The purpose of the adaptive immune response (ie, the elimination or neutralization of foreign antigen) is accomplished during the effector phase. Antigen-specific effectors exist in 2 major subsets:
Effector lymphocytes require 2 exposures to antigen for maximum effectiveness. The initial (priming, or activation) exposure occurs in the lymph node. The second (restimulation) exposure occurs in the peripheral tissue from which the antigen originated.
Effector T lymphocytes consist primarily of 2 types, as determined by their different responses on experimental assays and different cell surface molecules (Fig 2–5). Delayed hypersensitivity (DH) T lymphocytes usually express CD4 (and thus recognize antigen with MHC class II) and release IFN-γ and TNF-β. They function by encountering antigen presented by APCs in a tissue site, becoming fully activated, and releasing cytokines and mediators that recruit nonspecific, antigen-independent effector cells such as neutrophils, basophils, or monocytes (discussed in Chapter 1). As with helper T lymphocytes, Th1 and Th2 types of DH effector cells have been identified. Cytotoxic T lymphocytes express CD8 and serve to kill tumor cells and virus-infected host cells. They accomplish this function through the release of cytokines (eg, IFN-γ, TNF-α, and TNF-β) or specialized cytotoxic pore-forming and apoptosis-activating molecules such as perforin and granzymes. A third subset of effector lymphocytes, grouped as non-T, non-B lymphocytes, includes natural killer cells, lymphokine-activated cells, and killer cells.
Figure 2-5 Schematic representation of effector mechanisms during adaptive immunity. The tissue site (left) is not only where the immune response is initiated but is also ultimately where the immune response arc is completed—when effectors encounter antigen within tissue after their release into the circulation from the lymph node (right). The 3 most important effector mechanisms of adaptive immunity are cytotoxic T lymphocytes (CTLs), delayed hypersensitivity (DH) T lymphocytes (CD4-Th lymphocytes), and antibody-plasma cells derived from B lymphocytes.
(Illustration by Barb Cousins, modified by Joyce Zavarro.)
Antibodies, or immunoglobulins, are produced by plasma cells derived from B lymphocytes after appropriate antigenic stimulation with T-lymphocyte help. Plasma cells initially secrete IgM antibodies, followed later by production of other isotypes after antibody-class switching. Antibodies are released into the efferent lymph fluid (downstream from lymph nodes), draining into the venous circulation. Once bound to their specific epitope, antibodies mediate a variety of immune effector activities, including opsonization for phagocytosis and complement activation via the classical pathway.
Excerpted from BCSC 2020-2021 series: Section 9 - Uveitis and Ocular Inflammation. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.