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Adaptive immunity 

Adaptive immunity

Adaptive immunity

Paul Klenerman


July 30, 2015: This chapter has been re-evaluated and remains up-to-date. No changes have been necessary.

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date: 28 April 2017

Following the innate immune response, which acts very rapidly, the adaptive immune response plays a critical role in host defence against infectious disease. Unlike the innate response, which is triggered by pattern recognition of pathogens, i.e. features that are common to many bacteria or viruses, the adaptive response is triggered by structural features—known as antigens or epitopes—that are typically unique to a single organism.

Cells involved in the adaptive immune response—these are B lymphocytes and T lymphocytes, the latter divided into CD4+ (helper) and CD8+ (cytotoxic) populations. All of these lymphocyte subsets can potentially respond to a huge variety of antigens through the generation of great diversity in their antigen receptors (T-cell receptors and B-cell receptors), some of which is genetically encoded, but much is created by recombination between gene segments as the receptors are expressed.

Recognition of antigens—(1) B cells—a membrane-bound form of the soluble antibody molecules that the cell is destined to secrete acts as the B-cell receptor, which can bind to a range of antigens, including nonprotein antigens such as carbohydrates. (2) T cells—these can only survey antigens that have been cleaved to short peptides and presented on surface of cells bound in the groove of the hugely diverse MHC class I and class II molecules. Dendritic cells have a central role since they can not only present the peptides efficiently, but also provide critical extra signalling in the form of specialized ‘costimulatory’ surface molecules and soluble cytokines.

Response to antigens—once T cell and B cells have been triggered by antigen, they proliferate rapidly and display a range of effector functions. (1) B cells—secrete antibodies, initially in the form of immunoglobulin M (IgM), but subsequently ‘class switching’ to IgG. (2) T cells—(a) CD8+ T cells—response includes migration to sites of infection, killing of infected cells, and secretion of soluble mediators; (b) CD4+ T cells—play a key role in providing ‘help’ for B cells, e.g. in class switching, ‘help’ for proliferation of CD8+ T cells, and also conditioning of dendritic cells. CD4+ T cells which secrete a panel of cytokines promoting cell mediated immunity (such as interferon-γ‎ (IFNγ‎)) are described as Th1 (T helper 1), while others which secrete cytokines promoting B-cell functions (such as interleukin 4 (IL-4)) are Th2. and a third group which secrete IL-17 are termed Th17.

Immunological memory—once an infection is contained, the B- and T-cell populations contract and enter a phase of immunological ‘memory’. These memory populations are found largely in lymph nodes, although some ‘effector memory’ T cells may be found in nonlymphoid organs (e.g. liver). They are retained long term at much higher cell frequencies than are found in an unexposed person, and can respond to re-encounter with antigen with very rapid proliferation and effector function.

Regulation of immune responses—the functions of the adaptive immune system are tightly regulated to limit immune-mediated pathology. T cells develop initially within the thymus, where those which recognize host (‘self’) antigens are eliminated (‘central tolerance’). Self-reactive T cells may be further controlled in the periphery through a variety of mechanisms, including generation of a set of ‘regulatory’ T cells (Tregs). However, this multilayered control sometimes breaks down, thereby allowing pathological responses to harmless antigens (hypersensitivity) or self-antigens (autoreactivity), and pathogens such as HIV may exploit down-regulatory mechanisms to allow their long-term persistence in the body.

Clinical impact of understanding the adaptive immune system—this may be harnessed to generate novel diagnostics, therapies (e.g. monoclonal antibodies) and vaccines, but many challenges remain in translating our increasing knowledge about molecular control of adaptive immunity into protection against complex persistent infections.

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