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LymphImmuneSystem, Charleigh Ochoa Period 1 - Coggle Diagram

- - - - most clone cells become plasma cells, those that do not become plasma cells become memory cells
  - - - lag period: 3-6 days
      - peaks plasma antibody levels reached in 10 days
        
        antibody levels then decline
    - - re-exposure to same antigen gives faster/more effective response
        
        sensitized memory cells provide immunological memory
        
        respond within hours
        
        antibodies bond with greater affinity
        
        antibody levels can remain high for weeks to months
  - - - Naturally acquired: formed in response to actual bacterial or viral infection
      - Artificially acquired: formed in response to vaccine of dead or attenuated pathogens
  - - - Naturally acquired: antibodies delivered to fetus via placenta or to infant through milk
      - Artificially acquired: injection of serum, such as gamma globulin
        
        protection is immediate but ends when antibodies naturally degrade
- - - - can be complete antigen or hapten (incomplete)
      - contain antigenic determinants
      - can be self-antigen
    - - MHC Proteins
        
        coded by genes of MHC and unique to each individual
        
        contain groove that can hold piece of self-antigen or foreign antigen
- - - - T- or Y-shaped consisting of four looping polypeptide chains linked by disulfide bonds
    - - IgD
      - IgG
      - IgA
      - IgE
      - IgM
    - - do not destroy antigens; inactivate and tag them
        
        form antigen-antibody complexes
      - Defensive mechanisms
        
        Neutralization
        
        block specific sites on viruses or bacterial exotoxins
        
        prevent antigens from binding to receptors on tissue cells
        
        Agglutination
        
        allows for antigen-antibody complexes to become cross-linked into large lattice-like clumps
        
        Precipitation
        
        complexes precipitate out of solution
        
        easier for phagocytes to engulf
        
        Complement fixation
        
        maintain antibody defense against cellular antigens
- - - - external body membranes (skin & mucosae)
    - - antimicrobial proteins, phagocytes, & other cells
        
        inhibit spread of invaders
        
        inflammation most important mechanism
        
        Four Cardinal Signs
        
        Heat
        
        Swelling
        
        Redness
        
        Pain
        
        Stages
        
        Inflammatory chemical release
        
        Vasodilation and increased vascular permeability
        
        phagocyte mobilization
        
        fever
- - - - takes longer to react than innate
  - - - antibodies, produced by lymphocytes, circulate freely in body fluids
      - bind temporarily to target cell; mark for destruction
    - - lymphocytes act against target cell
        
        Directly - by killing infected cells
        
        Indirectly - by releasing chemicals that enhance inflammatory response; or activating other lymphocytes or macrophages
- - - - usually become helper T cells that can activate B cells, other T cells, and macrophages
        
        direct adaptive immune response
    - - become cytotoxic T cells that are capable of destroying cells harboring foreign antigens
        
        also become memory T cells
  - - - Antigen bonding
        
        T cell antigen receptors bind to antigen-MHC complex on APC surface
        
        TCR must recognize both MHC and foreign antigen it displays
        
        Binding of TCR to complex triggers multiple intracellular signaling pathways that start T cell activation
      - Co-stimulation
        
        complete T cell activation requires T cell to also bind to one or more co-stimulatory signals on surface of APC