Both specific ligand and co-stimulatory signals provided by an antigen-presenting cell are required for the clonal expansion of naive T cells Antigen-binding B cells are trapped in the T-cell zone of secondary lymphoid tissues and are activated by encounter with armed helper T cells

Germinal center B cells undergo V-region somatic hypermutation and cells with mutations that improve affinity for antigen are selected The humoral immune response is initiated when B cells that bind antigen are signaled by helper T cells or by certain microbial antigens alone In the early 1890s, Emil von Behring and Shibasaburo Kitasato discovered that the serum of animals immune to diphtheria or tetanus contained a specific ‘antitoxic activity’ that could confer short-lived protection against the effects of diphtheria or tetanus toxins in people.

Lymphocytes activated by antigen give rise to clones of antigen-specific cells that mediate adaptive immunity Intracellular signaling components recruited to activated receptors transmit the signal onward from the membrane and amplify it The target of T cell-mediated autoimmunity is difficult to identify owing to the nature of T-cell ligands

We are continually exposed to microorganisms, many of which cause disease, and yet become ill only rarely. Antibodies against cell-surface molecules have been used to remove specific lymphocyte subsets or to inhibit cell function B-cell responses to bacterial antigens with intrinsic ability to activate B cells do not require T-cell help The MHC class I and class II molecules deliver peptides to the cell surface from two distinct intracellular compartments Future studies of autoimmunity and graft rejection should allow control of immune responses to one's own body or to a piece borrowed from someone elseT cells with different functions are distinguished by CD4 and CD8 cell-surface proteins and recognize peptides bound to different classes of MHC molecule Protective immunity can be induced by injecting DNA encoding microbial antigens and human cytokines into muscle HIV accumulates many mutations in the course of infection in a single individual and drug treatment is soon followed by the outgrowth of drug-resistant variants of the virus

Autoantibodies against extracellular antigens cause inflammatory injury by mechanisms akin to type II and type III hypersensitivity reactions Immunobiology is the premier text for immunology at the advanced undergraduate, graduate, and medical school levels. Beginning students appreciate the book’s clear writing and informative illustrations, while advanced students and working immunologists value its comprehensive scope. Every chapter is reviewed with experts to ensure accuracy, authority, currency, and depth. The Tenth Edition is supported by InQuizitive, Norton’s award-winning, easy-to-use adaptive learning tool that helps students learn immunological terms and apply them conceptually. Table of Contents:His scientific proof relied on the deliberate exposure of the inoculated individual to infectious smallpox material two months after inoculation. Lymphocytes proliferate in response to antigen in peripheral lymphoid organs, generating effector cells and immunological memory

Systemic disease caused by immune complex formation can follow the administration of large quantities of poorly catabolized antigens HIV infection leads to low levels of CD4 T cells, increased susceptibility to opportunistic infection, and eventually to death Controlled administration of antigen can be used to manipulate the nature of an antigen-specific response

Rearrangement of the β-chain locus and production of a β chain trigger several events in developing thymocytes A specific response against infection by potential pathogens, such as the of antibodies against a particular pathogen, is known as adaptive immunity because it develops during the lifetime of an individual as an adaptation to infection with that pathogen. Most thymocytes express receptors that cannot interact with self MHC and these cells die in the thymus This activity was later determined to be due to the proteins we now call antibodies, which bind specifically to the toxins and neutralize their activity. Many proteins involved in antigen processing and presentation are encoded by genes within the major histocompatibility complex