Ayurvedic Approach to IMMUNOLOGY


 

 

 

Prof. Dr. S. N. Ohja

Prof. S. N. Ojha M.D. Ph.D

Principal, 

Padmashree Dr. D.Y. Patil College Of Ayurved & Research centre.

Pimpri, PUNE

 

————————————————————————————————————————————————————–

AYURVEDIC APPROACH TO IMMUNOLOGY 

 

Vyadhikshamatwa is defined as the capability of sharir to prevent the utpatti of the disease and also to resist almost all types of organism, toxins  nija & agantuj hetu that tend to damage the body constitution.

 

The ability of the body to defend itself against specific unwanted invading agents depends upon the biological defenses (Bala) of the sharir.

Bala is of 3 types

The natural, inherited body defence of sharir & mana is known as sahaja bala or innate  inmunity

Defence obtained with respect to ritu; (bala is increased in hemanta & shishira ritu) and bala obtained depending on development of dhatus considering the age

 

Neonates are in a state of physiological immunodeficiency during adolescence human body undergoes several immunological changes

—Specific foods like fresh fruits, vegetables and food rich in certain fatty acids may foster a healthy immune systems. Fruits like amalaki are rich source of Vit .C

IMMUNITY

Immunity is a biological term that describes a state of having sufficient biological defenses to avoid infection, disease, or other unwanted biological invasion.

Immunity involves both specific and non-specific components.

The non-specific components act either as barriers or as eliminators of wide range of pathogens irrespective of antigenic specificity.

Other components of the immune system adapt themselves to each new disease encountered and are able to generate pathogen-specific immunity.

TERMINOLOGY

 

  •  Adaptive immune system
  •  Antibody
  •  Antigens
  •  Antimicrobial peptides
  •  Apoptosis
  •  B lymphocytes
  •  B cell receptor of antigen
  •  Complement
  •  Co stimulatory molecules
  •  Cytokines
  • Dendritic cells
  •  Innate Immune System
  •  Large granular lymphocytes
  •  Natural Killer Cells
  •  Pathogen associated molecular patterns

(PAMP)

  •  Pattern recognition receptors (PRRs)
  •  T Cells
  •  T Cell receptor for antigen
  •  Tolerance
  •  CD  classification of human lymphocyte

differentiation antigens

INNATE IMMUNE SYSTEM

Innate immune defenses are non specific, meaning these systems respond to pathogens in a generic way.

MAJOR COMPONENTS OF INNATE IMMUNE SYSTEM

  •  Pattern recognition receptors (PRR)
  •  Antimicrobial peptides
  •  Complement components        
  •  Cytokines
  •  Cells

Macrophages,             Plasmacytoid dendritic cells

Myeloid dendritic cells,                 NK-T cells

Natural Killer cells (NK) Neutrophils

Eosinophils                                         Mast cells

Basophills                                            Epithelial cells.

COMPONENTS

Cellular – T Cell precursors in thymus

– Naïve mature T lymphocytes before antigen

exposure

– Memory T lymphocytes after antigen

exposure

– Helper T lymphocytes

– Cytotoxic T lymphocytes

Humoral – Bone marrow derived (B) lymphocyte

– Naïve B cells prior to antigen recognition

– Memory B cell after the antigen recognition

– Plasma cells that recreate specific antibody.

Cytokines            –

A further subdivision of adaptive immunity is characterized by the cells involved.

  •  Humoral immunity is the aspect of immunity that is mediated by secreted antibodies,

Humoral immunity is active when the organism generates its own antibodies.

passive when antibodies are transferred between individuals.

  •  Cell mediated immunity involves T-lymphocytes alone.

Cell mediated immunity is active when the organisms’ own T-cells are stimulated.

Passive when T cells come from another organism.

Passive immunity

  •  Passive immunity is the transfer of active immunity, in the form of readymade antibodies, from one individual to another.
  •  Passive immunity can occur naturally, when maternal antibodies are transferred to the fetus through the placenta, and can also be induced artificially, when high levels of human (or horse) antibodies specific for a pathogen or toxin are transferred to non-immune individuals.

 

  • Passive immunization is used when there is a high risk of infection and insufficient time for the body to develop its own immune response, to reduce the symptoms of ongoing or immunosuppressive diseases.
  •  Passive immunity provides immediate protection, but the body does not develop memory, therefore the patient is at risk of being infected by the same pathogen later.
  • Passive immunization is used when there is a high risk of infection and insufficient time for the body to develop its own immune response, to reduce the symptoms of ongoing or immunosuppressive diseases.
  •  Passive immunity provides immediate protection, but the body does not develop memory, therefore the patient is at risk of being infected by the same pathogen later.
  • Naturally acquired passive immunity
  • Maternal passive immunity is a type of naturally acquired passive immunity, and refers to antibody-mediated immunity conveyed to a fetus by its mother during pregnancy.
  • Maternal antibodies (MatAb) are passed through the placenta to the fetus by an FcRn receptor on placental cells. This occurs around the third month of gestation.
  •  IgG is the only antibody isotype that can pass through the placenta.
  • Passive immunity is also provided through the transfer of IgA antibodies found in breast milk that are transferred to the gut of the infant, protecting against bacterial infections, until the newborn can synthesize its own antibodies.
  • Artificially acquired passive immunity
  • It is a short-term immunization induced by the transfer of antibodies, which can be administered in several forms; as human or animal blood plasma, as pooled human immunoglobulin for intravenous (IVIG) or intramuscular (IG) use, and in the form of monoclonal antibodies (MAb).
  • Passive transfer is used prophylactically in the case of immunodeficiency diseases, such as hypogammaglobulinemia.
  •  It is also used in the treatment of several types of acute infection, and to treat poisoning.
  •  Immunity derived from passive immunization lasts for only a short period of time,
  • there is also a potential risk for hypersensitivity reactions,
  • serum sickness, especially from gamma globulin of non-human origin.
  • Passive transfer of cell-mediated immunity
  • Passive or “adoptive transfer” of cell-mediated immunity, is conferred by the transfer of “sensitized” or activated T-cells from one individual into another.
  •  It is rarely used in humans because it requires histocompatible (matched) donors, which are often difficult to find.
  • In unmatched donors this type of transfer carries severe risks of graft versus host disease.
  • It has, however, been used to treat certain diseases including some types of cancer and immunodeficiency.
  • This type of transfer differs from a bone marrow transplant, in which (undifferentiated) hematopoietic stem cells are transferred.

 

Naturally acquired active immunity

.Naturally acquired active immunity occurs when a person is exposed to a live pathogen, and develops a primary immune response, which leads to immunological memory.

This type of immunity is “natural” because it is not induced by deliberate exposure.

Many disorders of immune system function can affect the formation of active immunity such as immunodeficiency (both acquired and congenital forms) and immunosuppression.

Artificially acquired active immunity

Artificially acquired active immunity can be induced by a vaccine, a substance that contains antigen.

A vaccine stimulates a primary response against the antigen without causing symptoms of the disease.

There are four types of traditional vaccines:

  •  Inactivated vaccines are composed of micro-organisms that have been killed with chemicals and/or heat and are no longer infectious. Examples are vaccines against flu, cholera, bubonic plague, and hepatitis A. Most vaccines of this type are likely to require booster shots.
  •  Live, attenuated vaccines are composed of micro-organisms that have been cultivated under conditions which disable their ability to induce disease. These responses are more durable and do not generally require booster shots. Examples include yellow fever, measles, rubella, and mumps.
  •  Toxoids are inactivated toxic compounds from micro-organisms in cases where these (rather than the micro-organism itself) cause illness, used prior to an encounter with the toxin of the micro-organism. Examples of toxoid-based vaccines include tetanus and diphtheria.
  •  Subunit -vaccines are composed of small fragments of disease causing organisms. A characteristic example is the subunit vaccine against Hepatitis B virus.

Most vaccines are given by hypodermic injection as they are not absorbed reliably through the gut.

Live attenuated Polio and some Typhoid and Cholera vaccines are given orally in order to produce immunity based in the bowel.

Lymphocytes

  •  The cells of the adaptive immune system are special types of leukocytes, called lymphocytes.
  •  B cells and T cells are the major types of lymphocytes and are derived from hematopoietic stem cells in the bone marrow.
  •   B cells are involved in the humoral immune response,  whereas T cells are involved in cell-mediated immune response.
  • T cells recognize a “non-self” target, such as a pathogen, only after antigens (small fragments of the pathogen) have been processed and presented in combination with a “self” receptor called a major histocompatibility complex (MHC) molecule.
  • Subtypes of T cells: the killer T cell and the helper T cell.
  •  Killer T cells only recognize antigens coupled to Class I MHC molecules,
  • Helper T cells only recognize antigens coupled to Class II MHC molecules.
  • A third, minor subtype are the γδ T cells that recognize intact antigens that are not bound to MHC receptors.
  • the B cell antigen-specific receptor is an antibody molecule on the B cell surface, and recognizes whole pathogens without any need for antigen processing.
  • Each lineage of B cell expresses a different antibody, so the complete set of B cell antigen receptors represent all the antibodies that the body can manufacture.
  • Histological examination of the immune system

    The key primary lymphoid organs of the immune system are like thymus and bone marrow, and secondary lymphatic tissues such as spleen, tonsils, lymph vessels, lymph nodes, adenoids, and skin.

    Many components of the immune system are actually cellular in nature and not associated with any specific organ but rather are embedded or circulating in various tissues located throughout the body.

    Developmental immunology :

    The body’s capability to react to antigen depends on a

    •   person’s age,
    •   Antigen type,
    •   Maternal factors
    •   The area where the antigen is presented.

    Neonates are said to be in a state of physiological immunodeficiency, because both their innate and adaptive immunological responses are greatly suppressed. In neonates, opsonic activity and the ability to activate the complement cascade is very limited.

    Phagocytic activity is also greatly impaired in newborns.

    Maternal factors also play a role in the body’s immune response.

    At birth most of the immunoglobulin is present is maternal IgG.

    Because IgM, IgD, IgE and IgA don’t cross the placenta

    Although some IgA is provided in breast milk. These passively acquired antibodies can protect the newborn up to 18 months, but their response is usually short-live and of low affinity.

    During adolescence the human body undergoes several physical, physiological and immunological changes. These changes are started and mediated by different hormones.

     

    Depending on the sex either testosterone or 17-β-oestradiol, act on male and female bodies accordingly, start acting at ages of 12 and 10 years

    There is evidence that these steroids act directly not only on the primary and secondary sexual characteristics, but also have an effect on the development and regulation of the immune system.[7]

    The female sex hormone 17-β-oestradiol has been shown to regulate the level of immunological response.[10]

    Similarly, some male androgens, like testosterone, seem to suppress the stress response to infection; but other androgens like DHEA have the opposite effect, as it increases the immune response instead of down playing it.

    As in females, the male sex hormones seem to have more control of the immune system during puberty and the time right after than in fully developed adults.

    Other than hormonal changes physical changes like the involution of the Thymus during puberty will also affect the immunological response of the subject or patient.

    Clinical immunology :

    Clinical immunology is the study of diseases caused by disorders of the immune system (failure, aberrant action, and malignant growth of the cellular elements of the system).

    It also involves diseases of other systems, where immune reactions play a part in the pathology and clinical features.

    The diseases caused by disorders of the immune system fall into two broad categories:

    1) Immunodeficiency, in which parts of the immune system fail to provide an adequate response (examples include chronic granulomatous disease).

    2) autoimmunity, in which the immune system attacks its own host’s body (examples include systemic lupus erythematosus, rheumatoid arthritis, Hashimoto’s disease and myasthenia gravis).

    Other immune system disorders include different hypersensitivities, in which the system responds inappropriately to harmless compounds (asthma and other allergies) or responds too intensely.

    Disorders of human immunity

    The immune system is a remarkably effective structure that incorporates specificity, inducibility and adaptation.

    Failures of host defense do occur, however, and fall into three broad categories:

    1) Immunodeficiencies,

    2) Autoimmunity,

    3) Hypersensitivities.

    Immunodeficiencies :

    Immunodeficiencies occur when one or more of the components of the immune system are inactive.

    The ability of the immune system to respond to pathogens is diminished in both the young and the elderly, with immune responses beginning to decline at around 50 years of age due to immunosenescence.[68][69]

    In developed countries, obesity, alcoholism, and drug use are common causes of poor immune function.[69]

    However, malnutrition is the most common cause of immunodeficiency in developing countries.[69]

    Diets lacking sufficient protein are associated with impaired cell-mediated immunity, complement activity, phagocyte function, IgA antibody concentrations, and cytokine production.

    Deficiency of single nutrients such as iron; copper; zinc; selenium; vitamins A, C, E, and B6; and folic acid (vitamin B9) also reduces immune responses.[

    Additionally, the loss of the thymus at an early age through genetic mutation or surgical removal results in severe immunodeficiency and a high susceptibility to infection.

    Immunodeficiencies can also be inherited  Chronic granulomatous disease, where phagocytes have a reduced ability to destroy pathogens, is an example of an inherited,

    ‘acquired’.

    congenital, immunodeficiency. AIDS and some types of cancer cause acquired immunodeficiency.

    Autoimmunity :

    Overactive immune responses comprise the other end of immune dysfunction, particularly the autoimmune disorders.

    the immune system fails to properly distinguish between self and non-self, and attacks part of the body.

    Hypersensitivity :

    Hypersensitivity is an immune response that damages the body’s own tissues.

    They are divided into four classes (Type I – IV) based on the mechanisms involved and the time course of the hypersensitive reaction.

    Type I hypersensitivity is an immediate or anaphylactic reaction, often associated with allergy.

    Symptoms can range from mild discomfort to death.

    Type I hypersensitivity is mediated by IgE, which triggers degranulation of mast cells and basophils when cross-linked by antigen.

    Type II hypersensitivity occurs when antibodies bind to antigens on the patient’s own cells, marking them for destruction.

    This is also called antibody-dependent (or cytotoxic) hypersensitivity, and is mediated by IgG and IgM antibodies.[74]

    Immune complexes (aggregations of antigens, complement proteins, and IgG and IgM antibodies) deposited in various tissues trigger Type III hypersensitivity reactions

    Type IV hypersensitivity (also known as cell-mediated or delayed type hypersensitivity) usually takes between two and three days to develop.

    Type IV reactions are involved in many autoimmune and infectious diseases, but may also involve contact dermatitis (poison ivy).

    These reactions are mediated by T cells, monocytes, and macrophages.

    Physiological regulation :

    Hormones can act as immunomodulators, altering the sensitivity of the immune system.

    female sex hormones are known immunostimulators of both adaptive and innate immune responses.

    Some autoimmune diseases such as lupus erythematosus strike women preferentially, and their onset often coincides with puberty.

    By contrast, male sex hormones such as testosterone seem to be immunosuppressive.

    Other hormones appear to regulate the immune system as well, most notably prolactin, growth hormone and vitamin D. Conversely, some hormones are regulated by the immune system, notably thyroid hormone activity

    The age-related decline in immune function is also related to dropping vitamin D levels in the elderly.

    As people age, two things happen that negatively affect their vitamin D levels. First, they stay indoors more due to decreased activity levels.

    This means that they get less sun and therefore produce less cholecalciferol via UVB radiation.

    Second, as a person ages the skin becomes less adept at producing vitamin D.

    Sleep and rest.

    Complex feedback loops involving cytokines, such as interleukin-1 and tumor necrosis factor-α produced in response to infection, appear to also play a role in the regulation of non-rapid eye movement (REM) sleep.

    Nutrition and diet :

    The functioning of the immune system, like most systems in the body, is dependent on proper nutrition.

    It has been long known that severe malnutrition leads to immunodeficiency.

    Overnutrition is also associated with diseases such as diabetes and obesity, which are known to affect immune function.

    More moderate malnutrition, as well as certain specific trace mineral and nutrient deficiencies, can also compromise the immune response.[108]

    Specific foods may also affect the immune system; for example, fresh fruits, vegetables, and foods rich in certain fatty acids may foster a healthy immune system.

    Likewise, fetal undernourishment can cause a lifelong impairment of the immune system.

    In traditional medicine, some herbs are believed to stimulate the immune system,such as echinacea, licorice, ginseng, astragalus, sage, garlic, elderberry, and hyssop, as well as honey although further research is needed to understand their mode of action.

    Medicinal mushrooms like Shiitake, Lingzhi mushrooms, the Turkey tail mushroom, Agaricusblazei, and Maitake have shown some evidence of immune system up-regulation in in vitro and in vivo studies, as well as in a limited number of clinical studies.

    Manipulation in medicine

    The immune response can be manipulated to suppress unwanted responses resulting from autoimmunity, allergy, and transplant rejection, and to stimulate protective responses against pathogens that largely elude the immune system

    Immunosuppressive drugs are used to control autoimmune disorders or inflammation when excessive tissue damage occurs, and to prevent transplant rejection after an organ transplant.

    Anti-inflammatory drugs are often used to control the effects of inflammation.

    The glucocorticoids are the most powerful of these drugs; however, these drugs can have many undesirable side effects (e.g., central obesity, hyperglycemia, osteoporosis) and their use must be tightly controlled.

    Therefore, lower doses of anti-inflammatory drugs are often used in conjunction with cytotoxic or immunosuppressive drugs such as methotrexate or azathioprine.

    Cytotoxic drugs inhibit the immune response by killing dividing cells such as activated T cells. However, the killing is indiscriminate and other constantly dividing cells and their organs are affected, which causes toxic side effects.

    Immunosuppressive drugs such as ciclosporin prevent T cells from responding to signals correctly by inhibiting signal transduction pathways.

     

    In some cases, the drug itself is not immunogenic, but may be co-administered with an immunogenic compound, as is sometimes the case for Taxol.

    Manipulation by pathogens :

    The success of any pathogen is dependent on its ability to elude host immune responses.

    Therefore, pathogens have evolved several methods that allow them to successfully infect a host, while evading detection or destruction by the immune system.[

    An evasion strategy used by several pathogens to avoid the innate immune system is to hide within the cells of their host (also called intracellular pathogenesis).

    Here, a pathogen spends most of its life-cycle inside host cells, where it is shielded from direct contact with immune cells, antibodies and complement.

    Some examples of intracellular pathogens include viruses, the food poisoning bacterium Salmonella and the eukaryotic parasites that cause malaria (Plasmodium falciparum) and leishmaniasis (Leishmania spp.).

    Other bacteria, such as Mycobacterium tuberculosis, live inside a protective capsule that prevents lysis by complement.

    Many pathogens secrete compounds that diminish or misdirect the host’s immune response.

    Some bacteria form biofilms to protect themselves from the cells and proteins of the immune system.

    Such biofilms are present in many successful infections, e.g., the chronic Pseudomonas aeruginosa and Burkholderiacenocepacia infections characteristic of cystic fibrosis.

    Other bacteria generate surface proteins that bind to antibodies, rendering them ineffective; examples include Streptococcus (protein G), Staphylococcus aureus (protein A), and Peptostreptococcusmagnus (protein L).

    The simplest approach is to rapidly change non-essential epitopes (amino acids and/or sugars) on the surface of the pathogen, while keeping essential epitopes concealed.This is called antigenic variation. An example is HIV, which mutates rapidly, so the proteins on its viral envelope that are essential for entry into its host target cell are constantly changing. These frequent changes in antigens may explain the failures of vaccines directed at this virus.  In HIV, the envelope that covers the viron is formed from the outermost membrane of the host cell; such “self-cloaked” viruses make it difficult for the immune system to identify them as “non-self” structures.

 

4 responses to this post.

  1. Posted by Sunil Chauhan on November 22, 2011 at 10:10 pm

    Dear Sir,
    I want to contact you for discussion of my daughter’s case for elevated PTH level.

    Reply

    • As per our telephonic conversation, you are welcome to visit me at my college (Dr D Y Patil College Of ayurved Pimpri Pune) on working day, with prior notification.

      Thank you.

      Reply

  2. Thanks a lot sir,
    lecture is very informative all the things i wanted to know.

    Reply

  3. Posted by Tarun kumar Dwibedi. on March 22, 2012 at 1:38 am

    Thsnksnks 4 dis information,Sir.

    Reply

Leave a Reply

Fill in your details below or click an icon to log in:

WordPress.com Logo

You are commenting using your WordPress.com account. Log Out / Change )

Twitter picture

You are commenting using your Twitter account. Log Out / Change )

Facebook photo

You are commenting using your Facebook account. Log Out / Change )

Google+ photo

You are commenting using your Google+ account. Log Out / Change )

Connecting to %s

%d bloggers like this: