OxyFile #447

Specific Defense Mechanisms 


A.J. Lanigan


Ozone has the ability to kill or inactivate quite a number of 
pathogens (if it can make contact). Ozonides, agents that are 
formed by ozone in the blood, have a certain degree of ablity to 
do this same job. Many tout the abilty of ozone to perform in a 
test tube & assume an identical action occurs inside the body. It 
is possible to saturate a _test tube_ of material with ozone and 
measure the effectiveness afterwards. I have never had a person 
volunteer to be ground up & "tested" after an ozone treatment. So 
how do you find out if the treatment is doing any good? 

I have always stressed the need to establish a baseline before you 
start to compare how effective ozone (or any therapy) will be over 
time. Not to do this, IMO, leaves one to how one "feels" at the 
end of each period of work. Since most people who are serious end 
up investing hundreds if not thousands of dollars over time to 
pursue such work, hard evidence is very good to have in hand to 
put the issue to rest. Immune testing is one of the standard 
methods to determine if a therapy is performing or if changes need 
to be made. The fact that ozone reacts & is gone in nanoseconds 
and ozonides not long thereafter, it is the state of the immune 
system that has to be evaluated to see if it is capable of 
carrying out the battle to conclusion. Ozone plays a part in the 
general "non-specific" activation & modulation of the immune 
system. Immune "fax messages" such as cytokines, lymphokines, 
tumor necrosis factor(TNF), interferon(INF), interleukins(IL), 
etc. are known to increase during an ozone regimen. It is these 
profound increases that have led many researchers to the belief 
that ozone therapies' main value lies not in its ability to start 
a kill off of pathogens but to cause the immune system to finish 
that process and keep the body healthy over the long run. 

As one learns the importance of the immune system in a total 
approach to returning/conserving health, one needs to know how it 
works. Oxytherapy may be a trigger but here is the ultimate 
weapon. 

Have a happy day, a.j. 

SPECIFIC DEFENSE MECHANISMS: THE IMMUNE RESPONSE 

The immune system is a recognition system that distinguishes self 
from non-self. 

Antigen = A foreign substance which elicits a proliferation of 
cells that either attack specific invaders directly or produce 
antibodies. The immune response must be primed by the presence of 
an antigen. Exposure to a particular foreign agent enhances future 
response by that same invader. 

Vaccination = The immune response is presented with a nonvirulent 
or attenuated (weakened) form of a pathogen which initiates a 
long-term capability to respond quickly to the real infective 
agent. 

Active immunity occurs when the body is stimulated to produce 
antibodies. 

Passive immunity occurs when the body acquires injected 
antibodies. 

When antibodies cross the placenta from mother to fetus; When you 
get an injection of antibodies; Provides only temporary immunity 
since the antibodies circulate in the blood stream for only a few 
weeks or months. 


A. Duality of the Immune System 
 1.The immune system has two components mediated by two different 
   kinds of cell. 
    i.Humoral immunity results in production of antibodies which 
      circulate as soluble proteins in blood and lymph. (B cells) 
        a.Defends against free bacteria and viruses in body 
          fluids. 
   ii.Cell-mediated immunity is carried out by specialized cells 
      circulating in blood and lymph. (T cells) a.Protects against 
      bacteria and viruses that have already infected cells. 
        b.Also protects against fungi and protozoa. 
        c.Reacts against foreign tissue transplants and possibly 
          against cancerous cells. 


B. Cells of the Immune System 
 1.Lymphocytes = White blood cells responsible for the immune 
   response. 
    i.Originate from common stem cells in red bone marrow. 
   ii.Lymphocytes that continue maturation in bone become B cells 
      which function in humoral immunity. 
  iii.Lymphocytes that migrate to the thymus become T cells which 
      function in cell-mediated immunity. 
 2.As lymphocytes mature, they develop immunocompetence, a rigid 
   commitment to identify and respond to a specific antigen.
    i.Involves synthesis of surface receptor proteins (in B cells 
      these are bound copies of the antibody secreted during the 
      immune response). 
   ii.Each lymphocyte becomes programmed to recognize and respond
      to a specific antigen before it actually encounters that 
      antigen. The immune system is prepared for an almost 
      unlimited variety of potential pathogens that may never 
      invade the body. 
  iii.Immunocompetent cells then migrate to the lymph nodes and 
      spleen, where most first encounters with pathogens occur.
 3.Once activated by antigens, lymphocytes multiply and develop 
   into effector cells, derivatives equipped to respond to 
   antigens. 
    i.Effector cells are mobilized through circulatory and 
      lymphatic vessels. 

C. Antigens 
 1.In general, antigens are large molecules (MW=10,000 daltons or 
   more). 
    i.Most are proteins or large polysaccharides. 
   ii.Often are outer components of invading microbes (biochemical 
      markers not the whole organism). 
  iii.May be foreign molecules associated with other blood cells 
      or may be transplanted tissues. 
 2.Antigenic determinants = Localized surface regions of an 
   antigen recognized by antibodies. 
    i.May have many different determinants on one antigen; 
      therefore, one antigen may stimulate synthesis of many 
      different antibodies. 

D. Clonal Selection 
 1.The versatility of the immune system depends on the great 
   diversity of lymphocytes with different receptor specificities. 
 2.Clonal selection = The selective activation (by an antigen) of 
   a tiny fraction of quiescent lymphocytes, which grow and divide 
   to form a clone of effector cells. 

E. Immunological Memory 
 1.Primary immune response occurs when a first exposure to antigen 
   stimulates production of memory cells and effector cells. 
    i.Characterized by a lag period of several days (necessary 
      time to produce effector cells). 
 2.A secondary immune response occurs when another exposure to the 
   same antigen reactivates memory cells which, already sensitized 
   by the first exposure, rapidly produce more memory cells and a 
   large number of effector cells. 
    i.Faster, more effective and more prolonged than the primary 
      immune response. 
   ii.Memory cells may live for decades: effector cells live only 
      a few days. 
  iii.May confer lifetime immunity (e.g. mumps, chicken pox). 

F. The Humoral Immune Response 
 1.The humoral response is provoked by binding of antigens to 
   antibodies producing form B cell plasma membranes. 
 2.B cells are activated by: 
    i.Capping, when a polyvalent (having multiple copies of 
      antigenic determinants) antigen binds to several receptors 
      on an immunocompetent B cell surface, pulling receptors 
      together to form a cap which is taken into the cell by 
      endocytosis. 
   ii.A more common mechanism involving B cell interaction with T 
      cells, discussed later.
 3.Plasma cells = Effector cells that develop from B cells and 
   secrete as many as 2,000 antibody molecules per second during 
   their 4 to 5 day lifetime. These free, discharged antibodies 
   circulate in blood and lymph, binding and destroying antigens. 
 4.Antibodies constitute a class of immunoglobins (Ig), able to 
   recognize an antigen and assist in elimination. 
 5.The antigen-variable region interaction involves several weak 
   bonds which form between contiguous chemical groups on the 
   respective molecules. 
 6.There are 5 types of constant regions, hence 5 classes of 
   antibodies - IgM, IgG, IgA, IgD, and IgE. 
 7.In humoral effector mechanisms, soluble antibodies "tag" 
   molecules for destruction by a variety of effector mechanisms. 
 8.Antibodies are used widely in research and clinical testing 
   since they specifically recognize molecules. 
 9.Antibodies for vaccination or research used to be produced by 
   injection of an antigen into an animal. 
    i.A problem with this method was than animals make more than 
      one antibody since each antigen has many antigenic 
      determinants. 
   ii.The solution was monoclonal antibodies. 
10.With monoclonal antibodies, all cells producing antibodies are
   descendants of a single cell, thus, all produce identical 
   antibody molecules. 
    i.Made by hybridomas [fusion of a myeloma (tumor) cell to a 
      normal antibody] producing lymphocytes. 
11.The hybridoma is grown in an artificial medium. (Normal cells 
   do not grow indefinitely in culture, thus, the g=function to a 
   myeloma cell.) 
    i.Used in clinical assays such as pregnancy testing. 
   ii.Used in bone marrow transplants. 
  iii.May be coupled to a toxin, and then use the antibody's 
      specificity to target the toxin for a particular cell type 
      (potential use in chemotherapy). 

G. Cell-Mediated Immunity 
 1.T cells are the main agents of cell-mediated immunity. 
    i.Cannot be activated by free antigens. 
   ii.Respond only to antigenic determinants displayed on surfaces 
      of the body's own cells.
 2.T cell receptors = Specific proteins embedded in T cell plasma 
   membranes which allow recognition of bound antigens. 
    i.Recognizes only a self-nonself complex formed by an antigen 
      displayed on the cell surface by antigen presenting cells 
      (APCs) such as macrophages along with an MHC protein.
 3.MHC (major histocompatibility complex) = A group of 
   glycoproteins unique to each individual that are present on 
   cell surfaces.
    i.MHC I markers are present on all nucleated cells. 
   ii.MHC II markers are found only on macrophages, B cells and 
      some T cells.
 4.Histocompatibility restriction = The constraint on a T cell's 
   responsiveness. Although an MHC molecule can associate with 
   many different antigens, the T cell receptor is specific to one 
   antigen. 
 5.Activated T cells proliferate and form memory cells and 
   cytotoxic T cells that actually attack infected cells. 
 6.There are three main types of effector cells derived from T 
   cells:
    i.Helper T cells mobilize humoral and cell-mediated immune 
      responses. 
        a.Helper T cells activated by binding to APC. 
        b.Binding stimulates macrophages to release interleukin I, 
          a cytokine (chemical secreted by one cell as a regulator 
            of neighboring cells). 
        c.IL I stimulates T cells to grow, divide and produce more 
          helper T cells specific to the antigen-MHC complex. 
        d.These produce interleukin II, which stimulates further 
          helper T cell growth and division and amplifies 
          proliferation of cytotoxic T cells. 
        e.IL II also stimulate B cells to become activated (T 
          dependent antigens can activate only B cells stimulated 
          by interleukin II). 
   ii.Cytotoxic T cells are the only T cells that actually kill 
      other cells. 
        a.Identify targets by the fit of their receptor to an MHC- 
          antigen complex. 
        b.Kills cells by attaching to the cell surface and 
          releasing perforin, a protein that inserts into the
          plasma membrane forming a lesion that causes the cell to 
          lyse. 
        c.Probably attack cancer cells and foreign tissue grafts 
          and organ transplants. 
  iii.Suppressor T cells release cytokines that inhibit other 
      T cell and B cell activity. 
        a.Occurs late in the immune response to terminate immune 
          activities no longer required.