Immunity:- Barriers to entry, Nonspecific, Specific & Secondary Infection

Immunity:- Barriers to entry, Nonspecific, Specific & Secondary Infection

Sorry for any spelling mistakes made.

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  • Created by: sorcha
  • Created on: 05-10-11 21:08

Barriers to Entry

  • Earwax- Bacteriocidal
  • Mucus and Cilia- Prevent the entry of pathogens into lungs
  • Keriton in Skin- Waxy & imperiable to water and Pathogens
  • Blood clotting- Seals wounds
  • Lyposyme- in eyes, mouth and nose secretions break down the bacteria cell walls.
  • Vaginal secretions- acidic 
  • Acid in stomach- kills bacteria
  • Microbes - large numbers of harmless microbes that live on the skins surface reduce the colonization by other bacteria
  • Bacteria in intestines- Harmless bacteria competitively exclude pathogenic bacteria
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Non Specific Immune Response

  • Lysozyme:- an enzyme in nasal secreations, tears and saliva that breaks down the bacteria cell wall.
  • Inflammation:- Mast cells and dammaged white blood cells release histamine causing the arterioles to dilate. The capilleries become more permiable which causes blood flow to the are to increase therefore causing Plasma fluid, white blood cells and antibodies to leak out into the tissue. This causes Oedema
  • Phagocytosis:- white blood cells engluf, digest and destroy bacteria and foreign material. The phagocytes include neutrophils and monocytes.
  • Interferon. Virus infected cells produce Interferion. The production of theis chemical prevents the virueses to multiply. Interferon limits viral protein synthesis
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Specific Immune responses- Humoral- Activation of

  • Pathogen with antigens of surface is engulfed by macrophage
  • Macrophage presents antigens on its surface and becomes an Antigen-presenting cells (APC)
  • APC binds to T helper cells with complementary CD4 receptors
  • T helper cells is activated and divides into T memory cells and T helper cells. 


  • T Helper cell - when activated, these stimulate the B cells to divide and become cells capable of producing antibodies
  • T Killer cell - These destroy any cells with antigens on their surface membrane that are recognized as foreign or 'nonself' including infected body cells. 
  • T Memory Cell- A long-lived T Cell that bears receptors  for an antigen  during its encounter with a prior infection or vaccination 
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Specific Immune responses- Humoral- Clonal Select

  • Pathogen with antigens of its surface binds to B cell with complementary receptor
  • B cell becomes an antigen-presenting cell.
  • Activated T helper cell with complementary receptor binds to APC and produces cytokines ( proteins) that stimulate the B cell. (clonal selection)
  • The B Cell divides to give B Memory and B Effector cells. 
  • B Effector cells differentiate into plasma cells.
  • Plasma Cells secrete antibodies which bind to antigens identifying them for easier destruction. 
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Specific Immune responses- Humoral- Clonal Select

  • B Effector cells:- These differentiate to produce Plasma Cells, which release antibodies into the blood an Lymph.
  • B Memory Cells:- These cells remain in the body for months or years enabling an individual to respond more quickly to the same antigen. 
  • Cytokines :- The chemicals that T Helper Cells release that stimulate division and differentiation of the B cells
  • Antibodies:- Antibodies are protein molecules that belong to a class known as immunoglobulins. Antibodies bind to the antigens on the surface membrane. Antibodies act as labels allowing phagocytes to recognize and destroy the cell.  
  • Antigen:- Any substance foreign to the body that evokes an immune response that is capable of binding with an antibody or T cell
  • Clonal Selection:- The process of B cell division 
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Specific Immune responses- Cell mediated

  • Pathogen infects cell of host. The cell then presents the antigens and becomes an APC.
  • T killer cell with Complementary receptor binds to the APC.
  • The T killer cell divides to form two clones: Active and Memory T killer cells
  • Cytokines from T helper cells stimulate the differentiation.
  • The active T killer cells bind to infected cells presenting antigens.
  • The T Killer Cell releases chemicals that cause pores to form in the infected cell, causing Lysis
  • The infected cell dies.


  • Lysis:- disintegration of cell membrane. 
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Needs some serious spell checking!!!

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