Chapter 9: Immunity

Select the correct answer:

1. Plasma cells are

A. the same as memory cells

B. formed from blood plasma

C. B cells that are actively secreting antibody

D. inactive T cells carried in the plasma

Answer: C. B cells that are actively secreting antibody

Explanation: Plasma cells are differentiated B lymphocytes that produce and secrete large quantities of antibodies. They are the effector cells of the humoral immune response.

2. Antibodies combine with antigens

A. at variable regions

B. at constant region

C. only if macrophages are present

D. both A and C are correct

Answer: A. at variable regions

Explanation: Antibodies bind to antigens via their variable regions, which are specific to the antigen's epitope. The constant region determines the antibody class and effector functions.

3. In addition to the immune system, we are protected from disease by

A. a normal body temperature

B. hormones

C. antigens

D. mucous membrane and cilia

Answer: D. mucous membrane and cilia

Explanation: Mucous membranes and cilia are part of the first line of defense (physical barriers). They trap and expel pathogens from the respiratory tract.

4. Fever decrease the

A. interferon production

B. concentration of iron in the blood

C. activity of phagocytes

D. inflammation

Answer: B. concentration of iron in the blood

Explanation: Fever reduces the amount of free iron in the blood, which many bacteria need for growth. It also enhances the activity of phagocytes and interferon production.

5. T and B cells are

A. lymphocytes

B. macrophages

C. natural killer cells

D. red blood cells

Answer: A. lymphocytes

Explanation: T cells and B cells are the two main types of lymphocytes. T cells mature in the thymus, and B cells mature in the bone marrow.

6. When B-cells are presented with antigen they differentiate into

A. T-cells

B. helper T-cells

C. plasma cells

D. suppressor cells

Answer: C. plasma cells

Explanation: Upon activation by an antigen, B cells differentiate into antibody-secreting plasma cells and memory B cells.

7. When one receives a booster shot for polio which type of cell is most directly stimulated?

A. killer T cells

B. memory cells

C. phagocytes

D. suppressor cells

Answer: B. memory cells

Explanation: A booster shot stimulates memory B and T cells, which were formed during the initial vaccination, leading to a rapid and strong secondary immune response.

8. Natural killer cells kill virus infected and cancerous cells by:

A. phagocytosis

B. complement proteins

C. perforins and granzymes

D. antibodies

Answer: C. perforins and granzymes

Explanation: Natural killer (NK) cells release perforin (which forms pores in the target cell membrane) and granzymes (which enter and trigger apoptosis).

9. Colostrum provides

A. natural active immunity

B. artificial active immunity

C. natural passive immunity

D. artificial passive immunity

Answer: C. natural passive immunity

Explanation: Colostrum (first milk) contains maternal antibodies (IgA) that provide passive immunity to the newborn. The baby does not produce its own antibodies.

10. mAbs can help to combat diseases like:

A. measles

B. cancer

C. anorexia

D. haemophilia

Answer: B. cancer

Explanation: Monoclonal antibodies (mAbs) are used in cancer therapy to target specific cancer cells, delivering drugs or triggering immune responses.

11. A patient has a severe burn injury, compromising their skin barrier. Which of the following is most likely to occur?

A. Increased risk of infection due to loss of chemical and physical barriers

B. Decreased risk of infection due to increased immune response

C. No change in infection risk

D. Increased risk of autoimmune disease

Answer: A. Increased risk of infection due to loss of chemical and physical barriers

Explanation: The skin is a physical barrier and produces antimicrobial substances. Burns compromise this barrier, allowing pathogens to enter and increasing infection risk.

12. Dendritic cells are crucial for initiating an adaptive immune response. What would happen if dendritic cells were unable to present antigens?

A. The adaptive immune response would be enhanced

B. The innate immune response would be impaired

C. The adaptive immune response would be impaired

D. There would be no impact on the immune response

Answer: C. The adaptive immune response would be impaired

Explanation: Dendritic cells are antigen-presenting cells (APCs) that activate T cells. Without antigen presentation, T cells cannot be activated, and the adaptive immune response cannot be initiated.

13. Neutrophils use extracellular traps to kill pathogens. What is the primary advantage of this mechanism?

A. Targeted killing of specific pathogens

B. Ability to phagocytose large pathogens

C. Immobilization of pathogens in a localized area

D. Activation of complement system

Answer: C. Immobilization of pathogens in a localized area

Explanation: Neutrophil extracellular traps (NETs) are webs of DNA and antimicrobial proteins that trap and immobilize pathogens, preventing their spread and facilitating their killing.

14. NK cells play a crucial role in controlling viral infections and cancer. What would happen if NK cell function was impaired?

A. Increased risk of bacterial infections

B. Increased risk of viral infections and cancer

C. Decreased risk of autoimmune disease

D. No impact on immune function

Answer: B. Increased risk of viral infections and cancer

Explanation: NK cells are important for killing virus-infected cells and tumor cells. Impaired NK cell function leads to increased susceptibility to viral infections and cancer.

15. Interferons released by virus-infected cells trigger a response in neighboring cells. What is the primary purpose of this response?

A. To induce apoptosis in uninfected cells

B. To destroy RNA in infected cells

C. To activate the adaptive immune response

D. To prevent viral replication in neighboring cells

Answer: D. To prevent viral replication in neighboring cells

Explanation: Interferons bind to receptors on neighboring cells, inducing antiviral proteins that inhibit viral replication, thus limiting the spread of the virus.

16. Antibodies can bind to an antigen, forming an antigen-antibody complex. What would be the most likely outcome if antibodies were unable to opsonize bacteria?

A. Increased phagocytosis of bacteria

B. Decreased phagocytosis of bacteria

C. Increased activation of complement system

D. Decreased activation of NK cells

Answer: B. Decreased phagocytosis of bacteria

Explanation: Opsonization is the process by which antibodies coat pathogens, making them more recognizable and easier to phagocytose. Without opsonization, phagocytosis is less efficient.

17. Monoclonal antibodies have revolutionized the field of immunotherapy. What is a potential benefit of using monoclonal antibodies in cancer treatment?

A. Increased killing of virus infected cells

B. Targeted killing of cancer cells

C. Enhanced tumor growth

D. Increased risk of infection

Answer: B. Targeted killing of cancer cells

Explanation: Monoclonal antibodies can be designed to specifically target cancer cell markers, delivering cytotoxic drugs or triggering immune-mediated destruction of cancer cells while sparing healthy cells.

18. Vitiligo is an autoimmune disease characterized by skin depigmentation. What would be a potential consequence of vitiligo, in majority of patients, if left untreated?

A. Increased risk of skin cancer

B. Decreased risk of autoimmune disease

C. Increased risk of infection

D. Increased risk of systemic impact

Answer: A. Increased risk of skin cancer

Explanation: Vitiligo causes loss of melanocytes, which produce melanin that protects against UV radiation. Without melanin, patients are at increased risk of sunburn and skin cancer.

19. Transplant rejection occurs due to the immune system's ability to recognize foreign antigens. What would happen if a patient received a transplant from an identical twin?

A. Increased risk of graft-versus-host disease

B. Decreased risk of transplant rejection

C. Increased risk of autoimmune disease

D. No impact on immune function

Answer: B. Decreased risk of transplant rejection

Explanation: Identical twins have identical MHC (HLA) antigens. Therefore, the recipient's immune system will not recognize the transplanted organ as foreign, and rejection is unlikely.

20. Lymphokines, such as interleukins, play a crucial role in coordinating the immune response. What would be the consequence of impaired lymphokine production?

A. Enhanced activation of cytotoxic T cells

B. Reduced activation of immune cells

C. Increased production of antibodies

D. Enhanced phagocytic activity of neutrophils

Answer: B. Reduced activation of immune cells

Explanation: Lymphokines (cytokines) are signaling molecules that coordinate the immune response. Impaired production would lead to reduced activation, proliferation, and differentiation of immune cells.

1. What is immune response?

Answer: The immune response is the body's coordinated reaction to the presence of foreign substances (antigens) such as pathogens, toxins, or abnormal cells. It involves the activation of immune cells and the production of antibodies and cytokines to neutralize and eliminate the threat. It has two main components: the innate immune response (rapid, non-specific) and the adaptive immune response (slower, specific, and memory-forming). The immune response is essential for protecting the body against infections and diseases.

2. Name the three lines of defence against microbial attack.

Answer: The three lines of defence are:

1. First Line of Defence (Physical and Chemical Barriers): Skin, mucous membranes, cilia, tears, saliva, stomach acid, and antimicrobial peptides.

2. Second Line of Defence (Innate Immune Response): Phagocytes (neutrophils, macrophages), natural killer cells,

inflammation, fever, and complement proteins.

3. Third Line of Defence (Adaptive Immune Response): B cells and T cells, which provide specific, long-lasting immunity and memory.

3. How oil and sweat glands take part in defence against microorganisms?

Answer: Oil (sebaceous) glands secrete sebum, which contains fatty acids that lower the pH of the skin, creating an acidic environment that inhibits bacterial growth. Sweat glands secrete sweat, which contains lysozyme, an enzyme that breaks down bacterial cell walls. Sweat also contains salt and antimicrobial peptides. These secretions help maintain the skin's barrier function and prevent microbial colonization. Additionally, sweat flushes away potential pathogens from the skin surface.

4. Name the parts of antibody molecule.

Answer: An antibody molecule (immunoglobulin) is Y-shaped and consists of four polypeptide chains: two heavy chains and two light chains. It has two main regions:

Variable Region: Located at the tips of the Y, it contains the antigen-binding site. This region is highly variable and determines the specificity of the antibody for its antigen. Constant Region: Located in the stem of the Y, it determines the antibody class (isotype) and mediates effector functions such as complement activation and binding to phagocytes.

5. How interferons control spread of virus in the body?

Answer: Interferons are proteins released by virus-infected cells. They bind to receptors on neighboring uninfected cells, inducing the production of antiviral proteins. These proteins inhibit viral replication by blocking translation of viral RNA and

degrading viral RNA. This "antiviral state" prevents the virus from spreading to nearby cells. Interferons also activate immune cells like natural killer cells and macrophages, enhancing the overall antiviral response. They are part of the innate immune system.

6. How do antibodies kill pathogens?

Answer: Antibodies do not directly kill pathogens; they mark them for destruction and activate other immune mechanisms. They work through several mechanisms:

1. Neutralization: Antibodies bind to toxins or viruses, preventing them from attaching to host cells.

2. Opsonization: Antibodies coat pathogens, making them more recognizable and easier to phagocytose by macrophages and neutrophils.

3. Complement Activation: Antibodies bound to pathogens activate the complement system, which forms pores in the pathogen's membrane (membrane attack complex) and enhances phagocytosis.

4. Agglutination: Antibodies cross-link pathogens, clumping them together for easier removal.

5. Antibody-Dependent Cell-Mediated Cytotoxicity (ADCC): Antibodies bound to target cells (e.g., virus-infected cells) recruit NK cells to kill them.

7. Why does each antibody bind only to a specific antigen?

Answer: Each antibody binds only to a specific antigen because of the unique structure of its antigen-binding site (paratope) located in the variable region. The variable region has a specific amino acid sequence that creates a three-dimensional shape complementary to a specific epitope (antigenic determinant) on the antigen. This is analogous to a lock and key. The non- covalent interactions (hydrogen bonds, ionic bonds, hydrophobic interactions, van der Waals forces) between the paratope and epitope are highly specific. This specificity ensures that the immune response is precisely targeted.

8. Why is passive immunity temporary?

Answer: Passive immunity is temporary because it involves the transfer of pre-formed antibodies from an external source, rather than the recipient's own immune system producing them. The recipient's body does not generate memory cells, so no long-term immunity is established. The transferred antibodies are gradually degraded and cleared from the body over weeks or months. Once the antibody levels drop, protection is lost. Examples include maternal antibodies transferred to a fetus through the placenta or to a newborn through colostrum, and antibody injections (e.g., antivenom).

9. Name the disorders of immune system.

Answer: Disorders of the immune system include:

1. Immunodeficiencies: Weakened immune system (e.g., AIDS, SCID).

2. Autoimmune Diseases: Immune system attacks self-antigens (e.g., rheumatoid arthritis, type 1 diabetes, multiple sclerosis, systemic lupus erythematosus).

3. Allergies (Hypersensitivities): Overreaction to harmless antigens (e.g., hay fever, asthma, anaphylaxis).

4. Transplant Rejection: Immune response against transplanted organs.

5. Cancers of the Immune System: Leukemias and lymphomas.

10. What are the autoimmune diseases?

Answer: Autoimmune diseases are conditions in which the immune system mistakenly attacks the body's own healthy cells, tissues, and organs. This occurs when the immune system fails to recognize self-antigens and mounts an immune response against them. Causes include genetic predisposition, environmental triggers (infections, toxins), and hormonal factors. Examples include rheumatoid arthritis (joints), type 1 diabetes (pancreatic beta cells), multiple sclerosis (myelin sheath), systemic lupus erythematosus (multiple organs), and Hashimoto's thyroiditis (thyroid). Symptoms vary depending on the affected tissues.

11. Write the differences between:

(a) sebaceous gland and sweat gland

Answer: Sebaceous glands secrete sebum (oil) to lubricate skin and hair; sweat glands secrete sweat for cooling and excretion.

(b) macrophages and neutrophils

Answer: Macrophages are long-lived phagocytes found in tissues; neutrophils are short-lived, highly mobile phagocytes in blood.

(c) antibody-mediated immune response and a cell-mediated immune response.

Answer: Antibody-mediated (humoral) involves B cells and antibodies against extracellular pathogens; cell-mediated involves T cells against intracellular pathogens and abnormal cells.

(d) cytotoxic T cells and suppressor T cell

Answer: Cytotoxic T cells kill infected/cancerous cells; suppressor (regulatory) T cells suppress immune responses. (e) plasma cells and memory cells

Answer: Plasma cells secrete antibodies; memory cells provide long-term immunity for rapid secondary responses. (f) antibody and antigen

Answer: Antibody is a protein produced by B cells that binds to antigens; antigen is any substance that triggers an immune response. (g) innate immunity and acquired immunity

Answer: Innate immunity is rapid, non-specific, and present from birth; acquired immunity is slower, specific, and develops after exposure. (h) primary and secondary immune response

Answer: Primary response is slow and produces fewer antibodies; secondary response is rapid, stronger, and produces more antibodies due to memory cells.

1. Describe the human skin as an impenetrable barrier against invasion by microbes.

Answer: The human skin is the largest organ of the body and serves as the first line of defence against microbial invasion. It is a highly effective physical and chemical barrier.

1. Physical Barrier:

Epidermis: The outermost layer is composed of dead, keratinized cells that are tightly packed. Keratin is a tough, waterproof protein that is resistant to microbial enzymes and physical damage. Continuous Layer: The skin forms a continuous, intact covering over the body, preventing the entry of most microbes. Shedding: The outer layer of skin constantly sheds, removing microbes that have attached to the surface.

2. Chemical Barrier:

Sebum: Sebaceous glands secrete sebum, an oily substance containing fatty acids. This lowers the pH of the skin (around 5.5), creating an acidic environment that inhibits the growth of many bacteria and fungi. Sweat: Sweat glands secrete sweat, which contains lysozyme, an enzyme that breaks down the peptidoglycan cell walls of bacteria. Sweat also contains salt and antimicrobial peptides (defensins). Antimicrobial Peptides: Keratinocytes produce defensins and cathelicidins, which disrupt microbial membranes.

3. Microbiome:

The skin is home to a diverse community of commensal bacteria (normal flora). These bacteria compete with pathogens for nutrients and space, and some produce antimicrobial substances, preventing colonization by harmful microbes.

4. Immune Surveillance:

The skin contains Langerhans cells (dendritic cells) that capture antigens and present them to T cells in lymph nodes,

initiating an adaptive immune response if the barrier is breached.

In summary, the skin provides a formidable barrier through its physical structure, chemical secretions, commensal microbiota, and immune surveillance. Breaches in this barrier (e.g., burns, cuts) significantly increase the risk of infection.

2. What is the role of macrophages and neutrophils in killing bacteria?

Answer: Macrophages and neutrophils are phagocytic cells of the innate immune system that play a crucial role in killing bacteria.

1. Neutrophils:

Recruitment: Neutrophils are the most abundant white blood cells. They are rapidly recruited to sites of infection by chemotactic factors. Phagocytosis: They engulf bacteria by phagocytosis, forming a phagosome. Killing Mechanisms:

Respiratory Burst: Production of reactive oxygen species (ROS) like superoxide and hydrogen peroxide. Antimicrobial Proteins: Release of defensins, lysozyme, and proteases. Neutrophil Extracellular Traps (NETs): Release of DNA webs that trap and kill bacteria.

Life Span: Short-lived; they die after killing pathogens, forming pus.

2. Macrophages:

Resident and Recruited: Macrophages are found in tissues (e.g., alveolar macrophages, Kupffer cells) and are also recruited from monocytes. Phagocytosis: They engulf bacteria and cellular debris. Killing Mechanisms: Similar to neutrophils (ROS, antimicrobial proteins).

Antigen Presentation: After killing, they present antigens to T cells, linking innate and adaptive immunity. Life Span: Long-lived; they can survive and continue to phagocytose.

3. Cooperation:

Neutrophils provide a rapid, early response. Macrophages provide a sustained response and orchestrate the adaptive immune response.

In summary, macrophages and neutrophils are essential for killing bacteria through phagocytosis and various antimicrobial mechanisms. They are key components of the innate immune defence.

3. Explain the protective proteins of complementary system with diagram.

Answer: The complement system is a group of over 30 proteins in the blood plasma that play a crucial role in the innate and adaptive immune responses. They work in a cascade to destroy pathogens.

Protective Proteins and Functions:

1. C1-C9: The core components. C1 binds to antibodies or pathogen surfaces, initiating the cascade. C3 is the central protein, cleaved into C3a and C3b.

2. Factors B, D, P: Involved in the alternative pathway.

3. Mannose-binding lectin (MBL): Initiates the lectin pathway.

Functions:

Opsonization: C3b coats pathogens, enhancing phagocytosis. Chemotaxis: C5a attracts phagocytes. Inflammation: C3a and C5a stimulate histamine release, increasing blood vessel permeability.

Membrane Attack Complex (MAC): C5b, C6, C7, C8, and C9 form a pore in the pathogen membrane, causing lysis.

Diagram Description: (A diagram would show the three pathways: Classical (antibody-dependent), Lectin (MBL-dependent), and Alternative (pathogen surface-dependent), converging on C3. Then showing C3b opsonization, C5a chemotaxis, and MAC formation.)

Regulation: Complement proteins are regulated by inhibitors (e.g., C1 inhibitor) to prevent damage to host cells.

In summary, the complement system is a vital part of the immune defence, providing opsonization, inflammation, chemotaxis, and direct lysis of pathogens.

4. Explain in detail inflammatory response with diagram.

Answer: Inflammation is a localized, protective response to tissue injury or infection. It is characterized by redness, heat, swelling, and pain.

Steps:

1. Tissue Injury: Damaged cells release chemical signals (histamine, prostaglandins, bradykinin).

2. Vasodilation: Blood vessels dilate, increasing blood flow to the area (redness and heat).

3. Increased Permeability: Capillaries become more permeable, allowing plasma proteins and phagocytes to enter the tissue (swelling).

4. Phagocyte Recruitment: Neutrophils and macrophages migrate to the site (chemotaxis) and phagocytose pathogens and debris.

5. Clotting: Fibrin forms a clot to wall off the area and prevent spread of infection.

6. Resolution: Once the threat is removed, inflammation subsides, and tissue repair begins.

Diagram Description: (A diagram would show a blood vessel with vasodilation, increased permeability, and phagocytes migrating into the tissue.)

Benefits: Inflammation destroys pathogens, removes debris, and initiates tissue repair. Harmful Effects: Chronic inflammation can damage tissues (e.g., arthritis, atherosclerosis).

In summary, inflammation is a complex, coordinated response that protects the body but must be tightly regulated.

5. Explain temperature response against infection.

Answer: Fever is a systemic response to infection, characterized by an elevated body temperature. It is a protective mechanism.

Mechanism:

Pyrogens: Pathogens and immune cells release pyrogens (e.g., interleukin-1). Hypothalamus: Pyrogens act on the hypothalamus, raising the set point for body temperature. Response: The body responds by shivering and vasoconstriction to raise body temperature.

Benefits of Fever:

Inhibits Pathogen Growth: Many bacteria and viruses replicate poorly at elevated temperatures. Enhances Immune Response: Fever increases the activity of phagocytes, enhances interferon production, and speeds up tissue repair. Reduces Iron: Fever reduces free iron in the blood, which bacteria need for growth.

Risks:

Very high fever (above 40°C) can be dangerous, causing seizures, dehydration, and organ damage.

In summary, fever is an adaptive response that enhances the body's ability to fight infection. It is regulated by the hypothalamus and is usually beneficial but can be harmful if excessive.

6. What are the ways fever kills microbes?

Answer: Fever does not directly kill microbes but creates an environment that is unfavorable for their growth and enhances the host's immune response.

1. Inhibition of Pathogen Growth:

Many bacteria and viruses have optimal replication temperatures lower than the elevated body temperature. Fever slows their replication.

2. Enhanced Immune Function:

Phagocytosis: Fever increases the motility and phagocytic activity of neutrophils and macrophages. Interferon: Fever enhances the production and antiviral effects of interferons. Lymphocyte Activation: Fever promotes the proliferation and activation of T cells.

3. Nutrient Deprivation:

Fever reduces the concentration of free iron in the blood. Iron is essential for the growth of many bacteria. By sequestering iron, the body limits bacterial growth.

4. Tissue Repair:

Fever accelerates tissue repair processes.

In summary, fever is a multifaceted defence mechanism that inhibits microbial growth and enhances the immune response. It

does not kill microbes directly but creates conditions that are hostile to them.

7. Describe the role of monocytes in immune system.

Answer: Monocytes are a type of white blood cell (leukocyte) that play a crucial role in the immune system. They are produced in the bone marrow and circulate in the blood.

Functions:

1. Phagocytosis: Monocytes are phagocytic. They engulf and destroy pathogens, dead cells, and debris.

2. Differentiation into Macrophages: When monocytes migrate from the blood into tissues, they differentiate into macrophages. Macrophages are resident in tissues (e.g., alveolar macrophages, Kupffer cells) and are long-lived.

3. Differentiation into Dendritic Cells: Some monocytes differentiate into dendritic cells, which are potent antigen- presenting cells (APCs). They capture antigens and present them to T cells, initiating the adaptive immune response.

4. Cytokine Production: Monocytes and macrophages secrete cytokines (e.g., interleukins, TNF-α) that regulate inflammation and immune responses.

5. Antigen Presentation: They present antigens to T helper cells, linking innate and adaptive immunity.

In summary, monocytes are versatile immune cells that phagocytose pathogens and differentiate into macrophages and dendritic cells, playing a central role in both innate and adaptive immunity.

8. What is the role of T cells in cell mediated response.

Answer: T cells are lymphocytes that mature in the thymus. They are the primary mediators of cell-mediated immunity, which targets

intracellular pathogens (viruses, some bacteria) and abnormal cells (cancer cells).

Types of T Cells and Their Roles:

1. Helper T Cells (CD4+):

Recognize antigens presented by MHC class II molecules on APCs. Secrete cytokines that activate B cells, cytotoxic T cells, and macrophages. Are the "master regulators" of the immune response.

2. Cytotoxic T Cells (CD8+):

Recognize antigens presented by MHC class I molecules on infected or cancerous cells. Kill target cells by releasing perforin and granzymes (inducing apoptosis).

3. Regulatory T Cells (Tregs):

Suppress immune responses to prevent autoimmunity and limit collateral damage.

4. Memory T Cells:

Provide long-term immunity. Upon re-exposure to the same antigen, they rapidly proliferate and mount a strong secondary response.

In summary, T cells are essential for cell-mediated immunity. Helper T cells coordinate the response, cytotoxic T cells kill infected cells, and regulatory T cells modulate the response.

9. Describe the role of B cells in humoral antibody mediated immune response.

Answer: B cells are lymphocytes that mature in the bone marrow. They are the primary mediators of humoral immunity, which targets extracellular pathogens and toxins.

Roles:

1. Antigen Recognition: B cells have surface immunoglobulins (antibodies) that recognize specific antigens.

2. Activation: When a B cell binds an antigen, it internalizes it, processes it, and presents it on MHC class II molecules to helper T cells. Helper T cells then activate the B cell via cytokines and CD40 ligand.

3. Proliferation and Differentiation: Activated B cells proliferate and differentiate into:

Plasma Cells: Antibody factories. They secrete large quantities of antibodies specific to the antigen. Memory B Cells: Long-lived cells that provide immunological memory. Upon re-exposure to the antigen, they rapidly differentiate into plasma cells, producing a rapid and strong secondary response.

4. Antibody Production: Antibodies produced by plasma cells circulate in the blood and lymph, where they bind to antigens, neutralizing them, opsonizing pathogens, and activating complement.

In summary, B cells are essential for humoral immunity. They produce antibodies that neutralize and eliminate extracellular pathogens and toxins, and they provide long-lasting memory.

10. Describe the types of acquired immunity.

Answer: Acquired (adaptive) immunity is specific and develops after exposure to an antigen. It can be classified into active and passive immunity, and further into natural and artificial.

1. Active Immunity:

Definition: The body produces its own antibodies and memory cells in response to an antigen. Natural Active Immunity: Acquired through natural infection. Long-lasting. Artificial Active Immunity: Acquired through vaccination. Long-lasting. Mechanism: Activation of B and T cells, production of memory cells.

2. Passive Immunity:

Definition: The body receives pre-formed antibodies from an external source. No memory cells are produced. Temporary. Natural Passive Immunity: Antibodies transferred from mother to fetus (placenta) or newborn (colostrum). Artificial Passive Immunity: Antibodies injected (e.g., antivenom, immune globulin). Mechanism: Immediate protection but short-lived.

In summary, acquired immunity can be active (body produces antibodies) or passive (antibodies transferred). Active immunity is long-lasting, while passive immunity is temporary.

11. Describe the role of T cells and B cells in transplant rejection.

Answer: Transplant rejection is an immune response mounted by the recipient against the transplanted organ (graft). Both T cells and B cells play roles.

1. T Cells:

Recognition: T cells recognize foreign MHC (HLA) molecules on the donor organ. Helper T Cells (CD4+): Activate cytotoxic T cells and B cells. Cytotoxic T Cells (CD8+): Directly kill donor cells by recognizing foreign MHC class I molecules. Delayed-Type Hypersensitivity: T cells recruit macrophages, causing inflammation and damage.

2. B Cells:

Antibody Production: B cells produce antibodies against foreign MHC molecules. Hyperacute Rejection: Pre-existing antibodies can cause immediate rejection. Acute Rejection: Antibodies contribute to damage.

Prevention:

Tissue Matching: Matching donor and recipient MHC. Immunosuppressive Drugs: Cyclosporine, corticosteroids, etc., to suppress T and B cell responses.

In summary, both T cells and B cells mediate transplant rejection. T cells are the primary mediators of acute cellular rejection, while B cells and antibodies contribute to humoral rejection.

12. Explain why a transplant recipient is given immune suppressant drugs and determine what implications this has on his life.

Answer: Transplant recipients are given immunosuppressive drugs to prevent the immune system from rejecting the transplanted organ.

Why Immunosuppressants are Given:

The recipient's immune system recognizes the donor organ's MHC (HLA) antigens as foreign. Without suppression, T cells and B cells attack the graft, leading to rejection. Immunosuppressants inhibit the activation and proliferation of immune cells.

Implications on Life:

1. Increased Risk of Infection: Suppressed immune system makes the patient vulnerable to opportunistic infections (bacterial, viral, fungal).

2. Increased Risk of Cancer: Immune surveillance is reduced, increasing the risk of certain cancers (e.g., skin cancer, lymphoma).

3. Side Effects of Drugs: Hypertension, diabetes, kidney damage, osteoporosis, weight gain.

4. Lifelong Medication: Must take drugs daily for life.

5. Regular Monitoring: Frequent blood tests to monitor drug levels and organ function.

6. Lifestyle Changes: Avoiding crowds, practicing good hygiene, and managing stress.

In summary, immunosuppressive drugs are essential for graft survival but carry significant risks and lifestyle implications. Patients require lifelong monitoring and care.

13. Evaluate the discovery of monoclonal antibodies and justify how this accomplishment revolutionized many aspects of biological research.

Answer: Monoclonal antibodies (mAbs) are identical antibodies produced by a single clone of B cells (hybridoma). Their discovery by Georges Köhler and César Milstein in 1975 revolutionized biological research and medicine.

Revolutionary Aspects:

1. Specificity and Homogeneity: mAbs bind to a single epitope with high specificity and can be produced in unlimited quantities.

2. Diagnostics: Used in ELISA, Western blotting, immunohistochemistry, and flow cytometry for detecting diseases (e.g., pregnancy tests, HIV tests, cancer markers).

3. Therapeutics: Used to treat cancer (e.g., trastuzumab for breast cancer), autoimmune diseases (e.g., adalimumab for rheumatoid arthritis), and infectious diseases (e.g., palivizumab for RSV).

4. Research Tools: Used to identify and quantify proteins, study protein function, and purify molecules.

5. Targeted Therapy: Can be conjugated with drugs, toxins, or radioisotopes to deliver therapy specifically to target cells.

Justification:

mAbs have enabled precise targeting of molecules, leading to breakthroughs in understanding cellular processes. They have transformed medical diagnostics and therapeutics. They have facilitated the development of personalized medicine.

In summary, the discovery of monoclonal antibodies has had a profound impact on biological research and medicine, enabling precise detection, targeting, and treatment of diseases.