Adaptive Immunity Response 1
Lecture Overview on Adaptive Immunity
Topics Covered:
Adaptive Immunity: Cell-mediated
Antigens and Immunogenicity
MHC molecules
Key Principles of Adaptive Immunity
Specificity
Memory
Cell-mediated Immunity
Required Videos:
How The Immune System ACTUALLY Works
The Immune System Explained I by Kurzgesagt
Sources:
Openstax Microbiology Textbook: Chapter 18, Adaptive Immune Responses
Classification of Immune Responses
Immune responses are classified as either:
Innate immunity
Adaptive immunity
Referenced in Figure 26.1 of Brock’s Biology of Microorganisms, 16th ed.
Key Features of Adaptive Immunity
Primary Effector Cells:
Lymphocytes:
T lymphocytes (T cells)
B lymphocytes (B cells)
Characteristics of Adaptive Immunity:
Specificity: Targets distinct antigens.
Memory: Produces faster and stronger responses upon re-exposure to pathogens.
Self-tolerance: Does not attack host tissues.
Memory in Adaptive Immunity
Graph Explanation:
Demonstrates the primary and secondary immune responses related to antibody production after initial and secondary exposure to an antigen.
The secondary response is faster and yields a higher concentration of antibodies, as illustrated in Figure 18.2 of Microbiology, Openstax.
Major Histocompatibility Complex (MHC) Molecules
Definitions:
MHC molecules are known as "Self" proteins, unique to each individual.
Close relatives may have similar MHC profiles.
Also referred to as HLA (human leukocyte antigens).
MHC Molecules Identifying Self
Characteristics:
Surface proteins that are unique to every individual.
Two Classes of MHC:
MHC I:
Expressed on all nucleated human cells.
Binds to and displays antigens originating in the cytoplasm.
In absence of infection: MHC I displays self-antigen.
MHC II:
Expressed only on antigen-presenting cells (APCs): macrophages, dendritic cells, and B cells.
Binds to and displays antigens originating outside cells.
Serves as a crucial link between innate and adaptive immune responses as seen in Figure 18.11 of Microbiology, Openstax.
Lymphatic System Overview
Components:
Lymph
Lymphatic vessels
Lymph nodes
Organs Involved:
Bone marrow
Thymus
Spleen
Functions:
Collects excess fluid from tissues and returns it to the blood.
Provides sites for immune activation.
Lymphocytes circulate between the blood and lymph as referenced in a visual aid from cancer.gov.
Primary and Secondary Lymphoid Tissues
Primary Lymphoid Tissues:
Site of lymphocyte maturation:
Thymus: T lymphocytes mature here.
Bone Marrow: B lymphocytes mature here.
Secondary Lymphoid Tissues:
Encapsulated:
Spleen
Lymph nodes
Diffuse:
Mucosa-associated lymphoid tissue (MALT)
Gut-associated lymphoid tissue (GALT)
Blood Components: Serum vs. Plasma
When blood is drawn and spun, it separates into:
Liquid portion
Cell portion
If blood clots:
Liquid portion = Serum (NO clotting factors present).
If blood sample is not allowed to clot (using an anticoagulant):
Liquid portion = Plasma.
Understanding Lymph
Lymph formation process:
Plasma exits capillaries.
Cells and tissues are bathed in interstitial fluid.
Lymph nodes filter lymph before returning it to the circulatory system.
Reiterated: Plasma → interstitial fluid → lymph.
Origin of Blood Cells
All blood cells originate in the bone marrow as displayed in Figure 26.5 of Brock’s Biology of Microorganisms, 16th ed.
Specificity of Lymphocytes
Each lymphocyte contains antigen-specific receptors that are unique:
T cells: Mature in Thymus; have T cell receptors (TCR) for specific epitopes.
Function in both humoral and cell-mediated immunity.
B cells: Mature in Bone Marrow; have unique B cell receptors (BCR) that recognize specific epitope.
When secreted, BCR acts as an antibody.
Function primarily in humoral immunity.
Activation of Lymphocytes and Memory Cell Creation
Naïve lymphocytes are those prior to exposure to a specific antigen.
Primary Response:
First exposure to an antigen involves:
Antigen recognition by specific lymphocyte.
Proliferation of lymphocytes (clonal expansion).
Differentiation into:
Effector cells.
Memory cells.
Secondary Response:
Involves activation of memory cells leading to:
Faster and stronger response.
Often few to no disease signs/symptoms.
This represents immunological memory as illustrated in Figure 27.1 of Brock’s Biology of Microorganisms, 16th ed.
Pathogens and Adaptive Immune Response
Pathogens can replicate in:
Extracellularly: Grow outside host cells (in tissues and fluids).
Intracellularly: Grow inside host cells.
The adaptive immune response must recognize and respond to both types of pathogens:
Cell-mediated immunity:
Primary function of T cells to eliminate intracellular pathogens.
Antibody-mediated (humoral) immunity:
Primary function of B cell antibodies to eliminate extracellular pathogens.
Response Mechanism of B and T Cells
B cells respond primarily to extracellular pathogens.
T cells respond primarily to intracellular pathogens.
Extracellular antigens interact with MHC II-epitope complexes.
Intracellular antigens interact with MHC I-epitope complexes.
Cytotoxic T Cells and Cell-Mediated Immunity
Cytotoxic T Cells (TC):
Also known as T-cytotoxic (Tc) or cytotoxic T lymphocytes (CTLs).
Identified as CD8+ T cells.
Function:
TCR binds to specific MHC I-epitope complexes.
CD8 provides co-stimulation needed for activation.
Causes death of infected cells through:
Release of cytokines attracting NK cells and macrophages.
Release of perforins and granzymes leading to apoptosis of the target cell.
Further referenced in Norman-McKay's Microbiology textbook.
Interaction of TCR with MHCI
All nucleated cells process intracellular antigens through:
Proteasome:
Loads epitopes onto MHCI in the endoplasmic reticulum (ER).
The complex is then exported to the cell surface.
In uninfected cells:
MHCI-epitope complexes display self epitopes.
In infected cells:
MHCI-epitope complexes display pathogen-derived epitopes.
These complexes are recognized specifically by cytotoxic T cells (CTLs).
Activation of Cytotoxic T Cells (CTLs)
Activation process involves:
Interaction of naïve CTL with an infected cell displaying a specific antigen on MHCI.
Co-stimulation provided by CD8.
Following activation, CTLs release perforin and granzymes leading to controlled cell death (apoptosis) as shown in a figure of Microbiology, Openstax.
Outcomes of Lymphocyte Activation
Activation of lymphocytes leads to:
Proliferation of cells with the same specificity.
Creation of memory cells for future immunological responses.
Illustrated in Figures 12.14 and 12.19 of Norman-McKay's Microbiology textbook.
Mechanism of Infected Cell Death by CTLs
CTLs engage in apoptosis of infected cells, an essential part of the immune response.
Additional illustration provided in Figure 12.16 of Norman-McKay's Microbiology textbook.
Overview of Immune Response to Intracellular Pathogen: Cell-Mediated Immunity
Innate Immune Responses:
Features include:
Invasion of host cells.
Host cell injury leading to the release of cytokines.
Inflammation and involvement of NK cells.
Adaptive Immune Responses:
Mechanisms include:
Infected host cells display foreign antigens in complex with MHCI.
Activation of specific CTLs.
Proliferation and differentiation into effector and memory cells.
Ultimately results in the death of the infected host cells.
Memory cells persist to enable quick reactions in future infections.
Comparison: NK Cells vs. Cytotoxic T Cells (CTLs)
Feature | NK Cells | Cytotoxic T Cells (CTLs) |
|---|---|---|
Type of Immunity | Innate | Adaptive |
Timing | Rapid | Requires activation by antigen presentation (MHC I + specific antigen) |
Target | Detect cells lacking “self” MHC I | Recognize specific antigen peptides on MHC I |
Receptors | Non-specific | Antigen-specific (TCR) |
Effector Molecule | Perforins and granzymes | Perforins and granzymes |
Memory | No | Yes; forms long-lived memory T cells |
Main Targets | Virus-infected and tumor cells | Primarily virus-infected and tumor cells |
Co-stimulation | None | Requires CD8 |
Importance of MHC Class I
Functions:
Found on all nucleated cells (absent from RBCs).
Presents endogenous antigens, including:
Normal self-antigens.
Intracellular foreign antigens or altered self-antigens (such as tumors).
These antigens are displayed on the cell surface bound to MHC I and recognized by CD8+ CTLs.
When a foreign antigen is detected:
CTLs release perforin and granzymes, resulting in apoptosis of the infected cell.
Importance:
Facilitates monitoring of the health of all body cells by the immune system.
Loss of MHC I in infected or tumor cells can trigger attack by NK cells through “missing-self” recognition.
Learning Objectives from Lecture
Post-lecture, students should be able to:
Describe concepts of adaptive immune specificity, memory, and tolerance.
Differentiate between serum and plasma.
Describe lymph including its collection and filtration processes.
Identify primary and secondary lymphoid tissues and their basic roles.
Compare and contrast MHC I and MHC II relative to expression patterns.
Outline the sequence of events for processing and presenting intracellular antigens for both normal and infected cells.
Explain immunological memory in terms of primary and secondary immune response.
Present details on T cytotoxic cells regarding activation signals, differentiation, functions, and antigen elimination processes.
Differentiate between effector lymphocytes and memory lymphocytes.
Distinguish between CTLs and NK cells.