Specific Immunity

Specific Immunity

immune cells/ antibodies target specific antigens
1. production of antibodies against a specific antigen
2. adaptive
3. several days to become effective
Cell Mediated
1. principle cellular agent is the T cell
  1. T lymphocytes
    1. derived from lymphoblasts in the red bone marrow
      1. soon after birth migrate to various lymphatic tissues and organs in the body
        many stored in an inactive state as small lymphocytes
    2. gain immunological competence in the thymus gland
      1. less than 10% of the cells are selected.
      2. if thymus removed at birth, the animal will not develop cellular immunity
      3. become functional T cells
        only respond to very specific antigens - each of their membranes contains a unique type of membrane receptor that will bind to one type of antigen
        1000s of different kinds of competent lymphocytes.
    3. Activation
      1. foreign antigen engulfed by antigen presenting cells (APCs) i.e. macrophages, is presented as an antigen-MHC complex to a competent lymphocyte
        Only T cells with receptors that bind to that specific antigen can respond
        fewer than 1/10,000 T cells in the lymphatic tissue may respond
        now become sensitized (or activated by helper T cells)
        sensitized cell increases in size and divides mitotically to form a clone of cells similar to itself.
        these now differentiate into a variety of specialised cells (T cell subsets)
        cytotoxic T cell
        recognise and destroy cells with foreign antigens including infected body cells (viruses), bacteria, protozoa, fungi, cancer cells, organ transplants
        memory T cell
        remain in lymphatic tissue for many years; responsible for secondary immune response
        helper T cell
        enhance the immune response; 60% of circulating T cells; T helper 1 cells release Interleukins-2 --> stimulates other T cells; T helper 2 cells release Interleukin-4 --> stimulates proliferation of B cells
        suppressor T cell
        controversial, less understood. suggested to turn off the immune response when fewer antigens are present; release suppressor cytokines
        T cells now leave the lymph nodes and migrate to the site of infection and release a variety of cytokines and cytotoxins
        cytotoxic T cells combine with surface antigens on foreign cells releasing cytokines like perforin-1 which forms membrane pores
        helper T cells release interleukins at the infection site
  2. Natural Killer (NK)
    1. large, granular lymphocytes from the bone marrow
      1. granules contain perforins and proteases called granzymes
        induces apoptosis in infected or abnormal cells - perforins form pores in the cell membrane allowing granzymes and associated molecules to enter
    2. forming about 15% of the circulating lymphocytes
    3. release cytokines and perforins
    4. recognise stressed cells in the absence of typical immune system signals (presence of antibodies or presences of large molecular weight proteins and carbohydrates on the plasma membranes of foreign organisms)
      1. permits rapid response
  3. Dendritic Cells
  4. Macrophages
Antibody Mediated - Humoral
1. a function of the B lymphocytes
  1. immunological competence develops in the red bone marrow
    1. B cells move to the lymphoid tissues mainly the lymph nodes and spleen
      1. found in separate areas from T cells
  2. 1000s of competent B lymphocytes, each capable of responding to a particular antigen
    1. each B cell is programmed to encode a glycoprotein receptor that binds to a specific antigen
2. B Cell Activation
  1. complex involving several cells
    1. An APC presents an antigen-MHC complex to a sensitized T cell
      1. meanwhile, the B cell has interacted with the antigen, degraded it, and displays the peptide fragments on its surface antibodies
      2. activated helper T cell now bind to B cell and releases cytokines (Interleukin-4) which activate the B cell
        Once activated, B cells increase in size, divide and differentiate into plasma and memory cells.
        plasma cells are mature B cells with large amounts of RER that remain in the lymph node and release antibodies
        B memory cells continue to produce small amounts of antibody for many years (show the same secondary response as T ceclls)
        capable of producing lots of antibodies very quickly, secondary response much quicker
3. Antibodies
  1. highly specific proteins, immunoglobulins
    1. 4 polypeptide chains - 2 identical heavy chains (400+ amino acids) and 2 identical light chains (214 amino acids)
    2. constant C region; variable V region (3D shape that binds with the antigen)
      1. antigens have a number of antigenic regions or determinants which may be recognised by different antibodies
        binding sites on the V region interact with antigens --> antigen-antibody complex
      2. base of the C region (Fc) interacts with the cells of the immune system
  2. 5 classes of antibody - based on amino acid sequence of the heavy chain at the C region
    1. IgG
      1. 75% plasma Ig; binds to macrophages, neutrophils
        secondary response
      2. complement system
      3. effective against bacteria, viruses + can cross placenta
    2. IgM
      1. 10% plasma Ig; blood type
        primary response
      2. complement system
      3. effective against bacteria
    3. IgA
      1. 15% ig; body secretions - mucous, saliva, tears, milk
      2. viral and bacterial attachment
    4. IgD
      1. on B lymphocyte surface
      2. rarely secreted
      3. B cell receptor
    5. IgE
      1. bound to mast cells and basophils
      2. allergic response; anaphylactic response
      3. parasitic worms
4. Antibody Action
  1. don't directly destroy antigen - label for destruction
    1. agglutination - clumps antigenic agents on cells together
    2. precipitation - soluble antigen becomes insoluble and ppts out
    3. neutralisation - antibodies bind to specific sites on bacterial exotoxins or on viral surface antigens
Primary and Secondary Response
1. first exposure elicits a primary response ~3-14 days
2. subsequent exposure will usually cause a more rapid response - secondary immune response
  1. due to presence of memory cells bearing receptors to the antigen
  2. latent period shorter + less antigen required, pathogen destroyed before it can get established

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	Criado por Erica Lai mais de 9 anos atrás