Lecture 25 Studyguide - Immunology PDF

Viral mechanisms for evading host immunity 1. Alter surface antigens recognized by antibodies or TCRs by one or both of: Antigenic drift Antigenic shift => resulting variation creates strains no longer recognized by immune system The transcript introduces the concept of viral mechanisms for evading...

Viral mechanisms for evading host immunity 1. Alter surface antigens recognized by antibodies or TCRs by one or both of: Antigenic drift Antigenic shift => resulting variation creates strains no longer recognized by immune system The transcript introduces the concept of viral mechanisms for evading host immunity, focusing on alterations in surface antigens recognized by antibodies or T cell receptors. Here's a breakdown of the explanation: 1. Ultra Surface Antigens: Viruses may undergo changes in surface antigens to evade recognition and destruction by the host immune system. There are two main mechanisms discussed: Antigenic Drift: Involves gradual changes in surface antigens due to point mutations, resulting in strains that are no longer effectively recognized by the immune system. Antigenic Shift: Involves sudden and significant changes in surface antigens due to genetic reassortment between different viral strains, leading to the emergence of new strains that may not be recognized by pre-existing immunity. Both mechanisms lead to the evolution of viral strains that are less susceptible to immune detection and elimination. 2. Significance: 1 Viral evasion of host immunity through alterations in surface antigens poses a significant challenge for immune responses and vaccine development. These mechanisms contribute to the persistence and spread of viruses within populations and can lead to the emergence of new viral strains with increased virulence or pandemic potential. Understanding viral evasion strategies is crucial for developing effective countermeasures, such as vaccines and antiviral therapies, to combat infectious diseases. In summary, the transcript highlights the importance of alterations in surface antigens as a key mechanism by which viruses evade host immunity. Antigenic drift and shift enable viruses to evade immune detection and elimination, posing challenges for public health efforts to control infectious diseases. 1 2. Inhibition of antigen processing and Class I MHC presentation Different viruses inhibit different steps in the pathway Infected cells not recognized and killed by CD8+ T cells EBV = Epstein-Barr virus; HSV = Herpes simplex virus; CMV = Cytomegalovirus The transcript discusses the second mechanism by which viruses evade host immunity, which involves the inhibition of antigen processing and Class I MHC presentation. Here's a breakdown of the explanation: 1. Overview of Class I MHC Pathway: The figure illustrates the Class I MHC pathway, which is involved in presenting viral peptides on the surface of infected cells for recognition by cytotoxic T lymphocytes (CTLs). The pathway begins with the degradation of cytosolic proteins, including viral proteins, by the proteasome. Peptides generated from the degraded proteins are transported into the endoplasmic reticulum (ER) via the transporter associated with antigen processing (TAP) protein. In the ER, peptides bind to MHC class I molecules and are subsequently transported to the cell surface for presentation to CTLs. 2. Viral Interference with Class I MHC Pathway: Different viruses, such as Epstein-Barr virus (EBV), herpes simplex virus (HSV), and cytomegalovirus (CMV), can interfere with various steps in the Class I MHC pathway. These viruses may inhibit proteasomal activity, block transport of the TAP protein, inhibit MHC protein synthesis, 2 retain MHC proteins in the ER, or remove MHC class I molecules from the ER. By disrupting these steps, viruses prevent the presentation of viral peptides on the surface of infected cells, thereby evading recognition and destruction by CTLs. 3. Consequences of Viral Interference: Inhibition of the Class I MHC pathway results in infected cells escaping recognition by CTLs, allowing viruses to persist and replicate within the host. Viral interference with antigen processing and MHC presentation compromises the host immune response, facilitating viral immune evasion and potentially leading to chronic infections or disease progression. 4. Additional Mechanism Involving Natural Killer (NK) Cells: The transcript briefly mentions another mechanism involving the engagement of natural killer cell inhibitory receptors by viral decoy class I-like molecules. These viral molecules resemble MHC class I proteins and interact with natural killer cell receptors, activating inhibitory pathways and protecting infected cells from NK cell-mediated killing. In summary, the transcript outlines how viruses interfere with antigen processing and Class I MHC presentation, enabling them to evade recognition by cytotoxic T lymphocytes and persist within the host. Additionally, it mentions a separate mechanism involving viral decoy molecules that protect infected cells from natural killer cell-mediated killing.. 2 Other mechanisms viruses use to evade the immune 3. Coding for proteins that: Act as ligands for NK cell inhibitory receptors Function as decoy signal molecules that compete with cytokines Resemble immunosuppressive cytokines such as IL-10 Bind to and inhibit pro-inflammatory cytokines 4. Exhaustion of CTLs cells 5. Killing or inactivation of immune cells (e.g., HIV kills CD4+ T cells) The transcript discusses additional mechanisms used by viruses to evade the host immune system. Here's a detailed explanation of the points mentioned: 3. Coding for Proteins with Specific Functions: Some viruses encode proteins that act as ligands for inhibitory receptors on natural killer (NK) cells. By engaging these receptors, viral proteins inhibit NK cell-mediated killing of infected cells, allowing the virus to evade immune surveillance. Additionally, viruses may produce decoy signal molecules that compete with cytokines, which are signaling molecules involved in inflammation and immune responses. By mimicking cytokines without activating their receptors, viral decoy molecules dampen the host's inflammatory response, promoting viral persistence. Certain viruses produce proteins that resemble immunosuppressive cytokines like interleukin-10 (IL-10). These viral cytokine mimics suppress the host immune response, impairing antiviral defenses and facilitating viral replication and spread. Moreover, some viruses secrete proteins that bind to and inhibit pro-inflammatory cytokines, preventing them from activating immune cells and promoting inflammation. This inhibition of cytokine signaling further dampens 3 the host's immune response, aiding viral evasion strategies. 4. Exhaustion of CTLs (Cytotoxic T Lymphocytes): Prolonged exposure to viral antigens can lead to exhaustion of CTLs, a state characterized by reduced effector function and increased expression of inhibitory receptors. Exhausted CTLs lose their ability to effectively recognize and eliminate virus-infected cells, allowing the virus to persist within the host. This mechanism of immune evasion is particularly relevant in chronic viral infections where prolonged antigen exposure leads to CTL exhaustion, contributing to viral persistence and disease progression. 5. Killing or Inactivation of Immune Cells: Some viruses, such as human immunodeficiency virus (HIV), specifically target and infect immune cells, such as CD4+ T cells. By infecting and killing or inactivating immune cells, viruses impair the host's ability to mount an effective immune response, facilitating viral replication and immune evasion. HIV-mediated depletion of CD4+ T cells compromises the host's adaptive immune system, leading to immunodeficiency and increased susceptibility to opportunistic infections. Summary: Collectively, these mechanisms highlight the diverse strategies employed by viruses to evade host immunity and promote viral persistence. By encoding proteins that interfere with immune signaling pathways, dampen inflammatory responses, induce CTL exhaustion, or directly target immune cells, viruses effectively subvert the host's immune defenses and establish chronic infections. Understanding these evasion mechanisms is crucial for developing effective antiviral therapies and vaccines that can counteract viral immune evasion strategies and enhance host immunity against viral infections. 3 Vaccination success depends on properties of target microbe Vaccination most effective if microbe does NOT: Establish latency Undergo antigenic variation (i.e., mutation, exhibit life stages) Interfere with host immune responses Infect other animal hosts The transcript discusses factors that influence the success of vaccination, particularly in the context of targeting viruses. Here's a detailed explanation: 1.Establish Latency: 1. Some viruses have the ability to establish latency, where they remain dormant in the host's cells without causing active infection. Latency can pose challenges for vaccination because dormant viruses may not be effectively targeted by the immune response. Moreover, latency can provoke chronic inflammation, which may lead to exhaustion of cytotoxic T lymphocytes (CTLs), impairing the host's ability to control the virus upon reactivation. 2.Undergo Antigenic Variation: 1. Viruses can undergo antigenic variation through mechanisms like antigenic drift or antigenic shift. Antigenic variation refers to changes in the surface antigens of the virus, making it difficult for the immune system to recognize and target the virus effectively. This poses a challenge for vaccination because vaccines may become less effective against new viral variants that emerge over time. 3.Exhibit Different Life Stages: 4 1. Some pathogens, such as certain protists, undergo different life stages during their life cycle. Each life stage may express different antigens, making it challenging for the immune system to provide broad protection against all stages of the pathogen. Vaccination strategies need to account for the diversity of antigens expressed during different life stages to ensure comprehensive immune protection. 1.Interfere with Host Immune Responses: 1. Viruses may possess mechanisms to interfere with host immune responses, as discussed in the previous slides. By inhibiting key steps in the immune response, viruses can evade immune detection and clearance, reducing the effectiveness of vaccination efforts. 2.Infect Other Animal Hosts: 1. Some viruses have the ability to infect other animal hosts besides humans. Vaccination efforts may focus on human populations, but if animals serve as reservoirs for the virus, it can complicate control measures. Viral reservoirs in animal populations can lead to ongoing transmission and potential re-introduction of the virus into human populations, undermining vaccination efforts. Summary: Vaccination success depends on various factors related to the properties of the target microbe, particularly viruses. Understanding these factors is crucial for developing effective vaccination strategies that can overcome challenges such as latency, antigenic variation, diverse life stages, immune evasion mechanisms, and zoonotic transmission. By addressing these factors, researchers can improve the efficacy of vaccines and enhance immune protection against viral infections. 4 Immunity against bacteria, fungi, and parasites The transcript discusses the shift in focus from immunity against viruses to immunity against bacteria, fungi, and parasites. Here's a detailed explanation: 1.Introduction to Immunity Against Bacteria, Fungi, and Parasites: 1. The transcript indicates a transition in the discussion from immunity against viruses to immunity against bacteria, fungi, and parasites. This shift in focus reflects the diverse nature of pathogens and the need to understand specific immune responses tailored to combat different types of microorganisms. 2.Role of T Cells in Immunity: 1. The table mentioned in the transcript likely outlines the role of T cells in immunity against various pathogens. Specifically, CD4-positive helper T cells play a crucial role in orchestrating immune responses against bacteria, fungi, and parasites. These T cells respond to different types of pathogens 5 and contribute to the activation of other immune cells to eliminate the invading microorganisms. 3. Different Types of Effector Cells: 1. The transcript mentions that there are different types of effector cells involved in immunity against different pathogens. These effector cells are specialized in recognizing and targeting specific types of pathogens, including intracellular bacteria, helminths (parasitic worms), and extracellular bacteria and fungi. 4.Role of Interferon Gamma: 1. Interferon gamma (IFN-γ) is highlighted as a key cytokine involved in immunity against bacteria, fungi, and parasites. IFN-γ plays various roles in immune responses, including activating macrophages and promoting the clearance of intracellular pathogens. It is distinct from type 1 interferons, which are primarily associated with antiviral immunity. 5.Specific Immune Responses: 1. The transcript emphasizes that different types of pathogens elicit distinct immune responses. For example, intracellular bacteria may trigger responses involving CD4-positive helper T cells and IFN-γ, while helminths may stimulate different immune pathways. Understanding these specific immune responses is essential for developing targeted strategies to combat different types of infections. Summary: Immunity against bacteria, fungi, and parasites involves a diverse array of immune responses mediated by T cells and other effector cells. Specific cytokines, such as interferon gamma, play crucial roles in coordinating immune responses tailored to combat different types of pathogens. By understanding the distinct mechanisms involved in immunity against various microorganisms, researchers can develop effective strategies for preventing and treating infectious diseases caused by bacteria, fungi, and parasites. 5 Immunity to extracellular bacteria Can survive and reproduce in organ lumens, connective tissues and sometimes blood Pathogenic extracellular bacteria promote inflammation and produce toxins Innate immune response: complement, phagocytosis, inflammation Adaptive immune response: antibody-dependent neutralization & opsonization May induce cytokine-mediated, inflammatory damage to host Use various immunoevasion and/or immunoresistance strategies Extracellular bacteria are capable of reproducing outside host cells. For example, in organ lumens of the GI and respiratory tract, or in connective tissues or even the blood. Many species of extracellular bacteria are pathogenic – these cause disease through two main mechanisms. First, these bacteria induce inflammation, which results in tissue destruction at the site of infection. Second, many of these bacteria produce toxins that have diverse pathologic effects. Some toxins are cytotoxic while other toxins interfere with normal cellular functions without killing cells or induce production of cytokines. Some well known toxins include diphtheria toxin, which inhibits protein synthesis, and tetanus toxin, which inhibits neuromuscular transmission. The innate immune response to extracellular bacteria consists primarily of complement, phagocytosis, and an enhanced inflammatory response. Recall that complement activation leads to opsonization, which enhances phagocytosis of bacteria, stimulation of inflammatory signaling that recruits and activates leukocytes and promotes killing of ingested microbes, and generation of the membrane attack complex. Inflammation from complement 6 and other innate immune cells further drives the innate immune response. In comparison, the adaptive immune response to extracellular bacteria primarily involves humoral immunity in which antibodies neutralize microbes and toxins, and also opsonize bacteria to enhance phagocytosis and complement activation. Humoral responses against extracellular bacteria are directed against cell wall antigens or toxins and is the principal mechanism of defense against polysaccharide encapsulated bacteria. Protein antigens of extracellular bacteria also activate CD4+ helper T cells, which produce cytokines that induce local inflammation and enhance microbe killing activities of phagocytes. The principal host injury associated with extracellular bacteria is cytokine-mediated inflammation-associated damage due to neutrophil and macrophage activities. Large burst of cytokine release may occur – such bursts are sometimes termed a cytokine storm. In severe infections, sepsis or even septic shock may result. Many extracellular bacteria have developed mechanisms by which to evade or resist the host immune response. For example, some bacteria have developed polysaccharide rich capsules that resist phagocytosis and others vary their surface antigens as a way to evade humoral immunity. ChatGPT ChatGPT The transcript discusses the immune response against extracellular bacteria, highlighting specific features of these pathogens, the immune mechanisms involved in the response, and potential consequences of infection. Here's a detailed explanation: 1.Special Features of Extracellular Bacteria: 1. Extracellular bacteria typically reside outside host cells, surviving and reproducing in various body regions such as organ lumens, connective tissues, and sometimes the blood or extracellular fluid. They promote inflammation and produce toxins, necessitating a robust immune response to combat the infection. 2.Immune Response Against Extracellular Bacteria: 1. The immune response involves both innate and adaptive mechanisms. Complement activation plays a crucial 6 role in recognizing and responding to extracellular bacteria. Phagocytes, such as macrophages and neutrophils, engulf and destroy the bacteria through phagocytosis. Inflammation, characterized by redness, swelling, and other signs, accompanies the immune response. 3. Adaptive Immune Response: 1. In the adaptive immune response, antibodies play a key role in neutralizing toxins and opsonizing extracellular bacteria, facilitating their recognition and phagocytosis by immune cells. The production of specific antibodies targeted against the bacteria aids in their clearance from the body. 4.Consequences of Infection: 1. Infection with pathogenic extracellular bacteria may induce cytokine-mediated inflammatory damage to the host, impacting normal cells in the infection site. The inflammatory response is aimed at eliminating the bacteria but can cause collateral damage to surrounding tissues. 5.Immune Evasion Strategies: 1. Extracellular bacteria may employ various immune evasion or resistance strategies to evade detection or neutralization by the immune system. These strategies may include antigenic drift, mutations in surface structures, or alterations in cell wall thickness, among others. By evolving these mechanisms, bacteria can evade immune surveillance and persist within the host. Summary: The transcript provides insights into the immune response against extracellular bacteria, emphasizing the role of both innate and adaptive immune mechanisms in combating infection. It highlights the importance of complement activation, phagocytosis, antibody production, and inflammation in the defense against these pathogens. Additionally, it discusses potential consequences of infection and the strategies employed by bacteria to evade immune detection and clearance. 6 Immunity to intracellular bacteria Survive and even reproduce within phagocytes => inaccessible to Abs Innate immune response: phagocytes and NK cells Adaptive immune response: CD4+ T cells activate phagocytes to kill microbes May result in macrophage-associated damage Resistant bacteria may escape lysosomes or inactivate microbe-killing mechanisms Some bacteria are able to survive and even reproduce within phagocytes. Because these microbes are able to find a niche where they are inaccessible to circulating antibodies, their elimination requires mechanisms of cellmediated immunity. The innate immune response to intracellular bacteria is mediated mainly by phagocytes and natural killer cells. In comparison, the adaptive immune response against intracellular bacteria involves CD4+ T cell mediated recruitment and activation of phagocytes. More information on these responses is provided in the next slide. Many intracellular bacterial infections induce host responses that lead to tissue injury, and such damage is often due to macrophage activity. Intracellular bacteria often persist for long periods and cause chronic T cell and macrophage activation, which results in the formation of granulomas surrounding microbes. This inflammatory reaction may serve to localize and prevent spread of microbes but is also associated with severe functional impairment caused by tissue necrosis and scarring. 7 Intracellular bacteria have developed various strategies to resist elimination by phagocytes, including inhibition of lysosome function or escape into the cytosol, thus hiding from the microbe-killing mechanisms of lysosomes. Alternatively intracellular bacteria may directly inactivate microbe-killing substances such as reactive oxygen species. The discussion now shifts to intracellular bacteria, which are bacteria capable of surviving and reproducing within phagocytes. Unlike viruses that directly enter cells, these bacteria are engulfed by phagocytes, where they can survive and replicate. Since they are within cells, they are inaccessible to antibodies, making it challenging for humoral immunity to combat them. 1.Innate Immune Response: 1. Phagocytes, such as macrophages and natural killer cells, play a crucial role in the innate immune response against intracellular bacteria. Phagocytes attempt to kill the engulfed bacteria, but the bacteria may develop mechanisms to suppress phagocyte killing. Natural killer cells detect infected cells by recognizing surface markers indicating infection and work to eliminate them. 2.Adaptive Immune Response: 1. In the adaptive immune response, CD4-positive helper T cells interact with phagocytes to stimulate their killing of intracellular bacteria. These helper T cells provide instructions to phagocytes to enhance their ability to eliminate the engulfed bacteria. 3.Phagocyte-Associated Damage: 1. Macrophages, being primary phagocytes, are involved in combating intracellular bacteria but may inadvertently cause damage to surrounding tissues. This damage, known as macrophage-associated damage, results from the immune response's activity against the bacteria. 4.Bacterial Resistance Mechanisms: 1. Intracellular bacteria can develop resistance to the immune system's efforts. They may escape from phagosomes into the cytosol, where they can replicate and potentially lyse the host cell. Additionally, these bacteria may inhibit or deactivate the microbicidal mechanisms of phagocytes, enabling them to persist within the host cell. 5.Escape from Phagosomes: 1. Some intracellular bacteria have the ability to escape from phagosomes, allowing them to evade the immune 7 system's attempts to eliminate them. Once in the cytosol, they may reproduce and cause damage to the host cell. Overall, the discussion emphasizes the challenges posed by intracellular bacteria and the complex interplay between the immune system and these pathogens. While immune cells work to eliminate intracellular bacteria, the bacteria employ various strategies to evade detection and destruction, highlighting the need for a coordinated and robust immune response. 7 Immunity to fungi Fungal infections may be endemic or opportunistic Compromised immunity most important factor for significant fungal infection Fungal infections may be extracellular or intracellular Innate immune response: neutrophils and macrophages Adaptive immune response: humoral (extracellular), T cell-mediated (intracellular) Fungal infections are important causes of disease and death in humans. Some fungal infections are endemic and these infections are usually caused by fungi present in the environment and to spores and or humans. Other fungal infections are opportunistic – the causative organisms produce mild or no disease in healthy individuals but create severe disease in immunodeficient people. Compromised immunity is the most important predisposing factor for clinically significant fungal infections. Fungal infections may be extracellular tissues or intracellular, specifically within phagocytes. Therefore the immune responses to these microbes are often combinations of responses to extracellular and intracellular microbes. The innate immune system response to fungi primarily involves neutrophils, macrophages and ILC’s. Macrophages and dendritic cells produce cytokines that recruit and activate neutrophils directly or via activation of tissue resident ILCs. Neutrophils then employ fungicidal substances such as reactive oxygen species and lysosomal enzymes, and phagocytosis fungi for intracellular killing. 8 In terms of adaptive immune responses to fungi, humoral responses are generally directed at extracellular infections, while cell-mediated immunity is the major mechanism of adaptive immunity against intracellular fungal infections, similar to the situation for intracellular bacteria. Here's a breakdown of immunity to fungi and how the immune system deals with them: 1.Fungal Infections: 1. Fungal infections, while less commonly discussed compared to bacterial or viral infections, are significant in certain regions where they are endemic. In other parts of the world, they may be opportunistic infections, particularly in individuals with compromised immune systems. 2.Compromised Immunity: 1. Compromised immunity is a critical factor in significant fungal infections, which can potentially lead to severe illness or even death. Conditions such as HIV infection are associated with increased susceptibility to fungal infections. Aspergillus is one common fungal pathogen, but there are others. 3.Extracellular vs. Intracellular Fungi: 1. Fungi can be either extracellular or intracellular pathogens, similar to bacteria. Extracellular fungi exist outside host cells, while intracellular fungi can survive and replicate within host cells. 4.Innate Immune Response: 1. Neutrophils and macrophages play crucial roles in the innate immune response against fungi. They can engulf and eliminate fungal pathogens, particularly if the infection is extracellular. 5.Adaptive Immune Response: 1. The adaptive immune response differs based on whether the fungal infection is extracellular or intracellular. For extracellular infections, humoral immunity, mediated by antibodies, is critical. In contrast, for intracellular infections, cell-mediated immunity, involving T cells such as cytotoxic T lymphocytes (CTLs), is important. CTLs recognize fungal peptides presented on MHC Class I proteins and kill infected cells. 6.Specificity of Immune Response: 1. The immune response against fungal infections involves specific components of the immune system tailored to the type of pathogen encountered. Not all elements of the immune system are equally involved in every type of infection, highlighting the specificity and versatility of immune responses. 8 8 Immunity to parasites Protozoa and helminths Infections often chronic Innate immune response: phagocytosis (protozoa), inflammation (helminths) Adaptive immune response: varied humoral and cell-mediated Tissue damage varies with parasite and corresponding immune response Multiple, effective immunoevasion and immunoresistance strategies Parasitic infections contribute to major health problems, particularly in developing countries. Parasites include single cell protozoa and complex multicellular worms (helminths). Most parasitic infections are chronic because of weak innate immune responses and the ability of parasites to evade or resist elimination by adaptive immune responses. The major innate immune response to protozoa is phagocytosis. In comparison, helminthic parasites activate various mechanisms of innate immunity that promote inflammation. Different protozoa and helminths vary greatly in the structural and biochemical properties, lifecycles, and pathogenic mechanisms. These organisms generally elicit various adaptive immune responses, including humoral and cell-mediated responses, that vary with the organism. Tissue damage associated with infection varies with parasite and corresponding immune response. Both innate 9 and adaptive immune responses to parasites can contribute to tissue injury, largely through mechanisms discussed previously for other microbes. Parasites employ Multiple, effective immunoevasion and immunoresistance strategies, which complicates both immune defense and the development of effective treatments, including vaccines. Here's a summary of the immune response to parasites, including helminths (worms) and protozoa: 1.Chronic Infections: 1. Parasitic infections are often chronic, meaning the immune system struggles to completely clear the pathogens from the body. 2.Innate Immune Response: 1. The innate immune response against parasites often involves activation of phagocytes, such as macrophages, to engulf and attempt to eliminate the parasites. For worms, inflammation plays a significant role, with mast cells releasing enzymes and chemicals to combat the parasites. 3.Adaptive Immune Response: 1. The adaptive immune response to parasites varies depending on factors such as accessibility of the parasite and its protective mechanisms. Both humoral (involving antibodies) and cell-mediated (involving T cells) responses may be involved. For example, for worms with strong outer cuticles, adaptive immune responses may be limited. 4.Tissue Damage: 1. The extent of tissue damage caused by parasitic infections varies depending on the type of parasite and the specific immune response activated. Inflammation driven by worm infections may lead to more tissue damage compared to phagocytosis of protozoa. 5.Evasion Strategies: 1. Parasites employ various evasion and resistance strategies to evade the host immune system, similar to bacteria and viruses. These strategies can complicate the immune response and contribute to chronic infections. Overall, the immune response to parasites involves a complex interplay between innate and adaptive immunity, influenced by factors such as parasite type and host immune status. 9 9 Features of immunity to microbes The immune response is specialized to type of microbe Microbial survival and pathogenicity are tied to immunoevasion / immunoresistance Defects in immunity are important causes of susceptibility to infections Analysis of immune responses can provide info on status of infection There are several fundamental features of immunity to microbes, including: 1. The defense against microbes is mediated by the effector mechanisms of innate and adaptive immunity. The innate immune system provides early defense and the adaptive immune system provides a more sustained and stronger response. Many pathogenic microbes evolved to resist innate immunity and protection against such infections is dependent on adaptive immune responses. 2. The immune response is specialized to particular types of microbes. This maximizes the impact of the response. 3. The survival and pathogenicity of a microbe are closely tied to the ability of the microbe to evade or resist the effector mechanisms of immunity. Infectious microbes and the immune system have coevolved and are engaged in a constant struggle for survival. Some microbes establish latent or persistent infections in which the immune response controls but does not eliminate the micro. 4. Inherited and acquired defects in innate and adaptive immunity are important causes of susceptibility to infections. 5. Analysis of immune responses provides a valuable clinical tool to follow the state of an infection. For example, measurement of serum antibodies specific for particular microbe provides an indication of ongoing or previous 10 infection. The presence of IgM antibodies is indicative of recent infection whereas the presence of only IgG suggest past infection. Other tests involve assays for T cell responses and cytokine release. The transcript discusses various aspects of immunity to microbes, emphasizing key points about how the immune system responds to different types of pathogens and how this relates to infection outcomes. Here's a breakdown of the transcript: 1.Specialized Immune Response: The immune system is tailored to combat specific types of microbes, including bacteria, viruses, fungi, and parasites. Different mechanisms are employed against each type of microbe, reflecting the diverse strategies needed to effectively neutralize them. 2.Microbial Survival and Pathogenicity: The ability of a microbe to survive and cause disease (pathogenicity) is closely linked to its capacity to evade or resist the host immune response. Microbes that have evolved effective evasion or resistance mechanisms are more likely to cause severe infections, highlighting the importance of understanding these mechanisms in combating infectious diseases. 3.Defects in Immunity: Individuals with compromised immune systems are more susceptible to certain types of infections. While everyone can get infections, those with weakened immune systems are particularly vulnerable. Understanding these vulnerabilities can inform strategies for protecting high-risk individuals and preventing infections. 4.Analysis of Immune Responses: Studying immune responses to infections provides valuable insights into the status and progression of the infection. Monitoring specific markers such as immune cell levels and cytokine production can help assess the severity and effectiveness of interventions, guiding treatment strategies and disease management. Overall, understanding the interplay between the immune system and microbes is crucial for developing effective strategies to prevent, treat, and manage infectious diseases. By elucidating the mechanisms of immune evasion and resistance, researchers can devise targeted approaches to combatting pathogens and protecting public health. 10