IMMUNITY - CHAPTER 9

What is adaptive immunity

• antigen-specific immune response.

• antigen must be processed + recognised first.

• includes humoral and cellular immunity

Faster FUTUREE responses

humoral immunity

• Involves B cells

• Produces antibodies (target specific antigens)

• Uses complement proteins

• Works in extracellular fluid

• It's an antibody-based response

cellular immunity

• Uses T cells & macrophages to fight pathogens

• Releases cytokines

• No antibodies involved

what is lymph

• Clear fluid like plasma

• returns leaked fluid

• transports lymphocytes/APCs,

• site for lymphocyte maturation.

what happens in lymph nodes during immune response

• contain many B & T cells + macrophages filter lymph

• Macrophages show antigens to T cells

• APCs present antigens to Tᴴ cells

• Lymphocytes multiply → nodes swell (early sign of infection)

Where do B and T cells mature?

B cells mature in bone marrow

• RESPONSIBLE FOR HUMORAL IMMUNITY

T cells mature in thymus

• RESPONSIBLE FOR CELL MEDIATED IMMUNITY.

lymphatic system

• made of lymph, lymphatic vessels, primary and secondary lymphoid organ/tissue

main lymphocytes

T cells, B cells and natural killer cells

primary lymphoid organs and secondary lymphoid organs

primary - Bone marrow and thymus.

secondary - Spleen, lymph nodes, tonsils, adenoids, appendix, Peyer’s patches.

immunity, adaptive and innate

resistance to infectious disease

• innate immunity is natural, non specifc, fast and no memory

• adaptive immunity is aquired, specifc, slow and has ;memory’

antigens (more detail)

• molecule that triggers immune response

• epitope is The part of an antigen recognized by antibodies or T/B cells.

• ^specifc part of antigen that antibody binds

cells involved in cell mediated immunity

helper T cells, Cytotoxic T cells, Memory T cells

helper T cells : cell mediated immunity

• do not directly kill cells

  release cytokines to activate macrophages, B cells, and cytotoxic T cells,

Cytotoxic T cells : cell mediated immunity

Kill infected, cancerous, or foreign cells directly.

Memory T cells :cell mediated immunity

Persist after infection to provide fast responses if re-exposed.

How do helper T (TH) cells get activated?

1. APCs present antigens on MHC II to TH cells.
2. CD4 (t helper) binds MHC II (activates TH cell.)
3. TH releases cytokines →

apc

1. Pathogen engulfed by antigen-presenting cell (e.g. macrophage).

2. Pathogen broken down into antigen fragments.

3. Antigen binds to MHC II inside the cell.

4. Helper T cell binds to presented antigen → activates immune response.

cell mediated pathway

1. cell infected w bacteria/virus. foreign antigen fragments r created within cells

2. MHC 1 binds antigen fragment

3. MHC protein presents antigen to cytotoxic T cell

• if cell (not wbc) is infected w pathogen, antigens can be taken from pathogen and be presentd to MHC 1

• cytotoxic t cells bind to antigens presented

• cytotoxic t cells recognise cancerous cells

• activated cytotoxic t cells eliminate infected cells directy

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How do cytotoxic T (TC) cells get activated?

Infected normal cells present antigens on MHC I to TC cells.
CD8 binds MHC I → activates TC cell.
TC cells kill infected cells directly.

humoral immunity cells

Plasma cells, Memory B cells

Plasma cells

Plasma cells -

• after activation, B lymphocytes → plasma cells (bc B cell receptors bind to specific antigen)

• produce antibodies specific to antigen

Memory B cells

• stay long time in lymphoid tissue

• can differentiate into plasma cells during re- infection

clonal selection

• antigen selects B cell (bc receptors match), that will eliminate the antigen,

What is clonal expansion?

Rapid division of selected B cells to fight an infection.

plasma and memory B cell production, positives of memory B cell production

• as well as plasma cells, memory B cells also produced.

• when particular pathogen comes into contact, antibody production is faster

• using memory, skip clonal selection and go straight to clonal expansion.

Antibodies (aka immunoglobin)

• Made by B cells to neutralise pathogens

• 4 polypeptides: 2 heavy, 2 light

• Forms Y shape

• Tips of Y (variable region) bind to antigen

What are 5 main functions of antibodies?

Neutralisation, agglutination, opsonisation, precipitation, complement activation.

Neutralisation (toxins vs pathogens)?

Toxins: antibodies bind to toxin, block action.
Pathogens: antibodies bind to surface antigens of pathogens, block entry into host cells.

agglutination

Antibody clumps/binds to antigens

• activates phagocytes + complement cascade

precipitation

Antibodies bind soluble antigens → becomes precipitate, so they drop out of solution.

antibody opsonisation

antibodies Mark pathogen for phagocytosis.

What are the five classes of antibodies?

IgG, IgM, IgA, IgE, IgD

What does IgG do?

Main antibody in blood, long-term immunity.

What does IgM do?

First antibody produced in infection.

What does IgA do?

Found in mucosal areas (gut, airways).

What does IgE do?

Involved in allergic reactions.

What does IgD do?

activate B cells by detecting antigens.

T cell receptors

On T cells;

• recognises antigens bound on MHC.

• has 2 peptide chains, 1 binding site.

immunological memory

• First time b/t cell meets antigen = primary immune response

• Second encounter (same situation) = secondary response (mainly IgG)

• secondary response is Faster & stronger due to memory B and T cells made from primary response

immunity - source of antibodies and gaining immunity

source of antibodies

• active immunity

• passive immunity

gaining immunity

• natural immunity

• artificial immunity

passive immunity

antibodies aquired by a person from external source

• offers immediate, not long term immunity

natural immunity - passive

• antibodies enter person naturally

• e.g. antibodies from mother (placenta or breast milk)

natural immunity - artifical

• antibodies injected (e.g. antivenom, hepatitis A IgG)
  ➡ Provides immediate but short-term protection (no memory)

natural immunity - Active immunity

antibodies produced by an individuals own adaptive immune system.

types of active immunity

• Natural: infection triggers B cells to produce antibodies

• Artificial: vaccination stimulates antibody production
  ➡ Slower onset but long-term (memory B and T cells formed)

vaccine

uses weakened/dead pathogens to trigger antibody production, protecting against future infections.

4 types of vaccine

• Live attenuated , Inactivated/killed, Toxoids, Sub-unit

• Live attenuated

• strong, long-lasting (e.g. MMR)

• Inactivated/killed

• weaker, may need boosters (e.g. rabies)

• Toxoids

• inactivated toxins (e.g. tetanus)

• Sub-unit

• only parts of pathogen, weakest (e.g. HPV)

Why do live attenuated vaccines provide stronger immunity than inactivated vaccines?

• They produce stronger, longer-lasting immunity than inactivated vaccines, which often need boosters or multiple doses (2-3).