lymph node

4. dendritic cell presents it to t helper cell activating it → t helper cell releases cytokines → stimulates t cell that already encountered same antigen

5. t cell is activated, divides (mitosis), differentiates into:

   • cytotoxic t cells → make infected cells go through apoptosis

   • memory t cells

   • helper t cells to stimulate/activate b cells and cytotoxic t cells

antibody level production

• higher in 2nd compared to 1st bc memory b cells able to be activated more rapidly, allowing for faster production, = more antibodies to be made.

natural active immunity

natural → acquired immunity after being infected w pathogen naturally

active → body made antibodies & memory cells against pathogens antigen

1. come into contact w pathogen first time no antibodies against it

2. body takes days to have the correct plasma cell w matching antibodies for the particular antigen to produce immune response

3. experience symptoms of disease

4. antibodies made by body bind to antigen on pathogen and immune cells destroy it

   • 2-4 steps is clonal selection + expansion

5. body produced antibodies + memory cells against the pathogen = immunity

artificial active immunity

artificial → artificially introduce disabled pathogen or toxin in body. Uses medical intervention

VACCINES

• vaccines are injections used to activate the immune system to produce antibodies against the disease without causing the disease. It has dead/weakened/attenuated pathogens.

Different types of vaccines

living attenuated pathogens

• has living attenuated pathogens that dont cause disease but can still reproduce. Gives higher production and longer immunity & antibodies (reproducing = memory cells more produced)

dead pathogens

• has killed bacteria or inactive viruses. use heat or chemicals to kill it. NOT long lasting immunity (cause all dead, memory cell & antibody wont keep being made)

subunits of the pathogen

• sub units of pathogen, acting like antigen stimulating antibody production

harmless toxoids

• has bacterial toxins thatre harmless. For vaccines for pathogens that secrete poisonous toxins.

booster shots

• killed bacteria or inactive viral vaccines have weaker immune response = immunity is shorter

• booster shots taken to inc length of immunity

• vaccine 1st injected has clonal selection & expansion to make plasma cells for antibodies and to make memory cells

• vaccine 2nd injection, higher rate of antibody production cause memory cells are readily there and can convert to plasma cells for antibodies quicker than 1st injection.

passive natural immunity

passive → receive antibodies from outside source, no memory cells made

• ADV: immediate protection against that pathogen

• DISADV: not long lasting immunity

eg

• developing fetus receives maternal antibodies igG across placenta → gives protection as fetus immune system not matured until after birth. Antibodies also received from milk for protection from infection before it can produce their own antibodies

passive artificial immunity

blood

• u get infectious hepatitis A

• u get antibodies from someone who had hepatitis A, giving temporary protection bc body didnt make those antibodies and no memory cells made

anti venom

• bitten by snake, doc injects antibodies against the venom → neutralising the venom.

  • they milk snake of venom and inject it into horse for it to make antibodies and make antivenom

natural vs artificial, passive vs active

passive u receive antibodies, active u make antibodies

artificial is medical intervention, natural u get infected naturally

allergens

substances that a person reacts to, its any antigen causing the immune system to produce an abnormal and inappropriate overreaction when a person is exposed to it. Usually harmless to most people.

• inhaling, ingesting, touching, injected w the allergen

testing for allergens

• skin tests → small drops of allergen placed on skin using needle, if sensitive = local allergic reaction occur

sensitivity to allergen

• allergen enters body, and immune system sees allergen as non self and immune response activated

• igE antibodies r produced by b plasma cells at site of entry

• igE antibodies attach to mast cell receptors = primed mast cell → person is sensitive to particular antigen and next time it enters the person will have an allergic reaction

allergic reaction + treatment

1. next exposure to antigen, igE antibodies on primed mast cells recognise the allergen and bind to it

2. the binding activates the mast cell to go through degranulation

3. releasing chemical mediators like histamine = inflammatory response

   • inc. blood flow, redness, inc permeability of blood vessels, allergen symptoms like sneezing

4. mast cell release cytokine attracting more immune cells to attack allergen = more chemicals released = inflammation keeps going

treatment

• avoid the allergen, take antihistamine (blocks receptors on mast cells or blocks histamine communicating with other cells), wear a mask

• immunotherapy/desensitisation

  • injecting small doses of the allergen & gradually inc the dose.

  • to stimulate immune system, modifying/stopping strength of igE antibodies and effect on mast cells

  • immune system gets more tolerant to the allergen producing antibody thats not igE and prevent binding the allergen to mast cells.