Adaptive Immunity: The Third Line of Defense

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Adaptive Immunity: Overview

Definitions and General Principles

Adaptive immunity is the third line of defense in the immune system, providing protection after exposure to pathogens or viruses. It is characterized by its specificity, clonality, ability to distinguish between 'self' and 'non-self', creation of memory, and inducibility. The adaptive immune system consists of two main components: humoral and cellular immunity.

Specificity: Targets specific antigens.
Clonality: Generates clones of lymphocytes specific to an antigen.
Self vs. Non-self: Recognizes and responds only to foreign antigens.
Memory: Remembers previous encounters for faster response.
Inducibility: Activated only upon exposure to antigens.

Components of Adaptive Immunity

Humoral Immunity: B Cells and Antibodies

Humoral immunity is mediated by B cells, which originate from stem cells in the red bone marrow. B cells differentiate and migrate to lymphoid tissues such as the spleen and lymph nodes. Upon activation, B cells produce antibodies that specifically bind to antigens.

B Cell Formation: Stem cells differentiate into B cells, which migrate to lymphoid tissues.
Antibody Production: B cells produce antibodies (immunoglobulins, Ig) that bind to epitopes on antigens.
Antibody Structure: Antibodies have variable (V) regions for antigen binding and constant (C) regions that determine antibody class. The Fc region interacts with other immune components.

Antigen-binding site and epitope on antibody

Antibody Types and Functions

There are several classes of antibodies, each with distinct functions. The main types include IgG, IgM, IgA, IgE, and IgD.

Antibody Type	Known Functions
IgG	Enhances phagocytosis; neutralizes toxins and viruses; protects fetus and newborn
IgM	Especially effective against microorganisms and agglutinating antigens; first antibodies produced in response to initial infection
IgA	Protects mucosal surfaces
IgE	Involved in allergic responses and defense against parasites
IgD	Functions mainly as a receptor on B cells

Known functions of IgG and IgM antibodies

Targets for Antibodies: Antigens and Epitopes

Antigens are molecules found on the surface of pathogens, such as components of capsules, cell walls, flagella, or fimbriae. Epitopes are specific regions on antigens recognized by antibodies. Antigens are typically proteins or polysaccharides and vary between species, strains, or toxins.

Antibody binding to epitopes on bacterial cell

Haptens

Haptens are small molecules that are not antigenic unless attached to a carrier molecule. Once exposed, antibodies can bind to haptens independently of the carrier. Penicillin is an example of a hapten that binds to body proteins.

Hapten molecules binding to carrier molecule

B Cell Differentiation and Clonal Deletion

B cell differentiation ensures a variety of B cell receptors (BCRs) and prevents responsiveness to self-antigens. Clonal deletion removes B cells that recognize self-antigens, preventing autoimmunity.

T-Dependent B Cell Activation (Clonal Expansion)

T-dependent activation requires help from T helper cells. B cells bind to antigens, internalize them, and present antigen fragments on MHC proteins. T helper cells recognize the MHC-antigen complex and produce cytokines to activate B cells, leading to clonal expansion and formation of plasma and memory cells.

B cell binding and presenting antigen T helper cell activating B cell

T-Independent B Cell Activation

Some antigens, such as polysaccharides and lipopolysaccharides, can directly stimulate B cells without T cell help. This results in a weaker response and no memory cell formation.

T-independent antigen binding to B cell receptors

Antigen-Antibody Binding Results

Antibody binding to antigens leads to several outcomes:

Agglutination: Pathogens are bound together, restricting movement and facilitating phagocytosis.
Opsonization: Antibody coating enhances phagocyte binding and intake.
Neutralization: Antibodies block pathogen or toxin attachment to host cells.
Activation of Complement: Complement proteins bind to antibody-coated pathogens, causing lysis and attracting immune cells.
Antibody-dependent cell-mediated cytotoxicity: Immune cells such as eosinophils, macrophages, and natural killer cells are attracted to antibody-coated targets, leading to destruction.

Agglutination of bacteria by antibodies Opsonization: antibody coating enhances phagocytosis Neutralization: antibodies block pathogen and toxin attachment Activation of complement causes lysis

Cellular Immunity: T Cells

Formation and Differentiation of T Cells

T cells are responsible for cell-mediated immunity, combating infected cells and cancer. They originate from stem cells in the bone marrow and migrate to the thymus for differentiation. T cells then move to lymph nodes and spleen.

T cell differentiation and selection in thymus T cell selection: recognition of MHC and autoantigen

T Cell Thymic Selection

Thymic selection ensures T cells recognize MHC proteins and distinguish self from non-self. T cells that fail to recognize MHC or recognize self-antigens undergo apoptosis or become regulatory T cells.

T cell selection outcomes: apoptosis or survival

T Cell Activation

Pathogens are engulfed by phagocytic cells, which present antigen fragments on MHC proteins. T helper cells bind to the MHC-antigen complex and are activated by costimulatory molecules. Activated T helper cells produce cytokines, stimulate other immune cells, and can become memory cells or activate B cells.

Antigen presentation and T helper cell activation T helper cell activation and cytokine production Cytokines activate B cells and cytotoxic T lymphocytes

Killing of Virus-Infected Cells

Cytotoxic T cells (CTLs) are activated by T helper cells and recognize virus-infected or cancerous cells presenting abnormal antigens on MHC proteins. CTLs induce apoptosis in infected cells using perforin and granzymes.

CTL killing virus-infected cell Infected target cell lysed by CTL

Immunological Memory

Memory B Cells and Secondary Response

Memory B cells are formed during the primary immune response and enable a faster, stronger response upon subsequent exposures to the same antigen. The secondary response is characterized by higher IgG production.

Primary and secondary antibody response graph

Types of Adaptive Immunity

Adaptive immunity can be acquired naturally or artificially, and can be active or passive:

Naturally acquired active: Antigens enter the body naturally, inducing antibodies and specialized lymphocytes.
Naturally acquired passive: Antibodies pass from mother to fetus or infant.
Artificially acquired active: Antigens introduced in vaccines stimulate antibody production.
Artificially acquired passive: Preformed antibodies are introduced by injection.

Types of adaptive immunity: active and passive, natural and artificial

Application Problems

Apoptosis and Dendritic Cells

Apoptosis: Cells undergoing apoptosis are those that fail thymic selection or are targeted by cytotoxic T cells.
Induction of Apoptosis: Cytotoxic T cells induce apoptosis via perforin and granzymes.
Dendritic Cells: Dendritic cells are antigen-presenting cells that play a crucial role in adaptive immunity by presenting antigens to T cells. Without dendritic cells, the immune system would have impaired activation of T cells and reduced adaptive responses.

Dendritic cell structure

Additional info: The notes have been expanded with academic context to ensure completeness and clarity for microbiology students.