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Immuo Answers
Immuo Answers
Immuo Answers
Direct oncogenic activity: Some viruses, such as human papillomavirus (HPV) and Epstein-Barr
virus (EBV), have direct oncogenic activity that can lead to the transformation of infected cells into
cancer cells. These viruses induce the expression of viral oncogenes, such as E6 and E7 in the case of
HPV, which can activate cellular oncogenic pathways and promote tumor growth. The viral
oncogenes can also induce the expression of tumor antigens, such as HPV E6 and E7 antigens, which
can be recognized by the immune system.
Indirect oncogenic activity: Other viruses, such as hepatitis B virus (HBV) and hepatitis C virus
(HCV), have indirect oncogenic activity that can contribute to the development of cancer. These
viruses can cause chronic inflammation and damage to the liver, which can lead to the accumulation
of genetic mutations and the development of liver cancer. The chronic inflammation and damage can
also induce the expression of tumor antigens, which can be recognized by the immune system.
Insertional mutagenesis: Some viruses, such as retroviruses, can integrate their DNA into the host
cell genome and cause insertional mutagenesis. This process can disrupt the expression of cellular
genes and lead to the expression of abnormal proteins, some of which may be recognized by the
immune system as tumor antigens.
Overall, viruses can induce the expression of tumor antigens through various mechanisms, including
direct and indirect oncogenic activity and insertional mutagenesis. Understanding these mechanisms
is important for developing strategies to prevent virus-induced cancers and for developing cancer
immunotherapies that target viral tumor antigens.
Recognition: Immune cells in the recipient's body, such as T cells and B cells, recognize the
transplanted tissue or organ as foreign. This recognition occurs through the recognition of foreign
antigens on the surface of the transplanted cells, which are different from the recipient's own antigens.
Activation: Once the immune cells recognize the foreign antigens, they become activated and begin to
multiply, leading to an increased immune response against the transplanted tissue or organ.
Effector phase: The activated immune cells migrate to the transplanted tissue or organ and attack it. T
cells can directly attack and kill the transplanted cells, while B cells can produce antibodies that target
the transplanted tissue or organ.
Inflammation: The immune response against the transplanted tissue or organ can also lead to
inflammation, which can damage the tissue and impair its function.
Recognition Phase: During the recognition phase, the immune system of the recipient recognizes the
transplanted tissue as foreign. The major histocompatibility complex (MHC) molecules play a critical
role in this process. MHC molecules present peptides derived from foreign proteins to T cells, which
recognize and respond to these foreign peptides. MHC molecules are highly polymorphic, and
individuals differ in their MHC alleles. Therefore, the MHC compatibility between the donor and
recipient is critical for successful transplantation.
Activation Phase: If the transplanted tissue is recognized as foreign, the recipient's immune system
becomes activated. T cells are key players in this process. CD4+ T cells recognize foreign peptides
presented by MHC class II molecules, while CD8+ T cells recognize foreign peptides presented by
MHC class I molecules. Once activated, T cells undergo clonal expansion and differentiate into
effector T cells, which can migrate to the transplanted tissue and cause damage.
Effector Phase: During the effector phase, the activated T cells migrate to the transplanted tissue and
cause damage. CD4+ T cells can help activate other immune cells, such as B cells and macrophages,
which also contribute to graft rejection. CD8+ T cells can directly kill the transplanted cells, leading
to tissue damage and graft rejection.
Infectious Disease: Infectious disease can also influence transplantation. Donors and recipients can
be screened for infectious diseases, such as hepatitis B and C, HIV, and cytomegalovirus, to reduce
the risk of transmission.
Q 12 -Difference between HVGR and GVHR.
The host versus graft reaction (HVGR) and graft-versus-host reaction (GVHR) are two types of immune responses that can occur
following transplantation.
The HVGR occurs when the recipient's immune system recognizes the transplanted tissue as foreign and mounts an immune
response against it. This can lead to graft rejection, as the recipient's immune cells attack and destroy the transplanted tissue.
HVGR can occur in any type of transplantation, but it is most commonly observed in solid organ transplantation.
In contrast, GVHR occurs when the transplanted tissue contains immune cells, such as bone marrow or stem cells, that recognize
the recipient's tissues as foreign and mount an immune response against them. This can lead to a systemic immune response,
as the transplanted immune cells attack the recipient's tissues throughout the body. GVHR is most commonly observed in bone
marrow transplantation, where the transplanted bone marrow contains immune cells that can recognize the recipient's tissues
as foreign.
1. Mechanism of immune response: In HVGR, the recipient's immune system attacks the transplanted tissue. In GVHR,
the transplanted immune cells attack the recipient's tissues.
2. Types of transplantation: HVGR can occur in any type of transplantation, but it is most commonly observed in solid
organ transplantation. GVHR is most commonly observed in bone marrow transplantation.
3. Timing of immune response: HVGR typically occurs within the first few weeks following transplantation. GVHR can
occur within the first few weeks, but it can also occur several months or even years after transplantation.
4. Severity of immune response: HVGR can range from mild rejection to severe rejection, depending on the extent of the
immune response. GVHR can be life-threatening, as the systemic immune response can cause damage to multiple
organs.
Q 13 - Explain the role of cytokine therapy for the augmentation of Immune responses to
tumors.?
Ans - Cytokine therapy is a type of cancer immunotherapy that involves the use of cytokines to stimulate the immune
system to attack cancer cells. Cytokines are small proteins that act as signaling molecules in the immune system, and they
play a crucial role in regulating immune responses to tumors. The two main types of cytokines used in cancer
immunotherapy are interleukins and interferons.
Interleukins are cytokines that promote the growth and activation of immune cells, such as T cells and natural killer cells.
Interleukin-2 (IL-2) is the most commonly used cytokine in cancer immunotherapy, and it has been shown to stimulate the
proliferation and activation of T cells and natural killer cells. IL-2 therapy has been used to treat metastatic melanoma and
renal cell carcinoma, and it has been shown to induce complete or partial responses in a subset of patients.
Interferons are cytokines that have both antiviral and antitumor properties. Interferon-alpha (IFN-alpha) has been used to
treat several types of cancer, including melanoma, renal cell carcinoma, and leukemia. IFN-alpha can enhance the activity of
T cells, natural killer cells, and dendritic cells, and it can also induce cancer cell death direct.
Malignant and benign tumors are two types of growths that can develop in various tissues of the
body. The main differences between them lie in their potential for spreading and invading surrounding
tissues
Malignant tumors:
Malignant tumors are cancerous growths that can invade nearby tissues and spread to other parts of the body
through the bloodstream or lymphatic system.
They are made up of abnormal cells that do not function properly and can divide uncontrollably.
They can be life-threatening if not detected and treated early.
Examples of malignant tumors include lung cancer, breast cancer, leukemia, and melanoma.
Benign tumors:
Benign tumors are non-cancerous growths that typically grow slowly and do not spread to other parts
of the body.
They are made up of normal cells that have grown abnormally and may not function as they should.
They are usually not life-threatening but can cause complications if they grow too large or press
against vital structures.
Examples of benign tumors include moles, lipomas, and uterine fibroids.
Ans - Immunosuppressive agents are drugs that are used to prevent or reduce the rejection of transplanted
organs or tissues by the recipient's immune system. There are several types of immunosuppressive agents that
are used in transplantation, including
1. Calcineurin inhibitors: These drugs, such as cyclosporine and tacrolimus, inhibit the activity of the enzyme
calcineurin, which is involved in T cell activation. By inhibiting calcineurin, these drugs reduce the activity
of T cells and other immune cells that could attack the transplanted organ. They are commonly used in the
early stages after transplantation.
2. Antimetabolites: These drugs, such as azathioprine and mycophenolate mofetil, block the production of
DNA and RNA, which inhibits the division of rapidly dividing cells such as T and B cells. This results in
reduced immune activity and helps prevent the rejection of the transplanted organ.
3. Corticosteroids: These drugs, such as prednisone and methylprednisolone, have broad anti-inflammatory
and immunosuppressive effects. They are used to prevent and treat rejection and are typically used in
combination with other immunosuppressive agents.
4. mTOR inhibitors: These drugs, such as sirolimus and everolimus, target a protein called the mammalian
target of rapamycin (mTOR), which plays a role in T cell activation and proliferation. By inhibiting mTOR,
these drugs reduce the activity of T cells and other immune cells that could attack the transplanted organ.
5. Antibodies: These drugs, such as anti-thymocyte globulin and alemtuzumab, target specific immune cells
and deplete them from the body, reducing the overall immune response. This can help prevent rejection of
the transplanted organ.
Q 24- Analyze the various possible factors contributing to autoimmunity in detail.
Autoimmunity is a condition in which the immune system attacks the body's own tissues, mistaking them for foreign
invaders. There are several factors that contribute to the development of autoimmunity, including:
1.Genetic factors: Certain genes can increase the risk of developing autoimmune diseases. For example, certain human
leukocyte antigen (HLA) genes are associated with increased risk of developing autoimmune diseases such as rheumatoid
arthritis and type 1 diabetes.
2. Environmental factors: Exposure to certain environmental triggers such as infections, drugs, and chemicals can trigger
autoimmunity in genetically susceptible individuals. For example, viral infections such as Epstein-Barr virus and
cytomegalovirus have been linked to the development of autoimmune diseases such as multiple sclerosis and lupus.
3.Hormonal factors: Hormones such as estrogen and testosterone have been implicated in the development of
autoimmune diseases. For example, women are more likely to develop autoimmune diseases than men, and the risk of
developing autoimmune diseases increases after menopause when estrogen levels decline.
4.Immunological factors: Dysregulation of the immune system can contribute to the development of autoimmunity. For
example, defects in regulatory T cells, which normally prevent the immune system from attacking the body's own tissues,
can lead to autoimmune diseases.
5. Epigenetic factors: Epigenetic modifications such as DNA methylation and histone modifications can influence gene
expression and contribute to the development of autoimmune diseases.
Q – 23 Identify how the oncogenic viruses cause tumor formation.
Oncogenic viruses are viruses that have the ability to transform normal cells into cancer cells. These viruses can cause tumor
formation by integrating their genetic material into the host cell's DNA and altering the cell's normal growth and
differentiation processes. Here are some examples of how different oncogenic viruses cause tumor formation:
Human papillomavirus (HPV): HPV is a DNA virus that can cause cervical cancer and other types of cancer, such as anal,
vaginal, and oropharyngeal cancer. HPV integrates its DNA into the host cell's genome, leading to the overexpression of the
E6 and E7 oncogenes. These oncogenes can inactivate tumor suppressor proteins, such as p53 and Rb, and promote cell
proliferation and survival.
Epstein-Barr virus (EBV): EBV is a DNA virus that can cause Burkitt's lymphoma, Hodgkin's lymphoma, and
nasopharyngeal carcinoma. EBV infects B cells and can transform them into immortalized lymphoblastoid cell lines. EBV-
encoded proteins, such as LMP1 and LMP2, can activate cellular signaling pathways and promote cell survival and
proliferation.
Hepatitis B virus (HBV) and Hepatitis C virus (HCV): HBV and HCV are RNA viruses that can cause liver cancer. These
viruses can cause chronic inflammation in the liver, which can lead to the accumulation of DNA damage and the
development of cancer. Additionally, HBV can integrate its DNA into the host cell's genome and promote cell proliferation
and survival.
Human T-lymphotropic virus type 1 (HTLV-1): HTLV-1 is an RNA virus that can cause adult T-cell leukemia/lymphoma
(ATL). HTLV-1 infects T cells and integrates its DNA into the host cell's genome. The viral Tax protein can activate cellular
signaling pathways and promote cell proliferation and survival.
Ans - Sometimes, when a person receives an organ transplant from someone else (an allograft), their
immune system may not attack and reject the transplanted organ without the use of drugs that
suppress the immune system. This is because their immune system may recognize the transplanted
tissue as belonging to their own body, rather than a foreign invader.
This recognition and acceptance of the transplanted tissue is called immunological tolerance. It can
occur due to various mechanisms such as the elimination of self-reactive T cells during development
or the suppression of immune responses by regulatory T cells in the periphery.
In some cases, exposure to the transplanted tissue through controlled use of immunosuppressive
drugs can also lead to tolerance by inducing the development of regulatory T cells. However, the exact
mechanisms of immunological tolerance are not fully understood and can vary from person to person.
1. Molecular mimicry: This occurs when a foreign antigen shares a similar structure with a self-antigen.
The immune system generates a response against the foreign antigen, but the antibodies or T cells can
cross-react with the self-antigen, leading to autoimmune reactions.
2.
Epitope spreading: This occurs when an immune response is generated against a specific antigen, but
as the immune response progresses, other self-antigens that were previously not recognized by the
immune system are exposed. This can lead to an autoimmune response against these self-antigens.
3. Loss of immune tolerance: Immune tolerance refers to the ability of the immune system to distinguish
self-antigens from foreign antigens and not generate an immune response against self-antigens. The
loss of immune tolerance can result from defects in immune regulatory cells, such as T regulatory cells,
or due to genetic factors. This can lead to autoimmune reactions against self-antigens.
4. Environmental factors: Environmental triggers, such as infections, toxins, drugs, or stress, can
activate the immune system and break immune tolerance, leading to autoimmune reactions.
5. Genetic factors: Autoimmune diseases often have a strong genetic component, and certain genes have
been associated with increased susceptibility to autoimmune diseases.
Tumor formation is a complex process that involves several stages. The stages of tumor
formation are as follows:
1.Initiation: This is the first stage of tumor formation, which involves a mutation in a cell's
DNA that results in the activation of oncogenes or the inactivation of tumor suppressor
genes. This mutation can be caused by various factors, including exposure to radiation,
chemicals, or viruses. Examples include exposure to tobacco smoke leading to the mutation
of the KRAS gene in lung cancer or exposure to UV radiation leading to the mutation of the
BRAF gene in skin cancer.
2. Promotion: In this stage, the mutated cells are stimulated to divide and grow by various
factors such as hormones, growth factors, and inflammation. This stage can last for many
years and can involve repeated exposure to promoting agents. Examples include the
promotion of liver cancer by chronic hepatitis B or C infection, or the promotion of colorectal
cancer by a diet high in red meat.
3.. Progression: In this stage, the tumor cells become increasingly aggressive and acquire
additional mutations that allow them to invade surrounding tissues and metastasize to other
parts of the body. This stage is characterized by a loss of cell differentiation and an increase
in genetic instability. Examples include the progression of breast cancer from a small,
localized tumor to a larger, invasive tumor that spreads to the lymph nodes and other
organs.
3. Metastasis: This is the final stage of tumor formation, in which tumor cells break away
from the primary tumor and travel through the bloodstream or lymphatic system to
establish secondary tumors in other parts of the body. Metastasis is responsible for most
cancer-related deaths and is difficult to treat once it has occurred. Examples include the
metastasis of lung cancer to the brain or the spread of melanoma to the liver.
Stage I: The cancer is localized to a small area and hasn't spread to lymph nodes or
other tissues
Stage III: The cancer has grown larger and has possibly spread to lymph nodes or
other tissues.
Stage IV: The cancer has spread to other organs or areas of your body
1.Sensitization phase: This phase occurs when the recipient's immune system is first exposed to the
donor tissue. The immune system identifies the donor tissue as foreign and initiates an immune
response. During this phase, antigen-presenting cells (APCs) such as dendritic cells or macrophages,
present donor antigens to T cells in the lymph nodes. This leads to the activation and proliferation of T
cells that recognize the donor antigens.
2.Activation phase: Once the T cells have been activated, they migrate to the site of the transplant
and infiltrate the tissue. Here, they encounter donor cells and attack them through various
mechanisms, such as cytotoxicity, cytokine release, and recruitment of other immune cells. In addition
to T cells, B cells may also be activated and produce antibodies against donor antigens. The
activation phase can be divided into two sub-phases: the induction phase and the amplification phase.
a. Induction phase: This is the initial stage of the activation phase, during which T cells are activated
and primed to attack the donor tissue.
b. Amplification phase: This is the stage during which the immune response is amplified and leads to
tissue damage and inflammation. The amplification phase is characterized by the recruitment of other
immune cells, such as macrophages and natural killer (NK) cells, which contribute to tissue damage.
3.Effector phase: During this phase, the activated T cells and other effector cells attack the donor
tissue and cause tissue damage. The effector phase is responsible for the clinical signs of graft
rejection, such as organ dysfunction and inflammation. The effector phase can be divided into two
sub-phases: the acute phase and the chronic phase.
a. Acute phase: This is the initial stage of graft rejection and occurs within the first few weeks after
transplantation. It is characterized by tissue damage and inflammation, which may lead to graft
dysfunction.
b. Chronic phase: This is a slower, more progressive form of rejection that can occur months or even
years after transplantation. It is characterized by fibrosis and scarring of the transplanted tissue, which
can ultimately lead to graft failure.
In summary, the process of graft rejection involves the sensitization, activation, and effector phases,
each of which involves different immune cells and mechanisms of tissue damage. Understanding the
process of graft rejection is critical for developing strategies to prevent and manage transplant
rejection