Immunology : Semester 3 : PYQs
Credit 1: Cell surface molecules and receptors
2 mark
a) What are Toll like receptors?
a) Describe the role of Toll like receptors in innate immunity.
c) What is the role of pathogen recognition receptors?
a) What are defensins?
a) What are primary cell cultures and cell lines?
a) Explain the general properties of cytokines giving examples.
b) Explain the T cell accessory membrane molecules and its role in immune
activation.
5/7 mark
c) Regulation of classical pathway of complement activation.
b) Diagrammatically explain regulation of classical complement pathway.
b) Regulation of classical pathway of complement activation.
c) Explain the role of Antigen and Antigen - Antibody complexes in the
regulation of immune response.
a) Describe IL-2 pathway of signal tansduction. [7]
a) Explain IL-2 pathway - JAK/STAT of signal transduction. [7]
a) Explain JAK / STAT pathway for intracellular signaling.
c) Describe JAK / STAT signal transduction pathway.
b) Justify-TCR-CD3 complex is required for activation mechanism. [5]
b) Describe structure and function of TCR - CD3 complex. [5]
a) RAS/MAP kinase pathway.
c) Structure and functions of B cell receptor.
a) Describe structure and function of B cell receptor. [7]
a) Explain the structure of B-cell receptor.
a) Explain the role of B- cell reptors in immune activation.
a) Explain the structure & Function of toll like receptors.
b) Describe the role of Tyrosine kinase linked receptors.
c) Describe the role of cytokine receptors.
a) Explain the role of B cell receptor in immune activation.
b) Explain the structure of Toll-like receptors.
c) Explain cytokine receptor families.
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Credit 2: Regulation of Immune response
2 mark
d) What is negative selection?
b) What is the significance of negative selection?
b) What is sthe role of PAMPs in innate immune response.
5/7 mark
a) Explain Network theory of antigen antibody complex formation. [7]
b) How biological response modifiers can be used for cancer therapy. [5]
c) Explain the network theory for regulation of humoral immune response.
Explain the regulation of alternative pathway of complement system.
a) Justify, “There exists T cells which have role in immune regulation”.
b) Explain the functional evolution of immunoglobulins.
c) Explain the host immune responses to tumour.
b) Compare regulation of classical & alternative complement pathway.
Explain the mechanisms of tolerance induction.
a) Explain role of adhesion molecules in immune activation.
b) Explain cytokine mediated cross regulation of TH subsets.
a) Describe the symptoms of complement deficiencies.
Diagramatically describe T-cell mediated supression of immune response.
b) Explain the role of idiotypic network in immune regulation.
c) Describe the regulation of classical complement pathway.
c) How are T cell deficiency disorders treated?
Diagrammatically represent regulation of alternative complement pathway.
Immunological assay of cytokines.
a) Antigen antibody reaction kinetics.
d) Diagnosis of complement deficiencies.
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Credit 3: Experimental Immunology
2 mark
e) Write principle of Elispot assay.
d) What are knockout mice?
c) What is SCID mice?
5/7 mark
a) Explain the mechanisms of tolerance induction by giving experimental evidences.
b) Describe Idiotypic network theory and its experimental evidence.
b) Explain the methods used for funcitonal assay of macrophages. [5]
c) Describe functional assays for phagocytes.
a) How animal models are used in the study of atoimmunity and AIDS. [7]
c) Describe the use of animal models in studying AIDS.
b) Explain cytokine mediated cross regulation of T cells. [5]
b) Comment on T cell Mediated Supression of immune response. [5]
c) Explain the role of Antigen in regulation of immune response.
c) Draw the diagram of ELISPOT assay for quantification of cytokines
b) Describe Elispot assay. Give its applications. [5]
b) Describe ELISPOT assay and give its application.
Q5) Myasthenia Gravis (MG) and animal model of Experimental Autoimmune
Myasthenia Gravis (EAMG) is the most common autoimmune disorder of
neuromuscular transmission. The disease is caused by the breakdown of the
acetylcholine receptor (AChR) which is largely due to complement activation
at the NeuroMuscular Junction (NMJ). It is known that Complement Receptor
1 - Related gene/protein Y deficiency (Crry –/–) modulates the adaptive immune
response and EAMG outcome.
A study was carried to determine whether Crry –/– mice have impairment in
membrane -related inhibition of complement activation and show failure in
controlling complement homeostasis. EAMG was induced by four
subcutaneous injections of 20μg AChR emulsified in complete Freund’s
adjuvant (CFA). Mice were immunized along the back subcutaneously, at the
base of the tail and boosted twice with 20μg of tAChR in incomplete Freund’s
adjuvant 4 and 8 weeks after primary immunization. Control mock immunized
mice received an equal volume of PBS in CFA or IFA.
Q5) Spleen cells or LAK cells, in the presence or absence of recombinant IL-2,
were infused into mice with pulmonary sarcoma. The animals were evaluated
13 days later for the number of pulmonary sarcoma metastases. The LAK
cells were prepared by isolating lymphocytes from tumor-bearing animals and
incubating them in vitro with high concentrations of IL-2. The results are
expressed in the graph below :
Based on the data given, answer the following :
a) Explain in brief, LAK cells and Sarcoma. [4]
b) Diagrammatically illustrate the role of IL-2 in activation of immune
response. [4]
c) Discuss the outcome of the experiment. [4]
d) Comment on the possible extrapolation of this study for developing
immunotherapy for cancer.
c) Explain the use of knock-out mice in immunological research.
b) How does the host immune system respond to HIV infections.
c) ELISPOT assay.
Explain Jerne’s network theory for regulation of immune response system.
Use of animals models in research on autoimmune diseases.
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Credit 4: Tumor Immunology
2 mark
f) What is Hodgkin’s disease?
f) What is Hodgkin’s disease?
e) Define lymphoma and give its types.
5/7 mark
a) Describe escape mechanisms of tumors from host defense.
a) What are transgenic animals? How they are used in immunological research?
a) What are transgenic animals? Give their significance in experimental immunology
a) Discuss mechanisms of induction of immunological tolerance using transgenic animals.
a) Comment on the escape mechanisms of tumour from host defense system.
b) What are the methods used for diagnosis of tumours. [5]
b) Tumour markers. Short note.
b) Describe different types of tumours of lymphoid system. [5]
b) Discuss the role of intracellular signalling proteins in immune activation mechanisms.
b) Describe the role of adhesion molecules in immune activation.
a) Explain immunosurveillance theory. [7]
a) Cancer therapy. Short note.
b) Differentiate between tumor specific antigens and tumor associated antigens.
c) Describe tumor vaccine therapy with examples.
b) Animal models in HIV research.
a) Explain tumour markers and its use in diagnosis of tumours.
b) Explain phagocytic deficiencies and its diagnosis.
c) Explain the pathophysiology and diagnosis of Myasthenia gravis.
b) Explain the mechanisms of symptoms development in Myasthenia gravis.
Describe the characteristic features of benign and malignant tumours.
a) Explain immunotherapeutic approaches to Mycobacterium tuberculosis
infections.
What is the difference between benign and malignant tumours?
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a) Describe the pathophysiology in Salmonella infections.
c) Describe the immunotherapeutic approaches to bacterial infections.
c) Describe immunotherapeutic approaches to systemic Lupus Erythomatosus (SLE).
a) What are complement deficiencies and how are they diagnosed?
a) Describe the evolution of cellular immune defenses in invertebrates.
b) Explain the complexity of immune cells in different species of vertebrates.
c) Describe the diversity of humoral immunity components in different species of vertebrates.
a) Justify, “Clonal deletion is one of the mechanisms of establishing tolerance”.
b) Explain how the complement system is regulated after the assembly of different convertases has taken place.
Q2): a) Justify, “Immunoglobulin isotypes evolved from IgM, since it has many structural and functional limitations”.
b) Giving suitable examples, comment on - “Therapeutic applications of cytokines has many drawbacks”.
Q3): a) Describe immunological characteristics of different etiological classes of tumors.
b) Justify “Tumor specific antigens can be targeted for developing immunotherapy of cancer”.
c) Explain the host immune mechanisms against intracellular bacterial pathogens.
Q4) Write short notes on any four of the following : [16]
e) IL - 1 and pyrogenesis.
Q1) Attempt any two the following : [16]
Q2) Attempt any two the following : [16]
Q3) Attempt any two of the following. [16]
Q4) Write short notes on anyfour of the following : [16]
a) Role of IL - 1 in pyrogenesis.
b) Tumour vaccine therapy.
c) Tumour Necrosis factor.
d) ELISPOT assay.
e) Animal models for AIDS.
Q5) Asthma is a chronic inflammatory airway disease currently afflicting millions
of people worldwide. It is characterized by airway hyper responsiveness (AHR),
inflammation and remodeling, that are associated with reversible airflow
obstructions. Allergic asthma is the major phenotype of asthma.It is
characterized by Th2 -type inflammation, allergenspecific IgE induction and
mast cell involvement. Interleukin 33 (IL-33) represents one of the potential
signals from the epithelial cells that trigger the development of asthma.
This study investigated the potential of IL-33 to exacerbate antigen driven
asthma responses. An ovalbumin (OVA) asthma model was used in which
sensitized C57BL/6 mice were exposed to IL-33 before each OVA challenge.
Total inflammatory cells in BALF (Bronchoalveolar lavage fluid) were counted
after injecting the C57BL/6 mice with PBS, IL-33, OVA, and OVA + IL-33.
Fig 1 : Total inflammatory cells in BALF (Bronchoalveolar lavage fluid) were
counted.*p <0.05,**p < 0.01,***p < 0.001 (ANOVA, Bonferroni) Results
are pooled data from four independent experiments (mean +/-SEM of
n = 9-10 mice for each group).
a) According to the present study does IL -33 have a role in inducing airway
inflammation ? [8]
b) Explain the pathophysiology, diagnosis and prognosis of Asthma [8].
Q1) Attempt any two of the following : [10]
Q2) Attempt any two of the following : [10]
a)
Q3) Attempt any two of the following : [10]
a) Describe different factors affecting animal cell culture techniques.
b) Describe functional assays for phagocytes.
c) Explain the use of experimental animals in immunology research.
Q4) Attempt any two of the following : [10]
Q5) Attempt any two of the following : [10]
a) Explain host immune responses in tumors.
b) What are immune adjuvant’s & explain its role in cancer immunotherapy.
c) Enlist different tumors of lymphoid system. Describe Hodgkin’s disease.
Q6) Attempt any two of the following : [10]
a) Explain the pathophysiology in Leishmania.
b) Describe host immune response to Mycobacterium tuberculosis.
c) Describe the differences in immunotherapeutic approaches of bacterial,
viral & parasitic infections.
Q7) Attempt any two of the following : [10]
a) Describe the diagnosis & therapeutic approaches of humoral deficiencies.
b) Describe Systemic Lypus Erythomatosus (SLE) as autoimmune disorder.
c) What are the therapeutic approaches to humoral & T - cell deficiencies.
Q8) Attempt any two of the following : [10]
a) Compare the anatomical organisation of immune system in invertebrates
& vertebrates.
b) Explain the evolution of immunoglobulins.
c) Describe the strategies of survival of living form with respect to immune
system evolution.
Q1) Attempt any two of the following:
[Max. Marks : 80
[16]
a)
Giving the sources and types of interferons, explain its’ role in immune
response activation.
b)
Justify, “Spatial control is not the only mechanism involved in regulation
of complement pathways”.
c)
Describe the types and functions of T cell receptors.
Q2) Attempt any two of the following:
[16]
a)
b)
Justify, “All vertebrate species evolved with both functional arms of
immune system”.
c)
Q3) Attempt any two of the following:
a)
[16]
Describe the properties and applications of tumor specific and tumor
associated antigens.
P.T.O.
b)
c)
Give the similarities and differences in benign tumors and malignant
cancers, with suitable examples.
Explain the pathophysiology of systemic lupus erythomatosus.
Q4) Write short notes on any four of the following:
a) Functional assays for phagocytic function.
b) Animal models used for research in autoimmunity.
c) Determination of antibody affinity by equilibrium dialysis.
d) Stem cell therapy.
e)
[16]
Prognosis of asthma.
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2
Complement deposition was at NMJ was assessed by staining diaphragms
from wild type (WT) EAMG and Crry –/– EAMG mice for C3, C3 fragments
(C3b/iC3b) and C5b-9 (MAC). The results are expressed as percentage of
NMJ (%) with detected complement deposits. Minimum three sections with
10-15 NMJs from each diaphragm were quantified (n = 5 mouse per
experimental group ).
Based on the given data explain the following:
a)
b)
c)
Whether there is any significant quantitative difference in deposition of
C3, C3b/iC3b fragments and C5b-9 (MAC) at the NMJ of WT EAMG
and Crry –/– EAMG mice?
[4]
Whether Crry –/– mice have deficiency in membrane-related inhibition
of complement activation and thus show failure in regulating self
complement mediated cytotoxicity.
[4]
How the self cells are protected from complement mediated cytotoxicity?[8]
Q1) Attempt any two of the following:
[10]
Q2) Attempt any two of the following:
[10]
a) With the help of diagram explain T cell mediated suppression of immune
response.
b) Explain regulation of alternative complement pathway.
c) Explain the role of Antigen-antibody complexes in regulation of immune
response.
Q3) Attempt any two of the following:
a) Explain functional assays for phagocytes.
b) Which are different factors affecting cells in culture.
[5127]-301
2
[10]
P.T.O.
Q4) Attempt any two of the following:
c) Explain anchorage dependent cell culture technique.
[10]
Q5) Attempt any two of the following:
a) Explain escape mechanisms of tumours from host defence.
b) Explain the use of immune adjuvants in immunotherapy.
c) Explain how tumour markers can be used in diagnosis.
[10]
Q6) Attempt any two of the following:
[10]
c) Explain the pathophysiology in Leishmaniasis.
Q7) Attempt any two of the following:
[10]
Q8) Attempt any two of the following:
[10]
a) Describe evolution of cellular defence mechanisms in invertebrate species.
b) Explain the evolution of humoral defence mechanisms in the different
species of vertebrates.
c) Explain the evolution of immunoglobulins.
Q1) Attempt any two of the following:
[16]
a)
Explain role of cytokines in regulating the humoral and cell mediate
immune responses.
b)
Justify, “Self RBCs are protected from complement mediated lysis”.
c)
Explain role of CD3-TCR complex in activation of T cells.
Q2) Attempt any two of the following:
[16]
a)
b)
Justify, “All immunoglobulin molecules evolved from a common
primordial gene”.
c)
Explain the cytological transformations that occur in normal cell, which
may lead to neoplastic growth.
[5127] - 31
1
P.T.O.
Q3) Attempt any two of the following:
[16]
a)
Discuss use of different possible / experimental tumor vaccines, giving
examples.
b)
Explain the protective immune mechanisms in infections with intracellular
pathogens.
c)
Discuss diagnosis and prognosis of systemic lupus erythomatosus.
Q4) Write short notes on any four of the following:
a)
Septic shock syndrome.
b)
Pathophysiology of Herpes infections.
c)
Hemolytic plaque assay.
d)
e)
[16]
Q5) Interleukin-22 (IL-22), recently identified as a crucial parameter of pathology
in experimental liver damage, may determine survival in clinical end-stage liver
disease. Liver cirrhosis, the end-stage of various liver diseases, has a poor
prognosis. In the cirrhotic liver, IL-22 may be secreted to protect residual
healthy liver tissue. Assuming that IL-22 possesses hepatoprotective properties
in end-stage liver disease, IL-22 may be a relevant factor for prognosis of
liver cirrhosis.
[16]
In a prospective cohort study including 120 liver cirrhosis patients and 40
healthy donors were analyzed for systematic levels of IL-22 in relation to
survival and hepatic complications. A total of 71% of patients displayed liver
cirrhosis-related complications at study inclusion. A total of 23% of the patients
died during a mean follow-up of 196 ± 165 days. Elevated levels of IL-22
were associated with ascites (P = 0.006), hepatorenal syndrome (P < 0.0001),
and spontaneous bacterial peritonitis (P = 0.001).
Patients with elevated IL-22 (> 18 pg/ml, n = 57) showed significantly reduced
survival compared to patients with regular (< 18 pg/ml) levels of IL-22 (321
days versus 526 days, P = 0.003).
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2
IL-22 serum concentrations are elevated in patients with liver cirrhosis
(n = 120) compared with healthy individuals (n = 40). Dots indicate IL-22
serum levels in individual patients. The straight horizontal line indicates the
mean.
The dotted horizontal line indicates the upper limit of normal for IL-22 of 18
pg/ml. Error bars indicates the standard deviation. Comparison between the
two groups was performed using the Mann Whitney U-test.
a)
Explain use of conventional biochemical tumor markers in diagnosis of
cancer.
b)
Based on the given information and the data, discuss possible use of
IL-22 in prognosis of different liver diseases, finally culminating in liver
cirrhosis
Q1) Attempt any two of the following:
[10]
a)
Explain the role of TCR - CD3 complex in immune activation.
b)
Explain JAK/STAT signal transduction pathway.
c)
Explain the role of Toll - like receptors in the immune system.
Q2) Attempt any two of the following:
[10]
a)
Explain mechanisms of tolerance induction by giving experimental
evidences.
b)
Explain cytokine mediated cross regulation of TH subsets.
c)
Explain the role of Biological response modifiers in immune therapy.
[5227] - 301
1
P.T.O.
Q3) Attempt any two of the following:
[10]
a)
What are functional assays for cytokines? Explain any two functional
assays for cytokines.
b)
What are primary cell cultures and cell lines?
c)
Explain the use of transgenic animals in immunological research.
Q4) Attempt any two of the following:
[10]
a)
Explain the structure of B cell receptor.
b)
Explain regulation of alternative complement pathway.
c)
Explain functional assays for phagocytes.
Q5) Attempt any two of the following:
[10]
a)
Explain Immuno - surveillance theory.
b)
Explain tumour vaccine therapy with examples.
c)
Q6) Attempt any two of the following:
[10]
a)
Explain immunotherapeutic approaches to Salmonella infections.
b)
How does the host immune system respond to Mycobacterium
tuberculosis infections?
c)
Explain the pathophysiology in Herpes simplex infections.
[5227] - 301
2
Q7) Attempt any two of the following:
[10]
a)
Describe the symptoms of humoral deficiencies.
b)
Explain the mechanisms of symptoms development in Systemic Lupus
erythomatosus.
c)
Explain the immunotherapeutic approaches for Myasthenia gravis.
Q8) Attempt any two of the following:
[10]
a)
Explain the function of immune system components in invertebrates.
b)
Explain how phagocytosis functions evolved in invertebrate species.
c)
Describe the diversity of humoral immunity components in the different
species of vertebrates.
Q1) Attempt any two of the following :
[16]
a)
Explain the role of IL - 1 in immune activation and pyrogenesis.
b)
With the help of suitable diagram explain the role of Super antigen in
pathogenesis.
c)
Explain the mechanisms of tolerance induction.
Q2) Attempt any two of the following :
[16]
a)
Explain the Idiotype network theory and its role in immune regulation.
b)
Explain the escape mechanisms of tumours from host defence.
c)
[5227] - 31
1
P.T.O.
Q3) Attempt any two of the following :
[16]
a)
Explain role of Biological response modifiers in cancer therapy.
b)
Explain complement deficiencies and its diagnosis.
c)
Explain the animal models for AIDS.
Q4) Write short notes on any four of the following :
a)
Septic shock syndrome.
b)
Tumour vaccine therapy.
c)
Stem cell therapy.
d)
T cell deficiencies.
e)
Myasthenia Gravis.
[16]
Q5) Breast cancer is the most frequently occurring cancer in women. It is essential
to identify reliable prognostic factors to guide decision making during the
treatment of breast cancer in order to improve prognosis. In breast cancer,
carcinoembryonic antigen (CEA) and cancer antigen 15 - 3 (CA15 - 3) are the
two most widely used serum tumour markers in the clinical fields. The present
study aims to investigate the prognostic value of preoperative serum CEA and
CA 15 - 3 levels in breast cancer patients. Serum CEA and CA 15 - 3 in a total
of 432 patients who were treated for stage I - III invasive breast cancer at the
Affiliated Cancer Hospital of Zhengzhou University were investigated.
Disease - free survival (DFS) was defined to be from the time of surgery to the
local regional recurrence, distant metastasis, and death before recurrence. Serum
CEA and CA 15 - 3 levels were determined using an automatic electrochemistry
luminescence immunoassay system. The results are as follows:
[5227] - 31
2
Fig 1: Kaplan - Meier survival curves of patients with normal or elevated CEA
and CA15 - 3 levels. Disease-free survival (DFS) according to carcinoembryonic
antigen (CEA) (A) and cancer antigen 15 - 3 (CA15 - 3) (B)
a)
Explain whether Serum CEA and CA 15 - 3 concentration levels can be
used as tumour markers in breast cancer.
[8]
b)
Which are the different tumour markers used in diagnosis of various
tumours?
Q1) Attempt any two of the following:
[16]
a)
Explain the types of interferons and give its role in immune activation.
b)
Explain the structure of TCR-CD3 complex and its role in activation of
T cells.
c)
Explain T cell mediated suppression of immune response.
Q2) Attempt any two of the following:
[16]
a)
Explain the regulation of classical complement pathway.
b)
Explain the evolution of cellular immune responses in invertebrate species.
c)
Explain the cellular transformations during neoplastic growth.
Q3) Attempt any two of the following:
[16]
a)
Explain immune adjuvants and tumour vaccine therapy.
b)
Explain humoral and T cell deficiencies.
c)
Explain experimental animals used in immunological research.
[5327] - 31
1
P.T.O.
Q4) Write short notes on any four of the following:
a)
Super antigens.
b)
Biological response modifiers.
c)
Complement deficiencies.
d)
Hemolytic plaque assay.
e)
Systemic Lupus Erythomatosus (SLE).
[16]
Q5) Globally, colorectal cancer (CRC) is the third most common cancer diagnosed,
and is associated with high rates of incidence and mortality for both men and
women. Carcinoembryonic antigen (CEA) is a classic tumour marker for CRC,
and has been used to monitor CRC recurrence and as a prognostic factor for
CRC patients. However, the effectiveness of CEA as a preoperative and
postoperative marker for CRC remains to be evaluated. This study consisted
of 413 patients that were diagnosed with CRC who were enrolled in the
retrospective study. Serum levels of CEA were assayed prior to surgical
resection. Serum CEA levels in CRC patients were measured using CEA
Elecsys analyzers. One group was associated with elevated levels of serum
CEA (e.g., > 5 ng/mL) (n=153; 37.0%), While the second group was associated
with normal levels of serum CEA (e.g., <5 ng/mL) (n=260; 63%). The disease
free survival rates were studied.
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Fig 1: Disease-free survival curves for patients with stage II A colorectal cancer (A)
and stage III B colorectal cancer (B) based on preoperative serum levels of
carcinoembryonic antigen. (t/mo : time/months)
a)
According to the present study does elevated preoperative serum CEA
levels have effect on disease-free survival rates?
[8]
b)
Explain with examples how tumour markers can be used in prognosis
and treatment of cancers.
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