Immunosuprresants and stimulants

1. PHARMACOLOGY NOTES
RAMDAS BHAT
SRINIVAS COLLEGE OF PHARMACY 1
CHAPTER-3
IMMUNOPHARMACOLOGY
Prepared by,
RAMDAS BHAT (M. Pharm)
Asst. Professor
Srinivas College of Pharmacy
Mangalore
7795772463
Ramdas21@gmail.com

2. PHARMACOLOGY NOTES
RAMDAS BHAT
SRINIVAS COLLEGE OF PHARMACY 2
• Immunity refers to the ability of the body to identify and resist microorganisms that are
potentially harmful. This ability enables the body to fight or prevent infectious disease
and inhibit tissue and organ damage. The immune system is not confined to any one part
of the body.
• Immune stem cells, formed in the bone marrow, may remain in the bone marrow until
maturation, or they may migrate to different body sites for maturation.
• After maturation, most immune cells circulate in the body and exert specific effects. The
immune system has two distinct, but overlapping, mechanisms with which to fight
invading organisms:
1. Cell-mediated defences (cell-mediated immunity)
2. Antibody-mediated defences (humoral immunity)
1. Cell-Mediated Immunity (T Cells):
• The cell-mediated immunity (CMI) results from the activity of many leukocyte actions,
reactions, and interactions that range from simple to complex.
• This type of immunity depends on the actions of the T lymphocytes, which are
responsible for a delayed type of immune response.
The T lymphocytes defend against viral infections, fungal infections, and some bacterial
infections as follows.
• The T lymphocyte becomes sensitized by its first contact with a specific antigen,
• Subsequent exposure to an antigen stimulates multiple reactions aimed at destroying or
inactivating the offending antigen.
• T lymphocytes and macrophages (large cells that surround, engulf, and digest
microorganisms and cellular debris) work together in CMI to destroy the antigen.
• T lymphocytes attack the antigens directly, rather than produce antibodies (as is done in
humoral immunity). Cellular reactions may also occur without macrophages.
• If CMI is reduced, as in the case of acquired immunodeficiency syndrome (AIDS), the body
-is., unable to protect itself against many viral, bacterial, and fungal infections.
IMMUNOPHARMACOLOGY

3. PHARMACOLOGY NOTES
RAMDAS BHAT
SRINIVAS COLLEGE OF PHARMACY 3
2. Humoral Immunity (B Cells):
• Humoral immunity protects the body against bacterial and viral infections.
• Special lymphocytes (white blood cells), called B lymphocytes, produce circulating
antibodies to act against a foreign substance.
• This type of immunity is based on the antigen—antibody response.
• An antigen is a substance, usually a protein, that stimulates the body to produce
antibodies. An antibody is a globulin (protein) produced by the B lymphocytes as a
defence against an antigen.
• Specific antibodies are formed for specific antigen when the person is exposed to the
chickenpox virus (the antigen).
• Once manufactured, antibodies circulate in the bloodstream, sometimes only for a short
time, but in other cases for the lifetime of the person. When an antigen enters the body,
specific antibodies neutralize the invading antigen; this condition is called immunity.
• Thus, the individual with specific circulating antibodies is immune (or has immunity) to a
specific antigen.
• Immunity is the resistance that an individual has against disease.
• Cell-mediated and humoral immunity are interdependent; CMI influences the function of
• the B lymphocytes, and humoral immunity influences the function of the T lymphocytes.
Active and Passive Immunity:
Active and passive immunity involve the use of agents that stimulate antibody formation
(active immunity) or the injection of ready-made antibodies found in the serum of immune
individuals or animals (passive immunity).
Active Immunity:
When a person is exposed to certain infectious microorganisms (the source of antigens), the
body actively builds an immunity (forms antibodies) to the invading microorganism. This is
called active immunity. There are two types of active immunity: (1) naturally acquired active
immunity and (2) artificially acquired active immunity.
CLASSIFICATION
1. Inhibitors of lymphocyte gene expression- glucocorticoids- PREDNISOLONE
2. Calcineurin Inhibitors-specific T-cell inhibitors- CYCLOSPORINE, TACROLIMUS
3. M-TOR inhibitors- SIROLIMUS, EVEROLIMUS
4. Antiproliferative drugs- AZATHIOPRINE, METHOTREXATE, MYCOPHENOLATE MOFETIL
CYCLOPHOSPHAMIDE, CHLORAMBUCIL
5. Biological agents-
TNFα inhibitors- ETANERCEPT, INFLIXIMAB, ADALIMUMAB
IL-1 receptor antagonist: ANAKINRA, RILONACEPT
IL-2 receptor antagonist: DACLIZUMAB, BACILIXIMAB
6. Monoclonal antibodies-
Anti-CD3 antibody: MUROMONAB
Anti CD52 antibody: ALEMTUZUMAB
Inhibitors of immune cell adhesion- EFALIZUMAB
7. Tolerogens or inhibitors of immune cell co-stimulation- ABETACEPT, BELATACEPT
8. Polyclonal antibodies: Anti-thymocyte antibody (ATG), Rho(D) immune globulin
CALCINEURINE INHIBITORS:

4. PHARMACOLOGY NOTES
RAMDAS BHAT
SRINIVAS COLLEGE OF PHARMACY 4
CYCLOSPORINE:
• It is a calcineurine inhibitor and inhibitor of the humoral immunity as well as the cell
mediated response.
• They help in inhibition of production and release of Lymphokine (IL-2).
• They are acyclic polypeptide that has eleven amino acids.
MOA:
• When the antigen binds to the receptor of the antigen presenting site, they are expressed
over the surface of the MHC class -II receptor of the APC.
• The presented Antigen are now recognised by the T-cell that releases IL-2 and thus
activating other T-cells like T helper cells and T cytotoxic cells as well as activated the
plasma cells. Thus causes the immune response.
• Once the T cells recognises the Antigen expressed over the APC, Antigen binds to the T
cell receptors and thus activates cascade of mechanism inside the cell.
• The mechanism takes place by the activation of Phospholipase C.
• That in turn activates the Phosphoinisitol diphosphate (PIP2) that further activates the IP3
and DAG.
• The activation of IP3-DAG mechanism causes increases the intracellular Ca2+.

5. PHARMACOLOGY NOTES
RAMDAS BHAT
SRINIVAS COLLEGE OF PHARMACY 5
• Calcium released will now bind to the Calmodulin and forms the complex called as Calcium
calmodulin complex.
• This complex further on binds to the Calcineurin form calcineurin calcium calmodulin
complex (CCCC).
• This complex now dephosphorylates the NFAT (Nuclear factor of activated t cell). Thus,
causing the activation of NFAT.
• The activated NFAT now targets the IL-2 gene in the nucleus and thus activates the
formation of IL-2.
• The IL-2 now formed binds to the same IL-2 receptor of same T-cell by the process called
as Apocrine signalling.
• Due to which it will now activates other T cells.
• Calcineurin inhibitors are that class of drug that prevents the release of IL-2 from the T
cell and thus blocking the further activation of other T cells and B cells.
• Calcineurin inhibitors binds to the intracellular receptor called as the Cyclophilin-1
forming Calcineurin-Cyclophilin complex and prevents the complex formation of Calcium
calmodulin with the Calcineurin thus further blocking dephosphorylation process.
• Thus, the release of IL-2 is blocked and blocking further activation of other T cells and B
cells.
INDICATIONS:
Organ transplantation (to prevent Allograft rejection), Dermatitis, IV infusion in Bone marrow
transplant.
PHARMACOKINETICS
• variable, incomplete oral absorption
• Extensive hepatic metabolism, excreted in bile
• Used alone or in combination with prednisone and azathioprine (or other antineoplastic
drugs)
ADVERSE EFFECTS
• Nephrotoxicity,
• hepatotoxicity,
• hirsutism,
• neurotoxicity
• nausea, vomiting
• acne
• tremors
• haematuria.
CONTRAINDICATION:
Hypersensitivity and lactation.
DRUG INTERACTIONS due to induction and inhibition of hepatic cytochrome P450.
TACROLIMUS:
• They have a structure similar to the Erythromycin (macrolide antibiotic).

6. PHARMACOLOGY NOTES
RAMDAS BHAT
SRINIVAS COLLEGE OF PHARMACY 6
• They bind to intracellular protein of T-cell called as FKBP12 and this complex binds to CCCC
and thus prevents the dephosphorylation of NFAT.
• Release of IL-2 is prevented.
INDICATIONS: In allograft rejection.
CONTRAINDICATIONS: Hypersensitivity, Pregnancy, DM, Hyperkalaemia, Lactation.
SIDE EFFECTS: Anaemia, Thrombocytopenia, Nausea, vomiting, hypertension, headache,
insomnia, haematuria, chills, fever, hyperglycaemia, dyspnoea, rash, flushing, itching,
alopecia, blurred vision, photophobia.
PHARMACOKINETICS: t ½ is 10 hrs.
DRUG INTERACTION:
• When given with aminoglycosides it increases the toxicity of aminoglycoside
(OTOTOXICITY).
• Cisplatin decreases the activity of the drug.
INHIBITORS OF LYMPHOCYTE GENE EXPRESSION-
GLUCOCORTICOIDS-
PREDNISOLONE:
• Prednisolone is a glucocorticoid drug that are mainly used as the anti-inflammatory and
to treat Addison’s disease.
• Long term usage of prednisolone can cause immunosuppression.
MOA:
• Whenever there is a pain, inflammation or infection, the chemical mediators /infectious
agents or stimulus will activate the any cell (here we are studying regarding the
immunosuppression hence we can take it as the lymphocytes).
• The stimulus will now activate a factor called as Nucleic Factor Kappa B (NFKB) and this
activated factor will enter into the nucleus and it act over the DNA to cause the
transcription from the mRNA, that later undergoes the translation to form the
inflammatory cytokines.
• The cytokines will now activate other t cells like helper cells, cytotoxic cells and plasma
cells.
• Prednisolone is a is a glucocorticoid drug and is lipid soluble in action.
• They can easily enter the Plasma membrane and bind to the glucocorticoid receptor
present in the cytoplasm and this ligand receptor complex will bind to the NFKB and thus
preventing their entry into the nucleus and further preventing the translation of cytokines
(IL-1).
ADVERSE EFFECTS:
• All commonly occur because high doses used for immunosuppression

7. PHARMACOLOGY NOTES
RAMDAS BHAT
SRINIVAS COLLEGE OF PHARMACY 7
• Suppression of hypothalamic-pituitary adrenal axis (HPA) function
• Osteoporosis
• Hypertension
• Weight gain
• Hyperglycemia
• Euphoric personality changes
• Cataracts
CYTOTOXIC DRUGS:
AZATHIOPRINE:
• They are the immunosuppressant drugs that are the Purine analogue.
• They are more effective as the immunosuppressant than the antitumor drug.
• They are used in Rheumatoid arthritis and in SLE, IBD and renal transplant rejection.
MOA:
• Azathioprine is a pro drug of 6-Mercapto purine.
• 6-MP later metabolize to form 6-Thioguanine nucleotides that enters into the T cell and B
cell and interferes with the S phase of interphase where they incorporate as the faulty
purine bases in the newly forming DNA molecule.
• Cell cycle is now stopped and cell will now undergo apoptosis.
• Other metabolites of 6-MP will now inhibit the action of enzyme glutamine-5-
phosphoribosylpyrophosphate amido transferase that is required for the denovo
synthesis of the purine nucleotides thus causing the lack of the purine or addition of the
faulty purine in the DNA molecule thus causing the Cytotoxic effect.
INDICATIONS:
• Kidney transplantation to prevent allograft rejection.
• Idiopathic thrombocytopenia
• Rheumatoid arthritis
• Systemic lupus erythematosus and IBD.
• Bone marrow transplant.
ADVERSE EFFECTS:
• Nausea, Vomiting.
• Stomatitis,
• Hepatotoxicity and Jaundice
• Muscle wasting
• Leukocytopenia, Pancytopenia,
• Rashes, Flushing.
PHARMACOKINETICS:
• Metabolize in liver, excreted in urine, crosses placenta.
DRUG INTERACTIONS:

8. PHARMACOLOGY NOTES
RAMDAS BHAT
SRINIVAS COLLEGE OF PHARMACY 8
Not to be administered with other drugs.
CYCLOPHOSPHAMIDE:
• It is an alkylating agent.
• They have immunosuppressant action but does not damage the platelets.
MOA:
• Cyclophosphamide is a pro drug that enters into the liver and gets metabolized to form 5-
Hydroxy cyclophosphamide (5HC).
• The formed 5HC will now inhibit various enzymes that are required for the translation of
mRNA into the various amino acids. Thus, interfering in the protein synthesis.
• These drugs also cause the cross linkage of the DNA strands.
INDICATIONS:
• Combination with the surgery, radiations, lymphosarcoma, immunosuppression, multiple
myeloma, Hodgkin’s lymphoma, Lymphogranulomatosis.
DOSE:
• 2-3 mg/kg orally.
SIDE-EFFECTS:
• Cardiotoxicity at higher doses.
• Alopecia
• Pulmonary fibrosis.
• Leukopenia
• Diarrhoea
• Azoospermia
• Sterility
• Weight loss
• Haematuria
• Cystitis
CI (CONTRAINDICATIONS):
• Hypersensitivity, pregnancy and lactation.
PK:
• Metabolized in the liver, t1/2 is 4-6 hrs. Excreted in urine.
DRUS INTERACTIONS:
Increased bone marrow depression with thiazides and Allopurinol. Increased toxicity with
aminoglycoside.
METHOTREXATE (MTX)
• It is a yellow to orange crystalline powder, slightly soluble in water.
• It is readily absorbed when given by mouth and rapidly excreted through kidneys.

9. PHARMACOLOGY NOTES
RAMDAS BHAT
SRINIVAS COLLEGE OF PHARMACY 9
• It is a cytotoxic antimetabolite. It inhibits an enzyme which reduces folic acid synthesis in
cells, in this way cell division is stopped.
• It induced immunosuppression.
MECHANISM OF ACTION:
• lt inhibits (stops) an enzyme which reduces folic acid which is required for nucleic acid
formation in all body cells, specifically S phase of cell cycle.
• It is useful in head and neck carcinoma, lymphosarcoma.
INDICATIONS:
• It is used in acute lymphoblastic leukaemia, leukemic meningitis, carcinoma breast, lung,
head, neck carcinoma lymphosarcoma, rheumatoid arthritis, mycosis fungoides.
DOSAGE:
Lymphoblastic leukaemia: 20 to 40 mg per square meter body surface area twice
weekly, IM/IV. maintenance dose 15 to 30 mg per square meter twice weekly.
Choriocarcinoma: 15 to 30 mg daily for 5 days.
CONTRAINDICATIONS:
hypersensitivity, serious anemia thrombocytopenia, severe leukopenia, pregnancy, lactation.
SIDE EFFECTS: Vomiting, nausea, anorexia, stomatitis hematemesis, ulcers, urinary retention,
menstrual irregularity, spermatogenesis, anemia, leukopenia, thrombocytopenia, urticaria,
rash, gastrointestinal haemorrhage, folliculitis, acne, alopecia, ecchymosis, dizziness,
headache, convulsions, fatigue, chills, fever.
PHARMACOKINETICS:
Onset action 4 to 7 days. Peak plasma concentration 1 to 2 weeks duration of action 3 weeks,
crosses placenta, excreted in urine.
DRUGS INTERACTIONS: Sulfonamides, phenylbutazone, tetracyclines, aspirin, alcohol,
phenytoin, radiations, probenecid, increase toxicity. Folic acid decreases effect of
methotrexate.
MYCOPHENOLATE MOFETIL:
• It is an immunosuppressant drug.
• It inhibits inflammatory action and prolong the survival of allergenic transplant.
MECHANISM OF ACTION:
• It inhibits inflammatory responses which are mediated by the immune system of the body,
it prolongs the survival of allergenic transplant of organ transplanted.
• lt inhibits de novo purine biosynthesis (that promotes immune cell proliferation) by
inhibiting inosine 5'-monophosphate dehydrogenase enzyme (IMPDH), with a preferential
inhibition of IMP DH Il.
• IMPDH normally transforms inosine monophosphate (IMP) to xanthine monophosphate
(XMP), a metabolite contributing to the production of guanosine triphosphate (GTP).

10. PHARMACOLOGY NOTES
RAMDAS BHAT
SRINIVAS COLLEGE OF PHARMACY 10
• GTP is an important molecule for the synthesis of ribonucleic acid (RNA), deoxyribonucleic
acid (DNA), and protein.
• As a result of the above cascade of effects, mycophenolate mofetil reduces de-novo
production of guanosine nucleotides, interfering with the synthesis of DNA, RNA, and
protein required for immune cell production.
INDICATIONS: Organic transplant to prevent rejection.
DOSAGE: Adult: 1 gm 12 hourly initial dose be given 3 days prior to transplantation of renal
transplant patients.
CONTRAINDICATIONS: Hypersensitivity; pregnancy, lactation.
SIDE EFFECTS: Insomnia, headache, tremor, haematuria, hypophosphatemia, edema,
respiratory difficulty (Dyspnoea), bronchitis, rash, leukopenia.
PHARMACOKINETICS: Available as 250 mg capsule, 500 mg tablets. It rapidly absorbed and
excreted in urine faeces.
DRUG INTERACTIONS: Increased effect of acyclovir, ganciclovir, decreased action of
mycophenolate by antacids.
m-TOR INHIBITORS: (Eg: SIROLIMUS, EVEROLIMUS)
SIROLIMUS (RAPAMYCIN)
• Newer and more potent immunosuppressant drug.
• They are macrolide antibiotic same as that of the Tacrolimus.
MOA:
• They will inhibit IL-2 mediated immune response.
• They block the m-TOR (mammalian target of rapamycin)
• They bind to intracellular protein of T-cell called as FKBP12 and this complex binds to m-
TOR kinase that helps in the release of IL2.
• Release of IL-2 is prevented.
• IL-2 binding to its receptor are prevented as a result the further mechanism of t cell
proliferation is blocked.
ADVERSE EFFECTS
• Thrombocytopenia, hyperlipidaemia, rash lacks direct end organ toxicity but increased
incidence impaired renal function when combined with cyclosporine.
CYTOKINE INHIBITOR:
TNF INHIBITORS (DISEASE MODIFIERS TO TREAT RHEUMATOID ARTHRITIS)
• Etanercept: Recombinant version of TNF receptor
• Infliximab: Chimeric human/murine anti-TNF monoclonal antibody.

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• Anakinra: Human IL-1 receptor antagonist, Disease modifier agent for Rheumatoid
arthritis
ANTIBODIES:
• These are sometimes used as a quick and potent immunosuppressive therapy to prevent
the acute rejection reactions
POLYCLONAL ANTIBODIES
1. Antilymphocyte globulins (ALG).
2. Antithymocyte globulins (ATG).
MONOCLONAL ANTIBODIES
• Rho (D) immunoglobulin: Basiliximab, Daclizumab
ANTIBODIES PREPARATION
a) by immunization of either horses or rabbits with human lymphoid cells producing
mixtures of polyclonal antibodies directed against a number of lymphocyte antigens
(variable, less specific).
b) Hybridoma technology: produce antigen-specific, monoclonal antibody (homogenous,
specific). They are produced by fusing mouse antibody-producing cells with immortal,
malignant plasma cells. Hybrid cells are selected, cloned and selectivity of the clone can
be determined. Recombinant DNA technology can be used to replace part of the mouse
gene sequence with human genetic material (less antigenicity-longer half-life). Antibodies
from mouse contain Muro in their names. Humanized antibodies contain ZU (humanized)
or XI (chimeric) in their names.
ANTILYMPHOCYTE GLOBULINS (ALG) &ANTITHYMOCYTE GLOBULINS (ATG)
• Polyclonal antibodies obtained from plasma or serum of horses hyper-immunized with
human lymphocytes. Binds to the surface of circulating T lymphocytes, which are
phagocytosed in the liver and spleen giving lymphopenia and impaired T-cell responses &
cellular immunity.
KINETICS
• Given i.m. or slowly infused intravenously.
• Half-life extends from 3-9 days.
USES
• Combined with cyclosporine for bone marrow transplantation.
• To treat acute allograft rejection.
• Steroid-resistant rejection.
ADVERSE EFFECTS:
• Antigenicity.
• Anaphylactic and serum sickness reactions (Fever, Chills, Flu-like syndrome).
• Leukopenia, thrombocytopenia.
• Risk of viral infection.

12. PHARMACOLOGY NOTES
RAMDAS BHAT
SRINIVAS COLLEGE OF PHARMACY 12
MONOCLONAL ANTIBODIES
MUROMONAB-CD3
• Is a murine monoclonal antibody
• Prepared by hybridoma technology
• Directed against glycoprotein CD3 antigen of human T cells.
• Given I.V.
• Metabolized and excreted in the bile
MECHANISM OF ACTION
• The drug binds to CD3 proteins on T lymphocytes (antigen recognition site) leading to
transient activation and cytokine release followed by disruption of T-lymphocyte function,
decreased immune response.
• Block killing by cytotoxic T cells.
• Prednisolone, diphenhydramine is given to reduce cytokine release syndrome.
USES
• Used for treatment of acute renal allograft rejection & steroid-resistant acute allograft
• To deplete T cells from bone marrow donor prior to transplantation.
Adverse effects
• Anaphylactic reactions.
• Fever
• CNS effects (seizures)
• Infection
• Cytokine release syndrome (Flu-like illness to shock like reaction).
BASILIXIMAB AND DACLIZUMAB
• Obtained by replacing murine amino acid sequences with human ones.
• Basiliximab is a chimeric human-mouse IgG (25% murine, 75% human protein).
• Daclizumab is a humanized IgG (90% human protein).
• Have less antigenicity & longer half-lives than murine antibodies
MECHANISM OF ACTION
• IL-2 receptor antagonists
• Are Anti-CD25
• Bind to CD25 (α-subunit chain of IL-2 receptor on activated lymphocytes)
• Block IL-2 stimulated T cells replication & T-cell response system
• Basiliximab is more potent than Daclizumab.
• Given I.V.
• Half-life Basiliximab (7 days), Daclizumab (20 days) are well tolerated - only GIT disorders
USES
a) Given with CsA and corticosteroids for Prophylaxis of acute organ rejection in renal
transplantation.
IMMUNOSTIMULANTS:

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RAMDAS BHAT
SRINIVAS COLLEGE OF PHARMACY 13
Immunostimulant, also known as immunostimulatory, are substances (drugs and nutrients)
that stimulate the immune system by inducing activation or increasing activity of any of its
components. One notable example is the granulocyte macrophage colony-stimulant factor.
CLASSIFICATION:
a) Specific immunostimulants.
b) Non-specific immunostimulants.
a) Specific immunostimulants provide antigenic specificity in immune responses, such as
vaccine or any antigen.
b) Non-specific act irrespective of antigenic specificity to augment immune response of
other antigen or stimulate components of immune system without antigenic specificity,
such as adjuvant and non-specific immunostimulators.
TYPES OF IMMUNSTIMULANTS:
1. Bacterial vaccine.
2. Colony stimulating factors.
3. Interferons.
4. Interleukins.
5. Therapeutic vaccines.
6. Vaccine combinations.
7. Viral vaccines.
1. BACTERIAL VACCINES:
• Bacterial vaccines contain killed or attenuated bacteria that activate the immune system.
Antibodies are built against that particular bacterium, and prevents bacterial infection
later. An example of a bacterial vaccine is the Tuberculosis vaccine.
Use:
• BCG(TB) vaccine is used in many countries with a high prevalence of TB to prevent
childhood tuberculous meningitis and miliary disease.
Side effect of Tuberculosis vaccine:
Serious side effect of BCG(TB) vaccine, such as anaphylactic reaction (a serious allergic
reaction), are very rare.
2. COLONY STIMULATING FACTORS:
• Colony stimulating factors are glycoproteins that promote production of white blood cells
(mainly granulocytes such as neutrophils), in response to infection.
• An administration of exogenous colony stimulating factors stimulates the stem cells in the
bone marrow to produce more of the particular white blood cells.
• The new white blood cells migrate into the blood and fight the infection.

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RAMDAS BHAT
SRINIVAS COLLEGE OF PHARMACY 14
Use:
• Colony stimulating factors are used in patients who are undergoing cancer treatment that
causes low white blood cell counts (neutropenia) and puts the patient at risk of infections.
• Colony stimulating factors tend to reduce the time where patients are neutropenic.
3. INTERFERONS
Families:
Type I IFNs (IFN-α, β): induced by viral infections leukocyte produces IFN-α, Fibroblasts &
endothelial cells produce IFN-β
Type II IFN (IFN-γ):
Produced by Activated T lymphocytes
Interferon types and uses:
a) IFN- α: Hepatitis B & C infections
Treatment of cancer (malignant melanoma)
b) IFN-β: Multiple sclerosis
c) IFN- γ: treatment of chronic granulomatous diseases
Adverse effect:
• Including myelosuppression, hypertension, arrhythmias, alopecia, headache and
arthralgia.
• It can also cause neurotoxicity resulting in confusion, sedation and rarely seizures.
INTERLEUKINS:
Interleukins are a group of cytokines which are synthesized by lymphocytes, monocytes,
macrophages, and certain other cells. The function especially in regulation of the immune
system.
ex- Aldesleukin, Oprelvekin etc.
Use:
They are mainly used in treatment of cancer therapy.
VACCINE COMBINATION:
• Vaccine combinations merge antigens that prevent different diseases or that protect
against multiple strains of infectious agents causing the same disease, into a single
product.
• This reduces the number of injections required to prevent some diseases.
Use:
• Combination vaccines combined protection against two or more diseases into one shot.
• The measles, mumps and rubella vaccine (MMR) and diphtheria, tetanus and pertussis
vaccine(DTaP) each protect our child against three diseases & that means fewer delays in
disease protection for children.
Some example of common combination vaccines for children:

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RAMDAS BHAT
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• Comvax, which combines Hib and Hep B.
• Twnrix, which combines Hep A and Hep B.
• Pediarix, which combines DTaP, Hep B and IPV (polio).
• Kinrix, which combines DTaP and IPV (polio) Pentacel, which combines DTaP, IPV(polio)
and Hib.
Side effect s of Combination vaccine:
• Side effects from combination vaccines are usually mild.
• They are similar to those individual vaccines given separately.
• Sometimes combination vaccines are usually causing slightly more pain or swelling where
the shot was given.
• But the child got the shots individually, he or she might have pain or swelling in two or
three spots, instead of just one.
VIRAL VACCINE:
• Viral vaccines contains either inactivated virus or attenuated (alive but not capable of
causing disease) viruses.
• Inactivated or killed viral vaccines contain viruses, which have lost their ability to
replicated and in order for it to bring about a response it contains more antigen than live
vaccines.
• Attenuated or live vaccines contain the live from of the virus. These viruses are not
pathogenic but are able to induce an immune response.
Side effect:
• Common side effect is-Blood in the urine or stool.
• Pneumonia.
• Inflammation of the stomach or intestines.

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RAMDAS BHAT
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Sl No Chapter
Name
Long Essay Short Essay Short
Answer
Total Marks Duration
allotted
4 Immunopha
rmacology
1 1 02 10 03hrs
LONG ESSAYS:
1. Define immunosuppressant. Classify them with appropriate examples and write the
pharmacology of any one immunosuppressant drug.
SHORT ESSAYS:
1. Define Immunosuppressants. Explain the pharmacology of cyclosporine.
2. Discuss the Pharmacology of Methotrexate.
3. Discuss the Pharmacology of Mycophenolate mofetil.
SHORT ANSWERS
1. Enlist four immunostimulants.
2. Write uses of immunostimulants.
3. What are Colony-Stimulating Factors? Write their specific use.
4. What are Interferons? Give examples.
5. Write indications for recombinant interferons.
6. What is Levamisole? Write its uses.
7. Outline mechanism of action of Cyclosporin.
8. Mention calcineurin inhibitors. Write their uses.
9. What are cytotoxic agents? Write their significance in immunology.
10. Write briefly on immunosuppressant actions of Glucocorticoids.
11. Write uses of Glucocorticoids as immunosuppressants.
12. Write uses of Tacrolimus.
13. Mention immunosuppressant monoclonal antibodies.
14. Enlist cytokine inhibitors.
15. How does cyclophosphamide produce immunosuppression?
16. Define immunostimulant and immunosuppressant with two examples.
17. What is Thymosin? Mention its therapeutic uses.
18. What are mTOR inhibitors? Give examples.
19. What are TNF – α inhibitors? Give examples.
20. What are Interleukins? Mention their inhibitors.