Infected cell with microbes in cytoplasm

Infected cell with microbes in cytoplasm

CD8+ T cells (CTLs)

Killing of infected cell secretion, T cells stimulate the function and focus the activity of nonspecific effector cells of innate immunity (such as phagocytes and eosinophils), thereby converting these cells into agents of adaptive immunity.

• The adaptive immune response to microbes that are phagocytosed and live within the phagosomes of macrophages is mediated by TH1 cells, which recognize microbial antigens and activate the phagocytes to destroy the ingested microbes. Macrophages are major cells of host defense early after infection, that is, during innate immune responses (see Chapter 4). Their function is to ingest and kill microbes. Many microbes have developed mechanisms that enable them to survive and even to replicate within phagocytes, so innate immunity is unable to eradicate infections by such microbes. In these situations, TH1 cells function to enhance the microbicidal actions of macrophages and thus to eliminate the infection.

• The response to extracellular microbes, including many fungi and bacteria, is mediated by TH17 cells. These cells recruit neutrophils (and some monocytes), which ingest and destroy the microbes.

• The response to helminthic parasites is mediated by Th2 cells, which stimulate the production of immunoglobulin E (IgE) antibodies and activate eosinophils and mast cells to eliminate the helminths.

• The adaptive immune response to microbes that infect and replicate in the cytoplasm of various cell types, including nonphagocytic cells, is mediated by CD8+ cytotoxic T lymphocytes (CTLs), which kill infected cells and eliminate the reservoirs of infection ( Fig. 10-1B). If the infected cells lack intrinsic microbicidal ability, the infection can be eradicated only by destroying these cells. CTL-mediated killing is also a mechanism for elimination of microbes that are taken up by phagocytes but escape from phagosomes into the cytosol, where they are not susceptible to the microbicidal activities of phagocytes.

• T cell-dependent inflammation may damage normal tissues. Inflammation, consisting of leukocyte recruitment and activation, accompanies many of the reactions of CD4+ T lymphocytes and may be injurious under various conditions. This T cell-dependent injurious reaction is called delayed-type hypersensitivity (DTH), the term hypersensitivity referring to tissue damage caused by an immune response. DTH frequently occurs together with protective cell-mediated immunity against microbes and may be the cause of much of the pathology associated with certain types of infection (see Chapters 15 and 18).

Cell-mediated immune responses consist of the development of effector T cells from naive cells in peripheral lymphoid organs, migration of these effector T cells and other leukocytes to sites of infection, and either cytokine-mediated activation of leukocytes to destroy microbes or direct killing of infected cells (Fig. 10-2). The development of effector T cells involves the sequence of antigen recognition, clonal expansion, and differentiation that is characteristic of all adaptive immune responses; these processes were described in Chapter 9. In this chapter, we describe the reactions of effector T cells and their roles in host defense and tissue injury. We start with the process that brings effector T cells to the site of infection or tissue damage.

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