23: Adaptive Immunity II
- Page ID
- 146425
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\(\newcommand{\avec}{\mathbf a}\) \(\newcommand{\bvec}{\mathbf b}\) \(\newcommand{\cvec}{\mathbf c}\) \(\newcommand{\dvec}{\mathbf d}\) \(\newcommand{\dtil}{\widetilde{\mathbf d}}\) \(\newcommand{\evec}{\mathbf e}\) \(\newcommand{\fvec}{\mathbf f}\) \(\newcommand{\nvec}{\mathbf n}\) \(\newcommand{\pvec}{\mathbf p}\) \(\newcommand{\qvec}{\mathbf q}\) \(\newcommand{\svec}{\mathbf s}\) \(\newcommand{\tvec}{\mathbf t}\) \(\newcommand{\uvec}{\mathbf u}\) \(\newcommand{\vvec}{\mathbf v}\) \(\newcommand{\wvec}{\mathbf w}\) \(\newcommand{\xvec}{\mathbf x}\) \(\newcommand{\yvec}{\mathbf y}\) \(\newcommand{\zvec}{\mathbf z}\) \(\newcommand{\rvec}{\mathbf r}\) \(\newcommand{\mvec}{\mathbf m}\) \(\newcommand{\zerovec}{\mathbf 0}\) \(\newcommand{\onevec}{\mathbf 1}\) \(\newcommand{\real}{\mathbb R}\) \(\newcommand{\twovec}[2]{\left[\begin{array}{r}#1 \\ #2 \end{array}\right]}\) \(\newcommand{\ctwovec}[2]{\left[\begin{array}{c}#1 \\ #2 \end{array}\right]}\) \(\newcommand{\threevec}[3]{\left[\begin{array}{r}#1 \\ #2 \\ #3 \end{array}\right]}\) \(\newcommand{\cthreevec}[3]{\left[\begin{array}{c}#1 \\ #2 \\ #3 \end{array}\right]}\) \(\newcommand{\fourvec}[4]{\left[\begin{array}{r}#1 \\ #2 \\ #3 \\ #4 \end{array}\right]}\) \(\newcommand{\cfourvec}[4]{\left[\begin{array}{c}#1 \\ #2 \\ #3 \\ #4 \end{array}\right]}\) \(\newcommand{\fivevec}[5]{\left[\begin{array}{r}#1 \\ #2 \\ #3 \\ #4 \\ #5 \\ \end{array}\right]}\) \(\newcommand{\cfivevec}[5]{\left[\begin{array}{c}#1 \\ #2 \\ #3 \\ #4 \\ #5 \\ \end{array}\right]}\) \(\newcommand{\mattwo}[4]{\left[\begin{array}{rr}#1 \amp #2 \\ #3 \amp #4 \\ \end{array}\right]}\) \(\newcommand{\laspan}[1]{\text{Span}\{#1\}}\) \(\newcommand{\bcal}{\cal B}\) \(\newcommand{\ccal}{\cal C}\) \(\newcommand{\scal}{\cal S}\) \(\newcommand{\wcal}{\cal W}\) \(\newcommand{\ecal}{\cal E}\) \(\newcommand{\coords}[2]{\left\{#1\right\}_{#2}}\) \(\newcommand{\gray}[1]{\color{gray}{#1}}\) \(\newcommand{\lgray}[1]{\color{lightgray}{#1}}\) \(\newcommand{\rank}{\operatorname{rank}}\) \(\newcommand{\row}{\text{Row}}\) \(\newcommand{\col}{\text{Col}}\) \(\renewcommand{\row}{\text{Row}}\) \(\newcommand{\nul}{\text{Nul}}\) \(\newcommand{\var}{\text{Var}}\) \(\newcommand{\corr}{\text{corr}}\) \(\newcommand{\len}[1]{\left|#1\right|}\) \(\newcommand{\bbar}{\overline{\bvec}}\) \(\newcommand{\bhat}{\widehat{\bvec}}\) \(\newcommand{\bperp}{\bvec^\perp}\) \(\newcommand{\xhat}{\widehat{\xvec}}\) \(\newcommand{\vhat}{\widehat{\vvec}}\) \(\newcommand{\uhat}{\widehat{\uvec}}\) \(\newcommand{\what}{\widehat{\wvec}}\) \(\newcommand{\Sighat}{\widehat{\Sigma}}\) \(\newcommand{\lt}{<}\) \(\newcommand{\gt}{>}\) \(\newcommand{\amp}{&}\) \(\definecolor{fillinmathshade}{gray}{0.9}\)Adaptive immunity provides specific, long-lasting defense against pathogens through the coordinated actions of B cells and T cells. B cells recognize antigens directly with their B cell receptors (BCRs) and, with help from helper T cells (Th cells), become activated. Activated B cells differentiate into plasma cells that secrete antibodies to neutralize pathogens, enhance phagocytosis, or activate complement pathways. Some B cells become memory cells for faster responses upon re-exposure. T cells, on the other hand, recognize antigens presented by major histocompatibility complex (MHC) molecules. Helper T cells (CD4⁺) amplify immune responses by releasing cytokines, while cytotoxic T cells (CD8⁺) kill infected cells directly. Both T and B cells generate memory populations to ensure quicker, stronger responses during future infections.
Vaccines work by safely exposing the immune system to weakened, inactivated, or partial components of pathogens, prompting the development of memory B and T cells without causing disease. Types of vaccines include live attenuated, inactivated, subunit, conjugate, and mRNA vaccines. By training the adaptive immune system, vaccines provide effective, long-term protection against specific diseases, often preventing illness entirely or reducing its severity upon exposure.
Figure \(\PageIndex{1}\): Compared to the primary response, the secondary antibody response occurs more quickly and produces antibody levels that are higher and more sustained. The secondary response mostly involves IgG.- 23.1: T Lymphocytes - Overview
- The antibodies involved in humoral immunity often bind pathogens and toxins before they can attach to and invade host cells. Thus, humoral immunity is primarily concerned with fighting pathogens in extracellular spaces. However, pathogens that have already gained entry to host cells are largely protected from the humoral antibody-mediated defenses. Cellular immunity, on the other hand, targets and eliminates intracellular pathogens through the actions of T lymphocytes, or T cells.
- 23.2: T-Cell Receptors (TCR) and Helper T Cells
- This page explains T-cell receptors (TCRs) and their significance in the immune response, emphasizing the generation of TCR diversity through VDJ recombination. It details the activation of helper T cells by antigen-presenting cells (APCs) and their subsequent clonal expansion and differentiation into specific subtypes (TH1, TH2, TH17, and memory T cells), each with unique immune functions driven by cytokine influence.
- 23.3: Cytotoxic T Cells and Superantigens
- This page explains the activation of cytotoxic T cells (CTLs) by antigen-presenting cells (APCs) via MHC I and CD8, differentiating them from helper T cells that utilize MHC II and CD4. Upon activation, CTLs can eliminate infected cells through perforin and granzymes.
- 23.4: B Lymphocytes and Antibodies
- Humoral immunity refers to mechanisms of the adaptive immune defenses that are mediated by antibodies secreted by B lymphocytes, or B cells. This section will focus on B cells and discuss their production and maturation, receptors, and mechanisms of activation.
- 23.5: B Cell Activation
- This page explains two types of B cell activation: T cell-independent and T cell-dependent. T cell-independent activation, triggered by repetitive antigens, produces a brief IgM response without memory B cells. Conversely, T cell-dependent activation, involving helper T cells, elicits a stronger response with class switching and memory B cell formation, leading to a more potent secondary response with increased antibody levels and affinity upon re-exposure.
- 23.6: Vaccines
- By artificially stimulating the adaptive immune defenses, a vaccine triggers memory cell production similar to that which would occur during a primary response. In so doing, the patient is able to mount a strong secondary response upon exposure to the pathogen—but without having to first suffer through an initial infection. In this section, we will explore several different kinds of artificial immunity along with various types of vaccines and their mechanisms for inducing artificial immunity.
- 23.7: Variolation and Vaccination
- This page explores the history of variolation and vaccination, focusing on smallpox. Variolation began in 10th century China, involving risky inoculation from smallpox material, while Edward Jenner introduced vaccination in the late 18th century using cowpox as a safer method. Vaccination reduced risks associated with smallpox and paved the way for vaccines against many other diseases.
- 23.8: Classes of Vaccines
- This page discusses various types of vaccines—live attenuated, inactivated, subunit, toxoid, conjugate, and DNA—along with their pros and cons. Live attenuated vaccines provide strong immunity but can be risky for immunocompromised individuals. Inactivated vaccines are safer but less effective, while subunit vaccines lead to fewer side effects. Toxoid vaccines target bacterial toxins, conjugate vaccines improve responses in young children, and DNA vaccines are in development.