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Lecture Chapter 17 for Micro Biology class, Lecture notes of Biology

Lecture Chapter 17 for Micro Biology class

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2023/2024

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Lecture on the Adaptive Immune System (Chapter 17)
Introduction to the Adaptive Immune System
Today, we are focusing on the adaptive immune system, which plays a critical role in
protecting our body from specific pathogens. This system provides us with long-term
protection after encountering an antigen and producing antibodies against it. Most of the time,
this protection lasts a lifetime.
In Chapter 16, we covered innate immunity, which involves the body’s initial, nonspecific
response to pathogens that breach outer defenses like skin. Now, we’re going to talk about the
adaptive immune system, which specifically targets particular pathogens.
Key Characteristics of the Adaptive Immune System
1. Self-Tolerance:
oThe adaptive immune system must differentiate between self (our own cells) and
non-self (foreign invaders). This prevents it from attacking the body’s own cells.
oSelf-tolerance is largely governed by the major histocompatibility complexes
(MHCs). These are proteins on the surface of most cells, which help the immune
system recognize what belongs in the body.
2. Specificity:
oThe adaptive immune system targets specific antigens (molecules from
pathogens) and will respond only to those antigens. It doesn’t attack other
pathogens that don’t have the same specific antigen.
3. Minimal Self-Damage:
oIdeally, the adaptive immune system will target pathogens without causing harm
to the body’s own tissues. Overreaction, such as the response to superantigens,
can result in damage to healthy tissues.
4. Immunological Memory:
oAfter encountering a pathogen, the adaptive immune system develops memory.
This means that if the same pathogen enters the body again, the immune system
can mount a quicker, stronger response.
Self-Tolerance and MHC Complexes
The concept of self-tolerance is essential. The MHC proteins (Class I and Class II) are
responsible for this recognition:
oMHC Class I: Present on all nucleated cells and plays a key role in the
recognition of infected or abnormal cells.
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Lecture on the Adaptive Immune System (Chapter 17)

Introduction to the Adaptive Immune System Today, we are focusing on the adaptive immune system , which plays a critical role in protecting our body from specific pathogens. This system provides us with long-term protection after encountering an antigen and producing antibodies against it. Most of the time, this protection lasts a lifetime. In Chapter 16, we covered innate immunity , which involves the body’s initial, nonspecific response to pathogens that breach outer defenses like skin. Now, we’re going to talk about the adaptive immune system , which specifically targets particular pathogens. Key Characteristics of the Adaptive Immune System

  1. Self-Tolerance : o The adaptive immune system must differentiate between self (our own cells) and non-self (foreign invaders). This prevents it from attacking the body’s own cells. o Self-tolerance is largely governed by the major histocompatibility complexes (MHCs). These are proteins on the surface of most cells, which help the immune system recognize what belongs in the body.
  2. Specificity : o The adaptive immune system targets specific antigens (molecules from pathogens) and will respond only to those antigens. It doesn’t attack other pathogens that don’t have the same specific antigen.
  3. Minimal Self-Damage : o Ideally, the adaptive immune system will target pathogens without causing harm to the body’s own tissues. Overreaction, such as the response to superantigens , can result in damage to healthy tissues.
  4. Immunological Memory : o After encountering a pathogen, the adaptive immune system develops memory. This means that if the same pathogen enters the body again, the immune system can mount a quicker, stronger response. Self-Tolerance and MHC Complexes  The concept of self-tolerance is essential. The MHC proteins (Class I and Class II) are responsible for this recognition: o MHC Class I : Present on all nucleated cells and plays a key role in the recognition of infected or abnormal cells.

o MHC Class II : Found on antigen-presenting cells (APCs) like macrophages , dendritic cells , and B cells. These cells play a vital role in activating the adaptive immune response.  Autoimmune Diseases : When the immune system fails to recognize MHC proteins properly, autoimmune diseases can occur. However, autoimmune diseases are not typically caused by microbes, so we won’t focus on them in this lecture. The Three Lines of Immune Defense

  1. First Line of Defense : o Physical and chemical barriers like skin, mucous membranes, and secretions (e.g., saliva, tears).
  2. Second Line of Defense : o Innate immunity – Nonspecific responses like phagocytosis, fever, and the complement system.
  3. Third Line of Defense : o Adaptive immunity – Specific responses involving T cells and B cells. Divisions of the Adaptive Immune Response The adaptive immune response is divided into two branches :
  4. Humoral (Antibody-mediated) Response : o Involves B cells and the production of antibodies that target pathogens in the blood or extracellular fluid. o Antibodies bind to antigens on pathogens outside of the cells.
  5. Cellular (Cell-mediated) Response : o Involves T cells , which can target infected cells directly (e.g., cytotoxic T cells) or assist other immune cells (e.g., helper T cells). Development of Immune CellsB cells and T cells both originate in the bone marrow. They are initially undifferentiated , but they will mature into different types of immune cells based on signals they receive.
  6. B Cells : o Start in the bone marrow, mature there, and then migrate to various tissues via the lymphatic system. Once activated, B cells differentiate into plasma cells (which
  1. IgD :  Present on the surface of B cells.  Involved in activating B cells but less understood compared to other classes. Mechanisms of Antibody Action Antibodies work through several mechanisms:
  2. Agglutination : o Antibodies bind to multiple antigens on different pathogens, causing them to clump together. This makes it easier for the immune system to eliminate them.
  3. Opsonization : o Antibodies coat pathogens, facilitating their recognition and destruction by phagocytes (e.g., macrophages).
  4. Neutralization : o Antibodies bind to pathogens or their toxins, preventing them from entering host cells or exerting harmful effects.
  5. Antibody-Dependent Cell-Mediated Cytotoxicity (ADCC) : o Antibodies bind to large pathogens (like parasitic worms ) and recruit immune cells like eosinophils to release cytotoxic molecules that destroy the pathogen.
  6. Complement Activation : o Antibodies activate the complement system , which triggers a cascade of immune responses that can lead to the destruction of the pathogen through cell lysis. Conclusion The adaptive immune system is a complex and highly specialized defense system that includes both humoral and cellular responses. The humoral response uses antibodies produced by B cells to neutralize and eliminate pathogens, while the cellular response involves T cells that directly target infected cells. Together, these two branches form a powerful defense system that can specifically recognize and remember pathogens, offering long-lasting immunity. =================================== **Lecture on B-Cell Activation and Immune Response Mechanisms:
  7. Introduction to B-Cell Activation:**  Antibodies & Antigens:

o We've already discussed antibodies and antigens in previous sessions. Now, let's focus on how B-cells are activated to produce these antibodies. o The process we're about to explore is known as Clonal Selection Theory.  Overview: o B-cells are responsible for producing antibodies. o The activation of B-cells leads to their differentiation into plasma cells , which are responsible for producing antibodies.

2. Development of B-Cells:B-Cell Maturation: o B-cells are developed and matured in the bone marrow. o After maturation, they are released into the blood or lymph.  B-Cell Receptors: o B-cells have unique receptors (similar to antibodies) on their surface. o These receptors have a variable region that binds specifically to one unique antigen. 3. Genetic Mechanism Behind Receptors:Gene Rearrangement: o B-cells have genes in their chromosomes that code for the binding site of antibodies. This includes both variable and constant regions. o A segment of about 300 genes is responsible for forming the B-cell receptor. o Through a process called gene rearrangement , these genes are randomly mixed and matched, allowing for the creation of a vast variety of unique B-cell receptors. o This process allows humans to produce antibodies for virtually any antigen they might encounter.  Gene Rearrangement Process: o During development, different parts of the chromosome are transcribed and translated to form unique combinations. o This is a random process, generating a wide array of potential binding sites. 4. B-Cell Selection and Self-Tolerance:Self-Tolerance Testing: o B-cells undergo a second check before they leave the bone marrow.

8. The Role of Helper T-Cells:MHC Recognition: o T-cells need to recognize MHC markers on cells to determine whether a cell is infected or not. o T-cells have CD4 receptors (helper T-cells) and CD8 receptors (cytotoxic T- cells).  Antigen Presentation by Dendritic Cells: o Antigen-presenting cells (APCs), such as dendritic cells , phagocytize pathogens and then display the processed antigen on their MHC-II marker. o Helper T-cells recognize these presented antigens and are activated.  Helper T-Cell Activation: o When a helper T-cell encounters a dendritic cell displaying a pathogen's antigen on an MHC-II molecule, it gets activated. o The helper T-cell begins to self-stimulate by releasing cytokines, which in turn stimulate more T-cells and the activated B-cells. 9. Interaction Between Helper T-Cells and B-Cells:T-Cell and B-Cell Cooperation: o The activated helper T-cell will interact with a B-cell that has previously encountered the same pathogen. o The helper T-cell will provide additional signals (cytokines) to the B-cell, stimulating it to differentiate into plasma cells or memory cells.  Plasma Cells and Antibody Production: o Plasma cells produce antibodies specific to the pathogen's antigen. o The antibodies can then neutralize, agglutinate, or destroy the pathogen.  Memory Cells: o Some B-cells differentiate into memory cells , which stay in the body for long- term immunity. o Upon re-exposure to the same pathogen, memory cells can quickly differentiate into plasma cells, leading to a rapid antibody response. 10. Secondary Immune Response:Memory Cells in Action: o The second time the same pathogen invades, memory cells can rapidly produce antibodies without the need for the clonal selection process. o This secondary immune response is quicker, typically preventing the person from getting sick again.

11. Antibody Types:IgM & IgG: o The first antibodies produced during an immune response are IgM antibodies, followed by IgG antibodies after 2-3 days.  Class Switching: o Over time, the body may switch to producing other types of antibodies, such as IgA (for mucosal immunity) or IgE (for allergic responses). 12. Antibody Functions:  Once produced, antibodies can act in several ways to neutralize or eliminate the pathogen: o Opsonization : Antibodies help enhance phagocytosis. o Agglutination : Antibodies can clump pathogens together, making them easier to clear. o Neutralization : Antibodies can neutralize toxins or viruses by blocking their ability to bind to host cells. o Antibody-dependent cell-mediated cytotoxicity (ADCC) : Antibodies can trigger the destruction of infected cells by immune cells. o Activation of the Complement System : Antibodies can activate the complement system to enhance immune responses. Conclusion:  The process of clonal selection for B-cells and the activation of helper T-cells are crucial to the body’s ability to mount an effective immune response.  Memory cells play a central role in long-term immunity, ensuring a faster and more robust response during future infections. This mechanism of immune defense provides us with the foundation of immunity against various pathogens, creating a highly adaptable and specific response each time a pathogen is encountered. =========================================

1. Humeral vs. Cellular Immunity

We have already discussed the humoral immune response, which involves B cells and the production of antibodies to fight infections. However, the humoral response is mainly effective

5. Different Cell Lines and Their Actions

There are three different cell lines that can target and destroy cells through the release of perforins and granzymes:

  1. Natural Killer (NK) Cells : Detect changes in MHC-I markers and release perforins and granzymes to attack abnormal cells (like cancerous cells or infected cells).
  2. Eosinophils : These cells recognize IgE antibodies bound to foreign antigens and release perforins and granzymes.
  3. Cytotoxic T Cells : These cells recognize altered MHC-I markers on infected or abnormal cells and induce apoptosis by releasing perforins and granzymes.

6. Cytokines in the Immune System

Cytokines are signaling proteins that communicate between different immune cells, coordinating the immune response.  Interleukins (ILs) : These cytokines mediate communication between leukocytes (such as T cells and B cells). They are essential for the activation and proliferation of immune cells.  Chemokines : A subset of cytokines that specifically attract leukocytes to sites of infection or inflammation.  Interferons : These proteins help protect against viral infections by inhibiting viral replication and enhancing the immune response.  Tumor Necrosis Factor (TNF) : A cytokine involved in inflammatory responses and the destruction of cancer cells.

7. Immunological Memory and Vaccine Development

Memory cells are critical to immunological memory —the ability of the immune system to recognize and respond to pathogens it has encountered before.  After the first exposure to a pathogen (primary response), the immune system produces IgM antibodies, followed by IgG. This response takes about 7 days to reach full strength.  During secondary exposure to the same pathogen, memory cells rapidly activate, resulting in a much faster and stronger immune response. This secondary response is characterized by a high spike in IgG production, preventing illness. This is the basis for how vaccines work—by introducing antigens from pathogens to stimulate the production of memory cells, without causing disease.

8. Types of Immunity

Immunity can be classified into four types :

  1. Naturally Acquired Active Immunity : This occurs when an individual is exposed to a pathogen and their immune system produces antibodies in response. This is the typical immune response after an infection.
  2. Naturally Acquired Passive Immunity : This occurs when IgG antibodies are transferred from mother to fetus during pregnancy through the placenta or through breastfeeding, providing protection to the newborn.
  3. Artificially Acquired Active Immunity : This is the result of vaccination , where a person is exposed to antigens from a pathogen (either killed or weakened), stimulating the production of antibodies and memory cells.
  4. Artificially Acquired Passive Immunity : In cases where immediate protection is needed (such as snake bites or bee stings), antibodies are given to the individual through antiserum (antibody-rich serum from another person or animal). This provides temporary immunity, as the recipient does not generate their own antibodies.

9. Key Terms to Know

Serology : The study of the reactions between antibodies and antigens.  Antiserum : A serum that contains antibodies, used to treat infections when immediate protection is needed.  Immunoglobulins (Ig) : These are antibodies, such as IgG , IgM , IgA , which are crucial in the immune response.  Gamma Globulin : A serum protein fraction that contains immunoglobulins, which is often used in immunotherapy.

10. Summary of Chapter 17

To summarize, this chapter discusses the mechanisms behind the adaptive immune response , focusing on humoral immunity (involving B cells and antibodies) and cellular immunity (involving T cells, particularly cytotoxic T cells). Both are essential for fighting infections and protecting the body from harmful pathogens and abnormal cells. Key features include the production of memory cells for faster secondary responses, the role of cytokines in immune communication, and the different types of immunity (active and passive). This understanding also lays the foundation for vaccine development.