Podcast
Questions and Answers
Given a scenario where a novel pathogen evades initial innate immune responses and infects human cells, which of the following adaptive immune responses would be LEAST effective in controlling the infection during the early stages, assuming no prior exposure to the pathogen?
Given a scenario where a novel pathogen evades initial innate immune responses and infects human cells, which of the following adaptive immune responses would be LEAST effective in controlling the infection during the early stages, assuming no prior exposure to the pathogen?
- Activation of complement pathways via IgM antibodies, leading to direct pathogen lysis and opsonization.
- Differentiation of naive B cells into plasma cells producing low-affinity antibodies targeting surface antigens.
- Presentation of viral peptides on MHC class I molecules, stimulating cytotoxic T lymphocyte (CTL) mediated killing of infected cells.
- Proliferation of pre-existing memory T cells specific for conserved viral epitopes due to cross-reactivity, resulting in rapid cytokine release. (correct)
A patient presents with a rare immunodeficiency characterized by a complete absence of somatic hypermutation in B cells. Which of the following immunological outcomes is MOST likely to be observed in this patient?
A patient presents with a rare immunodeficiency characterized by a complete absence of somatic hypermutation in B cells. Which of the following immunological outcomes is MOST likely to be observed in this patient?
- Increased susceptibility to autoimmune diseases due to a failure of central tolerance mechanisms in developing B cells.
- Normal primary antibody response but a severely blunted secondary antibody response following re-exposure to the same antigen.
- Significantly reduced affinity maturation of antibodies, leading to impaired clearance of chronic infections and a limited range of antigen recognition. (correct)
- Compromised development of memory T cells due to the lack of costimulatory signals from B cells to T cells.
In the context of organ transplantation, which of the following mechanisms is the MOST significant contributor to chronic rejection, characterized by gradual loss of graft function over months to years?
In the context of organ transplantation, which of the following mechanisms is the MOST significant contributor to chronic rejection, characterized by gradual loss of graft function over months to years?
- Direct cytotoxicity by recipient NK cells recognizing missing self-MHC class I molecules on donor cells.
- Acute antibody-mediated rejection due to pre-existing antibodies against donor HLA antigens.
- T cell-mediated alloreactivity leading to cytokine production, inflammation, and fibrosis within the graft. (correct)
- Hyperacute rejection caused by complement activation and thrombosis immediately after transplantation.
A researcher is investigating a novel immunosuppressive drug that selectively inhibits the function of regulatory T cells (Tregs). Which of the following downstream effects would be the MOST likely consequence of this drug's action?
A researcher is investigating a novel immunosuppressive drug that selectively inhibits the function of regulatory T cells (Tregs). Which of the following downstream effects would be the MOST likely consequence of this drug's action?
A patient with a known genetic defect in the gene encoding the common gamma chain ($_c$) of cytokine receptors (IL-2R, IL-4R, IL-7R, IL-9R, IL-15R, IL-21R) is MOST likely to exhibit which of the following immunological phenotypes?
A patient with a known genetic defect in the gene encoding the common gamma chain ($_c$) of cytokine receptors (IL-2R, IL-4R, IL-7R, IL-9R, IL-15R, IL-21R) is MOST likely to exhibit which of the following immunological phenotypes?
In the context of cancer immunotherapy, which of the following strategies would be MOST effective in enhancing the anti-tumor activity of cytotoxic T lymphocytes (CTLs) within the tumor microenvironment, assuming the tumor cells do not express MHC class I molecules?
In the context of cancer immunotherapy, which of the following strategies would be MOST effective in enhancing the anti-tumor activity of cytotoxic T lymphocytes (CTLs) within the tumor microenvironment, assuming the tumor cells do not express MHC class I molecules?
A researcher discovers a novel bacterial toxin that specifically blocks the interaction between the T cell receptor (TCR) and MHC class II molecules on antigen-presenting cells (APCs). Which of the following immunological processes would be MOST directly inhibited by this toxin?
A researcher discovers a novel bacterial toxin that specifically blocks the interaction between the T cell receptor (TCR) and MHC class II molecules on antigen-presenting cells (APCs). Which of the following immunological processes would be MOST directly inhibited by this toxin?
Consider a scenario where a population of individuals is exposed to a novel viral strain exhibiting significant antigenic drift in its surface glycoproteins. Which of the following factors would MOST significantly influence the degree of protection conferred by pre-existing antibodies elicited against previous viral strains?
Consider a scenario where a population of individuals is exposed to a novel viral strain exhibiting significant antigenic drift in its surface glycoproteins. Which of the following factors would MOST significantly influence the degree of protection conferred by pre-existing antibodies elicited against previous viral strains?
A research team is developing a vaccine against a newly discovered intracellular bacterial pathogen that evades both humoral and cell-mediated immunity through downregulation of MHC class I and II expression. Which of the following vaccine strategies is MOST likely to induce a protective immune response?
A research team is developing a vaccine against a newly discovered intracellular bacterial pathogen that evades both humoral and cell-mediated immunity through downregulation of MHC class I and II expression. Which of the following vaccine strategies is MOST likely to induce a protective immune response?
Upon encountering a novel viral pathogen, plasmacytoid dendritic cells (pDCs) are activated and produce high levels of type I interferons (IFN-/). Which of the following downstream effects of type I interferon signaling is MOST critical for initiating an adaptive immune response against the virus?
Upon encountering a novel viral pathogen, plasmacytoid dendritic cells (pDCs) are activated and produce high levels of type I interferons (IFN-/). Which of the following downstream effects of type I interferon signaling is MOST critical for initiating an adaptive immune response against the virus?
Flashcards
Adaptive Immunity
Adaptive Immunity
Immunity that develops over time through exposure to antigens, providing a specific and targeted response to pathogens.
Humoral Immunity
Humoral Immunity
A type of adaptive immunity mediated by B cells, which produce antibodies to neutralize or mark antigens for destruction.
Cellular Immunity
Cellular Immunity
A type of adaptive immunity mediated by T cells, which directly kill infected cells or activate other immune cells.
Antibodies
Antibodies
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Opsonization
Opsonization
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Cytotoxic T Cells
Cytotoxic T Cells
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Antigen-Presenting Cells (APCs)
Antigen-Presenting Cells (APCs)
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Active Immunity
Active Immunity
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Passive Immunity
Passive Immunity
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Hypersensitivity Reactions
Hypersensitivity Reactions
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Study Notes
- Adaptive immunity, also known as acquired immunity, develops over time as a result of exposure to antigens.
- It is a specific and targeted response to pathogens or foreign substances.
- Adaptive immunity involves lymphocytes, which are white blood cells including B cells and T cells.
- It provides long-lasting protection through the formation of memory cells.
Key Characteristics
- Specificity enables adaptive immunity to recognize and target specific antigens.
- Diversity allows a response to a wide range of antigens due to variability in lymphocyte receptors.
- Memory allows the immune system to "remember" antigens after initial encounter, leading to faster, stronger responses upon subsequent exposure.
- Self-tolerance allows differentiation between self and non-self antigens, preventing attacks on the body's own tissues.
Types of Adaptive Immunity
- Humoral Immunity is mediated by B cells, which produce antibodies.
- Cellular Immunity is mediated by T cells, which directly kill infected cells or help activate other immune cells.
Humoral Immunity
- B cells recognize antigens via their B cell receptors (BCRs).
- Upon antigen binding, B cells activate and differentiate into plasma cells and memory B cells.
- Plasma cells produce large quantities of antibodies, also known as immunoglobulins (Ig).
- Antibodies bind to antigens, neutralizing them or marking them for destruction by other immune cells.
- Memory B cells provide long-term immunity by quickly responding to subsequent encounters with the same antigen.
Antibody Classes
- IgG is the most abundant antibody in serum, providing long-term immunity and crossing the placenta to protect the fetus.
- IgM is the first antibody produced during an immune response and is effective at activating complement.
- IgA resides in mucosal secretions (e.g., saliva, tears, breast milk), providing protection at mucosal surfaces.
- IgE is involved in allergic reactions and defense against parasites, binding to mast cells and basophils.
- IgD is found on the surface of B cells, playing a role in B cell activation.
Mechanisms of Antibody Action
- Neutralization: Antibodies bind to antigens, preventing them from infecting cells or causing damage.
- Opsonization: Antibodies coat antigens, making them more easily recognized and phagocytosed by macrophages and neutrophils.
- Complement Activation: Antibodies activate the complement system, leading to the lysis of pathogens and inflammation.
- Antibody-Dependent Cell-Mediated Cytotoxicity (ADCC): Antibodies bind to infected cells, marking them for destruction by natural killer (NK) cells.
Cellular Immunity
- T cells recognize antigens presented on the surface of cells by major histocompatibility complex (MHC) molecules.
- The two main types of T cells are Helper T cells (CD4+) and Cytotoxic T cells (CD8+).
- Helper T cells secrete cytokines that activate other immune cells, including B cells and cytotoxic T cells.
- Cytotoxic T cells directly kill infected cells, cancer cells, and foreign cells by releasing cytotoxic granules.
- Memory T cells provide long-term immunity by quickly responding to subsequent encounters with the same antigen.
Antigen Presentation
- Antigen-presenting cells (APCs) such as dendritic cells, macrophages, and B cells process antigens and present them on MHC molecules.
- MHC Class I presents antigens from inside the cell (e.g., viral proteins) to cytotoxic T cells.
- MHC Class II presents antigens from outside the cell (e.g., bacterial proteins) to helper T cells.
T Cell Activation
- T cell activation requires two signals: antigen presentation via MHC and costimulatory molecules on APCs.
- Upon activation, T cells proliferate and differentiate into effector T cells and memory T cells.
- Cytokines play a critical role in T cell differentiation and function, influencing the type of immune response.
Regulation of Adaptive Immunity
- Regulatory T cells (Treg) suppress the immune response, preventing autoimmunity and maintaining immune homeostasis.
- Immune checkpoint inhibitors (e.g., PD-1, CTLA-4) regulate T cell activity and prevent overstimulation of the immune system.
- Cytokines and other signaling molecules modulate the adaptive immune response, influencing its duration and intensity.
Development of Adaptive Immunity
- Adaptive immunity develops throughout life as a result of exposure to antigens.
- Active Immunity develops when the body produces its own antibodies and T cells in response to an antigen (e.g., infection or vaccination).
- Passive Immunity develops when antibodies are transferred from one individual to another (e.g., mother to fetus or through antibody injections).
Immunological Memory
- Immunological memory is a hallmark of adaptive immunity, providing long-lasting protection against pathogens.
- Memory B cells and memory T cells persist in the body after an infection has been cleared.
- Upon re-exposure to the same antigen, memory cells quickly differentiate into effector cells, leading to a faster and stronger immune response.
- Vaccination relies on the principle of immunological memory, by exposing the body to weakened or inactive pathogens to generate memory cells without causing disease.
Dysregulation of Adaptive Immunity
- Autoimmune Diseases occur when the immune system attacks the body's own tissues, resulting in chronic inflammation and tissue damage.
- Immunodeficiency Disorders result from defects in the immune system, leading to increased susceptibility to infections.
- Hypersensitivity Reactions are exaggerated immune responses to harmless antigens, causing allergic reactions or tissue damage.
- Cancer: The immune system may fail to recognize and eliminate cancer cells, allowing them to proliferate and spread.
Clinical Significance
- Vaccines harness adaptive immunity to provide long-lasting protection against infectious diseases.
- Immunotherapies utilize the adaptive immune system to target and destroy cancer cells.
- Transplantation requires careful management of adaptive immunity to prevent rejection of transplanted organs.
- Autoimmune Diseases require immunosuppressive therapies to control the dysregulated immune response.
Summary
- Adaptive immunity is a highly specific and versatile defense mechanism that adapts to new threats.
- It relies on lymphocytes to recognize antigens, generate targeted responses and form memory cells.
- This form of immunity protects against infections and other diseases.
- A dysregulation in adaptive immunity causes autoimmune disorders and other immune-related conditions.
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