Chapter 15 : Acquired Immunity against Bacteria

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Acquired Immunity against Bacteria, Page 1 of 2

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This chapter focuses on the generation and maintenance of the acquired immune response against bacterial pathogens and the pathological effects that may occur if this response is left uncontrolled or actively disregulated. The chapter outlines the general mechanisms of acquired immunity, and then, using specific examples, discusses how various bacterial pathogens induce and modulate this response. Lymphocytes communicate with high endothelial venules via receptor-ligand interactions, which induce lymphocyte transmigration. These adhesion molecules include selectins, integrins, and members of the immunoglobulin (Ig) superfamily. For infections with intracellular bacteria in particular, CD4 T cells dominate both the induction and effector phases of the immune response. Peptides that are presented by major histocompatibility (MHC) class I molecules are generated from endogenous proteins or proteins that are secreted into the cytoplasm. In light of this, CD8 T-cell responses are central to the immune response to viruses. For bacterial infections such as and , the capsule elicits significant Ab production but only after 2 years of age. Accordingly, the capsular polysaccharide vaccine initially used against elicited strong Ab-mediated protection only in children older than 2 years. Toxins produced by extracellular bacteria can be divided into exotoxins, which are secreted by the bacteria, and endotoxins, which form an integral part of the outer membrane of gram-negative bacteria and which are released on bacterial lysis.

Citation: Collins H, Kaufmann S. 2002. Acquired Immunity against Bacteria, p 207-222. In Kaufmann S, Sher A, Ahmed R (ed), Immunology of Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817978.ch15

Key Concept Ranking

Innate Immune System
Immune Systems
MHC Class I
MHC Class II
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Figure 1.

Pathways of Ag processing and presentation. A schematic representation of the pathways of processing of bacterially derived Ag for recognition by T cells is shown.

Citation: Collins H, Kaufmann S. 2002. Acquired Immunity against Bacteria, p 207-222. In Kaufmann S, Sher A, Ahmed R (ed), Immunology of Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817978.ch15
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Figure 2

Bacterial components that stimulate the host immune response. Structures from bacteria that stimulate macrophages to release cytokines that have a direct impact on the development of the acquired T-cell response are shown. P, phosphate groups.

Citation: Collins H, Kaufmann S. 2002. Acquired Immunity against Bacteria, p 207-222. In Kaufmann S, Sher A, Ahmed R (ed), Immunology of Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817978.ch15
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Generic image for table
Table 1

T-cell populations involved in host resistance to bacterial infections

Citation: Collins H, Kaufmann S. 2002. Acquired Immunity against Bacteria, p 207-222. In Kaufmann S, Sher A, Ahmed R (ed), Immunology of Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817978.ch15
Generic image for table
Table 2

Murine Ab isotypes important in bacterial infections

Citation: Collins H, Kaufmann S. 2002. Acquired Immunity against Bacteria, p 207-222. In Kaufmann S, Sher A, Ahmed R (ed), Immunology of Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817978.ch15

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