**4.2 Harmful aspects of autoimmunity resulting in autoimmune disorders**

There are two harmful aspects of autoimmunity, both of which have the potential to manifest in disease states, one being an adverse immune response against normal self, causing an autoimmune disease; and the other being tolerance of an abnormal cell line, so that cancer growth is permitted. These disease states, or autoimmune disorders, come about when the immune system's surveying ability is mislead into situations of improper response or non-response to changes in self. It is observed in many autoimmune diseases that modified self initiates and/or maintains pathogenic aab responses against a target ag, causing a disease state (Barabas et al., 2004c; Heymann et al., 1959), whereas in cancer, ags identifiable as cancer specific are minimally antigenic and not recognized as unwanted self, and therefore fail to induce an immune response that eliminates the cancer cells (Foss, 2002; Kim et al., 2007).

In many respects the autoimmune system responds correctly during the development and maintenance of autoimmune disorders. In fact, the immune system does what it is instructed to do or not to do by the "information" it receives. In the case of self reaction, for instance, the cells and the products of the cells of the autoimmune system are virtually predestined to react against altered self, in that altered self is non-self and non-self should provoke a pathogenic immune response. Unfortunately, such an immune response against altered self can cause an autoimmune disease, as the developing pathogenic aabs are crossreactive, i.e., in addition to reacting against the modified self ag that initiates and maintains their production, they also react with normal self, causing harm to the tissue and providing

Four Aspects of Autoimmunity and How to Regain Tolerance to Self

from an Autoimmune Disease Utilizing the Modified Vaccination Technique 577

disease process will continue. The level of pathogenic IgG aab must be at zero for no

In contrast to the common belief, we and a few other scientists believe that the normal target ag on its own will not under normal circumstances initiate a pathogenic IgG aab response (Barabas et al., 2004c; Barabas et al., 2006a; Rich, 1996; Totoritis & Rubin, 1985; Weir & Elson, 1969; Weir & Pinckard, 1967). Administration of native ags during autoimmune disease states, e.g. during slowly progressive Heymann nephritis (SPHN), other experimental situations, do not make the disease process progress more intense (Barabas et al., 2006a; Bielekova et al., 2000; Peakman & Dayan, 2001; Prakken et al., 2004). Rather the opposite, in most instances they reduce the pathogenic immune response (Barabas et al., 2004c; Barabas et al., 2006a). It seems that even during a disease state the native target ag preferentially stimulates IgM aab production. The IgM aabs being cross-reactive, their increased levels remove from the circulation both the disease contributing native target ag and the disease

It is worth noting, in reference to a broader context, that the initiation and intensification of an autoimmune disease are undoubtedly complex, and may involve numerous factors or

 dysfunctional autoimmune system response (e.g. reduced phagocytosis and reduced specific IgM aab production due to age, malnutrition, vitamin deficiency,

 presentation of modified self aags or exogenous self-like ags to dendritic cells prior to antigenic information being processed by T and B cells for plasma cells to produce

regulatory molecules (cytokines, chemokines, etc.) attempting to accelerate or

 complement systems or components playing dominant roles in aag and aab reactions during an autoimmune disease (in both pathogenic and non-pathogenic immune

a. assisting in the complement-dependent clearance of modified/unmodified self that causes the autoimmune disease (Gaipl et al., 2001; Taylor et al., 2000; Zwart et al.,

b. in contributing to the continuously layered aag/aab depositions, e.g. in the glomeruli (Barabas et al., 2003; Barabas et al., 2004b; Barabas et al., 2004c) (pathogenic immune response) causing complement mediated C3, C59b injury (Barabas et al., 2003; Barabas

 overwhelming infection by an infectious agent presenting a whole range of potentially antigenic peptides that may initiate autoimmune disease by molecular mimicry;

potentially self reactive clones of T cells can react with self because of immune

in a few instances self ags can act to initiate and maintain pathogenic autoimmune

Notwithstanding the influence of such other factors, the set of processes described above appear to be fundamental to autoimmune disease involving misdirected auto-reaction, and understanding them has assisted in the development of a powerful technique to deal with

et al., 2004c) resulting in compromised glomerular filtration;

responses against self, e.g. when regulatory T cells are out of control.

autoimmune disease, as we will describe further below.

autoimmune disease process to be detectable in the host (Barabas et al., 2004b).

causing modified target ag (Barabas et al., 2007a), contributing to remission.

processes besides those described above, such as:

overwhelming infection, etc.);

decelerate autoimmune processes;

genetic predisposition;

pathogenic IgG aabs;

responses) (Blom, 2010):

2004);

environmental factors;

regulation failure;

more substrate for the reaction to continue. In the case of cancer, on the other hand, the cells and the products of the autoimmune system do not react with the minimally altered self on cancer cell surfaces and the cancer cells are not be eliminated, therefore allowing the cancer to prevail (Foss, 2002).

#### **4.2.1 Initiation and maintenance of an autoimmune disease**

The induction and maintenance of autoimmune diseases, as well as the associated immunopathological and functional changes, have been extremely well studied in experimental animals (Andres et al., 1986; Barabas et al., 1969; Barabas & Lannigan, 1969; Grupe & Kaplan, 1969; Heymann et al., 1959; Kerjaschki, 1993; Kerjaschki, 2000b; Kerjaschki & Farquhar, 1982); and by comparative study the etiology and pathogenesis of human autoimmune diseases are equally well understood (Davidson & Diamond, 2001; Kretz-Rommel et al., 1997; Kretz-Rommel & Rubin, 1999; Sinha et al., 1990; Theofilopoulos, 1995; Tung, 1994; Von Herrath & Oldstone, 1995). In most instances for an autoimmune disease to begin, a modified self (Barabas et al., 2004c) or self-like (molecular mimicry) (Ebringer et al., 1997; Ebringer, 2003; Mokhtarian et al., 1999; Orbach & Shoenfeld, 2007) ag has to present itself as a foreign-like, exogenous-like ag to the cells of the immune system. There are numerous agents that are able to modify self ags (toxins, chemicals, infectious agents, drugs, adjuvants, vaccines, smoking, chemical dyes, UV irradiation, etc.) and initiate a pathogenic IgG aab response (Barabas et al., 2004c; Conti et al., 2008; Davidson & Diamond, 2001; Hess, 1999; Heymann et al., 1959; Rao & Richardson, 1999; ten Veen & Feltkamp, 1972) (initially a primary immune response, as the immune system has not previously been exposed to the modified ag). If the modifying agent is continuously present in the system, then the modified self ag will continue to stimulate the appropriate T and B cells to maintain the production of pathogenic IgG aabs by the plasma cells (secondary ab response) (Barabas et al., 2003). The developing pathogenic IgG aabs are cross-reactive (Barabas & Lafreniere, 2005). They react with the modified self ag and the normal target ag in an organ. ICs made up of modified self and anti-modified self IgG aab form as a result. The fate of these ICs is twofold. In part they are neutralized and eliminated. However, insofar as they are not fully or quickly enough removed from the body they operate to maintain the pathogenic IgG aab production.

The pathogenic IgG aabs also react with the target ag not just as it appears in the circulation, but also *in situ* within the organ where it originates; e.g. in HN circulating antinephritogenic IgG aabs attack renal tubular BB localized nephritogenic ags and release them into the circulation (Barabas et al., 2003; Barabas et al., 2006c). Released aags will join IC deposits on the epithelial side of the glomerular basement membrane enlarging the deposits and thus causing morphological and functional injury to the kidney (Barabas et al., 2003). Continuously produced pathogenic IgG aabs and aags continually released from the damaged normal renal tubules will continue to enlarge the deposits in the glomeruli together with complement components, causing a chronic progressive autoimmune kidney disease (Barabas et al., 2003). The progression of disease processes or diminution of disease intensity depends mainly on the presence of the modifying agent in the system, because as stated above the immune response outcome depends on the presentation of the ag to the cells of the immune system. The continuous alteration of self by the modifying agent in the system drives the pathogenic autoimmune response to produce high levels of circulating pathogenic IgG aabs. As long as a pathogenic IgG aab is present in the circulation, the disease process will continue. The level of pathogenic IgG aab must be at zero for no autoimmune disease process to be detectable in the host (Barabas et al., 2004b).

In contrast to the common belief, we and a few other scientists believe that the normal target ag on its own will not under normal circumstances initiate a pathogenic IgG aab response (Barabas et al., 2004c; Barabas et al., 2006a; Rich, 1996; Totoritis & Rubin, 1985; Weir & Elson, 1969; Weir & Pinckard, 1967). Administration of native ags during autoimmune disease states, e.g. during slowly progressive Heymann nephritis (SPHN), other experimental situations, do not make the disease process progress more intense (Barabas et al., 2006a; Bielekova et al., 2000; Peakman & Dayan, 2001; Prakken et al., 2004). Rather the opposite, in most instances they reduce the pathogenic immune response (Barabas et al., 2004c; Barabas et al., 2006a). It seems that even during a disease state the native target ag preferentially stimulates IgM aab production. The IgM aabs being cross-reactive, their increased levels remove from the circulation both the disease contributing native target ag and the disease causing modified target ag (Barabas et al., 2007a), contributing to remission.

It is worth noting, in reference to a broader context, that the initiation and intensification of an autoimmune disease are undoubtedly complex, and may involve numerous factors or processes besides those described above, such as:

genetic predisposition;

576 Autoimmune Disorders – Current Concepts and Advances from Bedside to Mechanistic Insights

more substrate for the reaction to continue. In the case of cancer, on the other hand, the cells and the products of the autoimmune system do not react with the minimally altered self on cancer cell surfaces and the cancer cells are not be eliminated, therefore allowing the cancer

The induction and maintenance of autoimmune diseases, as well as the associated immunopathological and functional changes, have been extremely well studied in experimental animals (Andres et al., 1986; Barabas et al., 1969; Barabas & Lannigan, 1969; Grupe & Kaplan, 1969; Heymann et al., 1959; Kerjaschki, 1993; Kerjaschki, 2000b; Kerjaschki & Farquhar, 1982); and by comparative study the etiology and pathogenesis of human autoimmune diseases are equally well understood (Davidson & Diamond, 2001; Kretz-Rommel et al., 1997; Kretz-Rommel & Rubin, 1999; Sinha et al., 1990; Theofilopoulos, 1995; Tung, 1994; Von Herrath & Oldstone, 1995). In most instances for an autoimmune disease to begin, a modified self (Barabas et al., 2004c) or self-like (molecular mimicry) (Ebringer et al., 1997; Ebringer, 2003; Mokhtarian et al., 1999; Orbach & Shoenfeld, 2007) ag has to present itself as a foreign-like, exogenous-like ag to the cells of the immune system. There are numerous agents that are able to modify self ags (toxins, chemicals, infectious agents, drugs, adjuvants, vaccines, smoking, chemical dyes, UV irradiation, etc.) and initiate a pathogenic IgG aab response (Barabas et al., 2004c; Conti et al., 2008; Davidson & Diamond, 2001; Hess, 1999; Heymann et al., 1959; Rao & Richardson, 1999; ten Veen & Feltkamp, 1972) (initially a primary immune response, as the immune system has not previously been exposed to the modified ag). If the modifying agent is continuously present in the system, then the modified self ag will continue to stimulate the appropriate T and B cells to maintain the production of pathogenic IgG aabs by the plasma cells (secondary ab response) (Barabas et al., 2003). The developing pathogenic IgG aabs are cross-reactive (Barabas & Lafreniere, 2005). They react with the modified self ag and the normal target ag in an organ. ICs made up of modified self and anti-modified self IgG aab form as a result. The fate of these ICs is twofold. In part they are neutralized and eliminated. However, insofar as they are not fully or quickly enough removed from the body they operate to maintain the pathogenic IgG aab

The pathogenic IgG aabs also react with the target ag not just as it appears in the circulation, but also *in situ* within the organ where it originates; e.g. in HN circulating antinephritogenic IgG aabs attack renal tubular BB localized nephritogenic ags and release them into the circulation (Barabas et al., 2003; Barabas et al., 2006c). Released aags will join IC deposits on the epithelial side of the glomerular basement membrane enlarging the deposits and thus causing morphological and functional injury to the kidney (Barabas et al., 2003). Continuously produced pathogenic IgG aabs and aags continually released from the damaged normal renal tubules will continue to enlarge the deposits in the glomeruli together with complement components, causing a chronic progressive autoimmune kidney disease (Barabas et al., 2003). The progression of disease processes or diminution of disease intensity depends mainly on the presence of the modifying agent in the system, because as stated above the immune response outcome depends on the presentation of the ag to the cells of the immune system. The continuous alteration of self by the modifying agent in the system drives the pathogenic autoimmune response to produce high levels of circulating pathogenic IgG aabs. As long as a pathogenic IgG aab is present in the circulation, the

**4.2.1 Initiation and maintenance of an autoimmune disease** 

to prevail (Foss, 2002).

production.

	- a. assisting in the complement-dependent clearance of modified/unmodified self that causes the autoimmune disease (Gaipl et al., 2001; Taylor et al., 2000; Zwart et al., 2004);
	- b. in contributing to the continuously layered aag/aab depositions, e.g. in the glomeruli (Barabas et al., 2003; Barabas et al., 2004b; Barabas et al., 2004c) (pathogenic immune response) causing complement mediated C3, C59b injury (Barabas et al., 2003; Barabas et al., 2004c) resulting in compromised glomerular filtration;

Notwithstanding the influence of such other factors, the set of processes described above appear to be fundamental to autoimmune disease involving misdirected auto-reaction, and understanding them has assisted in the development of a powerful technique to deal with autoimmune disease, as we will describe further below.

Four Aspects of Autoimmunity and How to Regain Tolerance to Self

Terres, 1963; Xu et al., 2005; Yao et al., 2007).

Journal, 2007 Winter;6(4):12-18.]

modified vaccination technique

from an Autoimmune Disease Utilizing the Modified Vaccination Technique 579

1998; Whitfill et al., 1995; Xu et al., 2005; Yao et al., 2007). So far most of the pertinent investigations have described the role that ag:ab ICs play in immune response upon injection of such complexes at various ratios, and how enhanced ab production occurs during primary and secondary ab responses (Barabas et al., 2007d; Heyman, 2000; Stoner &

To date, we are the only group to have described how specifically composed ag:ab complexes can redirect the immune response for the health benefit of the vaccinated host (Barabas et al., 2004b; Barabas et al., 2006c; Barabas et al., 2006b; Barabas et al., 2007c; Barabas et al., 2009a; Barabas & Lafreniere, 2005). The possibility of such an approach has just recently become a reality, following the categorization of autoimmunity into four clearly definable functioning immunological responses (Figure 2) against self (Barabas et al., 2008a;

Fig. 2. Beneficial or harmful aspects of pathogenic and non-pathogenic immune responses. The diagram illustrates the beneficial and harmful aspects of pathogenic and nonpathogenic aspects of autoimmunity. The MVT can restore non-pathogenic tolerance, ending an autoimmune disease. [Figure reproduced by permission from BioProcessing

Abbreviations: AAb, autoantibody; AAg, autoantigen; Ab, antibody; Ag, antigen; MVT,

#### **4.2.2 Inability to recognize and remove abnormal cell lines**

Throughout life abnormal cell lines (some being cancerous) can emerge. They are most often recognized as non-self and removed by the cells of the autoimmune system. NK cells play a dominant role in this regard (Cheent & Khakoo, 2009; Foss, 2002; Topham & Hewitt, 2009).

Cancer specific non-self antigenic markers on the cell surfaces of emerging cancer cells are sometimes weakly antigenic; for this reason, they do not lend themselves to immune recognition and provoke immune response (Foss, 2002; Kim et al., 2007). In addition, tumour ags associated with cancer cell surfaces are camouflaged or protected on the cell membranes of these self-like cancer cells. The combination of minimal antigenicity and firm integration into and protection by the cell surface membrane means that even after cell death, these cancer specific ags do not detach to form individual small MW antigenic fragments that might be recognized as non-self for immune response processing. Further, if these cells are growing in a well vascularised space and allowed to spread into secondary sites without undermining influences such as ischemia, lack of nutrients, vitamins, or trace minerals, immune attack, etc. then the emerging cancer cells are more readily accepted as self. Several factors, such as old age, compromised immune system function (e.g. from treatment with immunosuppressive agents), overwhelming infections, exposure to harmful substances (smoking, alcohol, chemicals, drugs, etc.), and tumour derived soluble factors, can interfere with the normal functioning of the cells of the immune system in carrying out the surveillance of the somatic cells of our internal environments (Kim et al., 2007).

The lack of adjuvant in a mixture of the disintegrated components of dead cancer cells which include cell membrane associated ags has been shown to prevent pathogenic immune response against cancer specific ags, though it also prevented immune response against normal cell membrane associated ags (Ichim, 2005). And as we have noted elsewhere, normal self ags administered in adjuvants can induce pathogenic autoimmune responses, causing autoimmune disease – especially in the case of experimental autoimmune diseases (Barabas et al., 2004c; Heymann et al., 1959). Therefore, although a pathogenic autoimmune response is required against the cancer specific ag in order to kill (lyse) the cancer cells in the system, the use of an adjuvant to induce such an autoimmune response would likely have a deleterious effect against normal self as well. The question is how to overcome the immune system's inability to respond only against the non-self parts of cancer cells without causing harm to their normal functioning counterparts either in the organ where the primary tumour originated or elsewhere.

#### **5. MVT for the prevention and cure of diseases caused by chronic immune disorders**

Our MVT, which involves the administration of IC formed with condition-specific components that initiate and maintain a predetermined immune response, has the potential to prevent chronic ailments, and to cure already present diseases (Barabas et al., 2004b; Barabas et al., 2006c; Barabas et al., 2006b; Barabas et al., 2009a). This is the first time that the promise has existed to prevent, treat, and cure endogenous ag induced mishaps in humans specifically and without side effects.

The study of the affects of injection of ag:ab ICs at different ratios is not new, nor is the use of ICs in increasing ab production (Klaus, 1978; Kunkl & Klaus, 1981; Nie et al., 1997; Stoner et al., 1975; Stoner & Terres, 1963; Terres et al., 1972; Terres & Stoner, 1962; Terres & Wolins, 1959; Terres & Wolins, 1961) and even in vaccination (Haddad et al., 1997; Jeurissen et al.,

Throughout life abnormal cell lines (some being cancerous) can emerge. They are most often recognized as non-self and removed by the cells of the autoimmune system. NK cells play a dominant role in this regard (Cheent & Khakoo, 2009; Foss, 2002; Topham & Hewitt, 2009). Cancer specific non-self antigenic markers on the cell surfaces of emerging cancer cells are sometimes weakly antigenic; for this reason, they do not lend themselves to immune recognition and provoke immune response (Foss, 2002; Kim et al., 2007). In addition, tumour ags associated with cancer cell surfaces are camouflaged or protected on the cell membranes of these self-like cancer cells. The combination of minimal antigenicity and firm integration into and protection by the cell surface membrane means that even after cell death, these cancer specific ags do not detach to form individual small MW antigenic fragments that might be recognized as non-self for immune response processing. Further, if these cells are growing in a well vascularised space and allowed to spread into secondary sites without undermining influences such as ischemia, lack of nutrients, vitamins, or trace minerals, immune attack, etc. then the emerging cancer cells are more readily accepted as self. Several factors, such as old age, compromised immune system function (e.g. from treatment with immunosuppressive agents), overwhelming infections, exposure to harmful substances (smoking, alcohol, chemicals, drugs, etc.), and tumour derived soluble factors, can interfere with the normal functioning of the cells of the immune system in carrying out

the surveillance of the somatic cells of our internal environments (Kim et al., 2007).

tumour originated or elsewhere.

specifically and without side effects.

**disorders** 

The lack of adjuvant in a mixture of the disintegrated components of dead cancer cells which include cell membrane associated ags has been shown to prevent pathogenic immune response against cancer specific ags, though it also prevented immune response against normal cell membrane associated ags (Ichim, 2005). And as we have noted elsewhere, normal self ags administered in adjuvants can induce pathogenic autoimmune responses, causing autoimmune disease – especially in the case of experimental autoimmune diseases (Barabas et al., 2004c; Heymann et al., 1959). Therefore, although a pathogenic autoimmune response is required against the cancer specific ag in order to kill (lyse) the cancer cells in the system, the use of an adjuvant to induce such an autoimmune response would likely have a deleterious effect against normal self as well. The question is how to overcome the immune system's inability to respond only against the non-self parts of cancer cells without causing harm to their normal functioning counterparts either in the organ where the primary

**5. MVT for the prevention and cure of diseases caused by chronic immune** 

Our MVT, which involves the administration of IC formed with condition-specific components that initiate and maintain a predetermined immune response, has the potential to prevent chronic ailments, and to cure already present diseases (Barabas et al., 2004b; Barabas et al., 2006c; Barabas et al., 2006b; Barabas et al., 2009a). This is the first time that the promise has existed to prevent, treat, and cure endogenous ag induced mishaps in humans

The study of the affects of injection of ag:ab ICs at different ratios is not new, nor is the use of ICs in increasing ab production (Klaus, 1978; Kunkl & Klaus, 1981; Nie et al., 1997; Stoner et al., 1975; Stoner & Terres, 1963; Terres et al., 1972; Terres & Stoner, 1962; Terres & Wolins, 1959; Terres & Wolins, 1961) and even in vaccination (Haddad et al., 1997; Jeurissen et al.,

**4.2.2 Inability to recognize and remove abnormal cell lines** 

1998; Whitfill et al., 1995; Xu et al., 2005; Yao et al., 2007). So far most of the pertinent investigations have described the role that ag:ab ICs play in immune response upon injection of such complexes at various ratios, and how enhanced ab production occurs during primary and secondary ab responses (Barabas et al., 2007d; Heyman, 2000; Stoner & Terres, 1963; Xu et al., 2005; Yao et al., 2007).

To date, we are the only group to have described how specifically composed ag:ab complexes can redirect the immune response for the health benefit of the vaccinated host (Barabas et al., 2004b; Barabas et al., 2006c; Barabas et al., 2006b; Barabas et al., 2007c; Barabas et al., 2009a; Barabas & Lafreniere, 2005). The possibility of such an approach has just recently become a reality, following the categorization of autoimmunity into four clearly definable functioning immunological responses (Figure 2) against self (Barabas et al., 2008a;

Fig. 2. Beneficial or harmful aspects of pathogenic and non-pathogenic immune responses. The diagram illustrates the beneficial and harmful aspects of pathogenic and nonpathogenic aspects of autoimmunity. The MVT can restore non-pathogenic tolerance, ending an autoimmune disease. [Figure reproduced by permission from BioProcessing Journal, 2007 Winter;6(4):12-18.]

Abbreviations: AAb, autoantibody; AAg, autoantigen; Ab, antibody; Ag, antigen; MVT, modified vaccination technique

Four Aspects of Autoimmunity and How to Regain Tolerance to Self

2006b) (prophylactic vaccination);

response; therapeutic vaccination);

response);

**7. Conclusion** 

immune responses.

infections in humans.

and powerful;

from an Autoimmune Disease Utilizing the Modified Vaccination Technique 581

 immunization post-disease-induction with the same IC, when the autoimmune disease was in its chronic progressive phase, terminated the disease causing immune events (Barabas et al., 2004b; Barabas et al., 2006b) (increased levels of specific IgM aabs removed both the pathogenic immune response inducing modified ag and the disease contributing native aag from the system, thereby terminating pathogenic immune

corrective immune response induction was immediate (similar to secondary ab

there was no need for adjuvant application as immune response was quick, specific,

 the MVT was not a mere supplementary therapeutic option for prevention or treatment of the endogenous ag induced disorder; rather, it was key; by ab information transfer, utilizing the immune system's natural abilities. We achieved production in the vaccinated host of the same ab (i.e., the corrective immune response), with the same

tolerance to self was accomplished specifically and without side effects (utilizing the

There are several reasons why up to now chronic disorders have been mainly treated with drugs and not by immune intervention. Perhaps the most important reason was that we were unable to present the offending ag(s) (i.e., the antigenic information) to the cells of the immune system in a suitable form to elicit corrective immune response outcomes. However, we have learned how to prepare and present exogenous ags such as bacterial/viral products to the body in attenuated or inactivated forms – usually in adjuvants – to elicit protective

We have developed a new vaccination methodology called MVT that is able to downregulate immunopathological events in an experimental autoimmune kidney disease in animals and is also able to upregulate immune responses against an exogenous ag. This method, which is the third method of vaccination to be developed, has the potential not only to prevent but with equal effectiveness cure certain autoimmune diseases and chronic

Autoimmunity encompasses four possible immunological events against self, two beneficial and two harmful aspects (Figure 2). The two beneficial aspects of autoimmunity function throughout life to preserve the internal integrity of the organism by maintaining tolerance to normal self while preventing corrupted self from taking hold. The maintenance of antigenic

The autoimmune system achieves its aim on one hand (the first beneficial aspect of autoimmunity) by degrading cellular debris – from cells damaged by various agents (e.g. chemicals, drugs, smoke, toxins, etc.) and from cells which have come to the end of their lifespan – into reusable small MW peptides. The efficient clearance of cellular waste is assisted by non-pathogenic IgM aabs prior to their degradation by phagocytic cells. These specific IgM aabs are the main agents of the maintenance of tolerance to self, and fulfill a

homeostasis is the most important function of the autoimmune system.

specificity against the target ag, as was present in the injected IC; and

MVT) by downregulating and terminating pathogenic immune events.

the occurrence of the autoimmune kidney disease (Barabas et al., 2004b; Barabas et al.,

Barabas et al., 2009a), and the development of our understanding of autoimmune disease etiology and pathogenesis, in particular the role of non-pathogenic and pathogenic aabs (Figure 1) in both disease development and in its prevention and cure (Barabas et al., 2004b; Barabas et al., 2006c; Barabas et al., 2006b) (e.g. in autoimmune disease).

NOTE:


The immune system's natural ability can be utilized to bring about corrective immune responses which can cure/terminate chronic ailments by proper presentation of the target ag. In other words, the ag that causes or contributes to the disease can also terminate it, provided the antigenic information is presented to the cells of the immune system in the proper format.

The vaccination method we have developed – which is essentially the third vaccination rubric to have arisen, coming as it has after the conventional active and passive immunization techniques – promises to be able to deal with chronic ailments that are presently only treatable with drugs. Called MVT, it is so named because every time a vaccine is produced it must be formulated of components that are tailor-made to induce a specific corrective immune response. In order to achieve specificity – and to avoid collateral damage to normal body constituents – the production of absolutely pure and specific target ags and their abs is required. This can be done by present techniques, and soon more sophisticated methodologies will be available.
