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IMMUNOMODULATORS
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IMMUNITY Immunity may be defined as the ability of an animal’s body to
react to a foreign antigen and eliminate it, in the interest of the safety of the animal.
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IMMUNITY
INNATE/NATURAL
ACQUIRED/ADAPTIVE
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INNATE IMMUNITY Innate immunity: It is not dependent on prior antigen
exposure(priming), is primitive and of relatively low affinity, but is broadly active.
Effectors: Granulocytes, Monocytes, Macrophages, Natural killer cells, Mast cells & Basophils.
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ADAPTIVE IMMUNITY Adaptive Immunity: It is antigen-specific, depends on antigen
priming, and can be of very high affinity. Mediators are T&B lymphocytes, shows immunological
memory.
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Active Immunity Type of immunity due to the development of antibodies by
the individual himself. It can be natural and species specific. Eg: The relative immunity of horses, dogs and rats to TB or it
can be acquired by the introduction of an antigen.
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Passive Immunity Immunity acquired by the transfer of antibodies from a donor
to a recipient. It can be acquired naturally. Eg: By a fetus receiving maternal antibodies across the
placenta, or artificially by the administration of anti-serum containing Ig antibodies.
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IMMUNOMODULATORS Immunomodulators are substances that have been shown to
modify the immune systems response to a threat upon it. They modulate and potentiate the weapons of your immune
system keeping them in a highly prepared state for any threat it may encounter. With this balancing effect, all subsequent immune responses improve.
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IMMUNOMODULATION Immunomodulation is the process of modifying an immune
response in a positive or negative manner by administration of a drug or compound.
Immunomodulators are biological or synthetic substances, which can stimulate, suppress or modulate any of the immune system including both adaptive and innate arms of the immune response.
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Many proteins , amino acids ,natural compounds have shown a significant ability to regulate immune responses, including interferons-ϒ,steroids , DMG.
These are biological or synthetic substances, which can stimulate, suppress or modulate any of the immune system including both adaptive and innate arms of the immune response.
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Immunomodulators
Immunoadjuvants Immunostimulants Immunosuppressants
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IMMUNOMODULATORS
Immunoadjuvants: These agents are used
for enhancingvaccines efficacy and
therefore, could be considered specificimmune stimulants.
Immunostimulants: These agents are
inherently nonspecificin nature as they
envisaged to enhance body’s
resistance against infection.
Immunosuppressants: These are a structurally
andfunctionally
heterogeneous group of drugs, which are often
concomitantly administered in
combination regimens to treat
various types of organ transplant rejection and
autoimmuneDiseases.
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Immunoadjuvants
These agents are used for enhancing efficacy of vaccines and therefore, could be considered as specific immune stimulants.
Eg: Freund’s adjuvant, However since it contains Bacillus Calmette Guiren it is not appropriate for human use.
Immunoadjuvants hold the promise of being the true modulators of the immune response, it has been proposed to exploit them for selecting between cellular and humoral, Th1 and Th2, immunoprotective and immunodestructive and resgenic (IgE) versus Immunoglobulin G (IgG) types of immune responses.
Lack of availability of a suitable adjuvant for human has been one of the important stumbling blocks in our ability to develop various vaccines.
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Immunosuppressant drugs These agents could be used for the control of pathological
immune response in autoimmune diseases, graft rejection, graft vs. Host disease, hypersensitivity immune reaction, immune pathology associated with infections.
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Immunostimulant drugs These agents are envisaged to enhance body’s resistance
against infections and may be against allergy, autoimmunity and cancer as well.
These agents are inherently non-specific in nature, but they can act through both innate and adaptive arms of immune response.
In healthy individuals the immunostimulants are expected to serve as prophylactic or promotive agent ie. As immune potentiators by enhancing the basal level of immune response.
In individuals with impairment of Immune system as an immunotherapeutic agent.
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IMMUNOMODULATORS
IMMUNOADJUVANTS
FREUND’ S ADJUVANT
IMMUNOSUPRESSANTS
CALCINEURIN INHIBITORS
GLUCOCORTICOIDS
ANTIPROLIFERATIVE AGENTSMONOCLONAL ANTIBODIES
IMMUNOSTIMULATORSLEVAMISOLE
THALIDOMIDE
BCGRECOMBINANT
CYTOKINES
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IMMUNODEFICIENCY
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. It is common in both the young and the elderly, with immune responses beginning to decline at around 50 years of age due to immunosenescence.
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Causes Developed countries – obesity, alcoholism, drug use. Developing countries – Malnutrition Diets lacking sufficient proteins. Single nutrient deficiency such as Iron, copper, zinc,
selenium, Vitamins A,C,E and B6 and folic acid. Loss of thymus: at an early age due to genetic mutation or
surgical removal.
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Autoimmunity Overactive immune responses comprise the other end of
immune dysfunction, particularly the auto-immune disorders. Here the immune system fails to properly distinguish
between self and non-self, and attacks part of the body. Under normal circumstances , many T cells and antibodies
react with self-peptides.
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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 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
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 .
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AYURVEDIC CONCEPT
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रसायन रसानाम् रक्तादीनामयनमाप्यायनम्.......। स.ुसू 24/23
That which carries the rasa to the different parts of the body.
रसायनम् च तञेयम् यत् जराव्याधि� नाशनं। यथा अमृता रुदन्ति�त च गुगुलुश्च हरीतकी॥ Those Dravyas which destroy Jara and vyadhi are
Rasayanas.
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Examples of Rasayana Dravya
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Drugs with property similar to Rasayanas
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Some Ayurvedic Immunomodulators **
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बलम् It is another important Ayurvedic concept similar to immunity. It is derived from Ojas. It is not a dravya but is a bhava. It is divided into 3 : Sahaja (congenital),
Kalaja(Seasonal/According to Age), yukthija(acquired). Out of these,Sahaja type resembles innate immunity and
yukthija resembles acquired immunity.
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ओजः ओजस् तु तेजो �ातूनाम् शुक्रा�तानाम् परम् स्मृतम। हृदयस्तम् अपिप व्यापिप देहस्थि2पितपिनबन्धनम् ॥ स्निस्नग्�म् सोमात्मकम् शुध्दम् ईषत् लोपिहत पीतकम् । यत् नाशे पिनयतम् नाशे यस्मिस्मन् पितष्ठपित पितष्ठपित ॥ पिनष्पद्य�ते यतो भावा पिवपिव�ा देहसश्रयाः ।
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व्याधि�क्षमत्वम् व्याधि�क्षमत्वम् व्याधि�बलपिवरोधि�त्वम् व्यध्युत्पादप्रपितबन्धकत्वम् इपित यावत् । न च सवाDणिF शरीराणिF व्याधि�क्षमत्वे समथाDपिन भवन्ति�त ।
- च.सू 28/7 Vyadhikshamatva is the ayurvedic counter-part of passive
immunity , it is defined as the ability of the body to prevent diseases and also its ability to not result in diseases even when exposed to pathogens.
Charaka acharya also mentions that vyadhikshamatva is not the same for all bodies.
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REFERENCE
“ AN OVERVIEW ON IMMUNOMODULATION ” -Priyanka Saroj, Mansi Verma, K. K. Jha, Manju pal , Journal of Advanced Scientific Research .• **IMMUNOMODULATORS : A REVIEW OF STUDIES ON
INDIAN MEDICINAL PLANTS AND SYNTHETIC PEPTIDES, PART 1 : MEDICINAL PLANTS – S.S AGARWAL , V.K SINGH , PINSA pp 179 – 204, 1999.
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