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Vice Chair, Harvard Medical School

The Sabin polio vaccine consists of three attenuated polio virus strains and is highly immunogenic spasms on right side of head 500 mg ponstel. Moreover muscle relaxant skelaxin 800 mg purchase line ponstel, just as polio itself can be transmitted by fecal contamination of public swimming pools and other failures of hygiene muscle relaxant kava buy ponstel with a visa, the vaccine can be transmitted from one individual to another by the orofecal route muscle relaxant homeopathy order ponstel once a day. Infection with Salmonella likewise stimulates a powerful mucosal and systemic immune response and, as we saw in Section 14-21, has been attenuated for use as a vaccine and carrier of heterologous antigens for presentation to the mucosal immune system. On the one hand, presentation of soluble protein antigens by the oral route often results in tolerance, which is important given the enormous load of foodborne and airborne antigens presented to the gut and respiratory tract. As discussed in Sections 14-10 and 13-28, the ability to induce tolerance by oral or nasal administration of antigens is being explored as a therapeutic mechanism for reducing unwanted immune responses. On the other hand, the mucosal immune system can respond to and eliminate mucosal infections such as pertussis, cholera, and polio. The proteins from these microorganisms that stimulate immune responses are therefore of special interest. One group of powerfully immunogenic proteins at mucosal surfaces is a group of bacterial toxins that have the property of binding to eukaryotic cells and are protease-resistant. A recent finding of potential practical importance is that certain of these molecules, such as the E. In mice, nasal insufflation of either of these mutant toxins together with tetanus toxoid resulted in the development of protection against lethal challenge with tetanus toxin. The latest development in vaccination has come as a surprise even to the scientists who first developed the method. The story begins with attempts to use nonreplicating bacterial plasmids encoding proteins for gene therapy: proteins expressed in vivo from these plasmids were found to stimulate an immune response. This response does not appear to damage the muscle tissue, is safe and effective, and, because it uses only a single microbial gene, does not carry the risk of active infection. This technique has been shown to be effective in animals and might be suitable for mass immunization, although it has yet to be tested in humans. The effectiveness of a vaccine can be enhanced by targeting it to sites of antigen presentation. An important way of enhancing the effectiveness of a vaccine is to target it efficiently to antigen-presenting cells. The first is to prevent proteolysis of the antigen on its way to antigen-presenting cells. Preserving antigen structure is an important reason why so many vaccines are given by injection rather than by the oral route, which exposes the vaccine to digestion in the gut. The second and third approaches are to target the vaccine selectively, once in the body, to antigen-presenting cells and to devise methods of engineering the selective uptake of the vaccine into antigen-processing pathways within the cell. Techniques to enhance the uptake of antigens by antigen-presenting cells include coating the antigen with mannose to enhance uptake by mannose receptors on antigen-presenting cells, and presenting the antigen as an immune complex to take advantage of antibody and complement binding by Fc and complement receptors. A more complicated set of strategies involves targeting vaccine antigens selectively into antigen-presenting pathways within the cell. For example, human papillomavirus E7 antigen has been coupled to the signal peptide that targets a lysosomal-associated membrane protein to lysosomes and endosomes. A vaccinia virus incorporating this chimeric antigen induced a greater response in mice to E7 antigen than did vaccinia incorporating wild-type E7 antigen alone. These specialized epithelial cells lack the mucin barrier and digestive properties of other mucosal epithelial cells. Instead, they can bind and endocytose macromolecules and micro-organisms, which are transcytosed intact and delivered to the underlying lymphoid tissue. In view of these properties, it is not surprising that some pathogens target M cells to gain entry to the body. The counterattack by immunologists is to gain a detailed molecular understanding of this mechanism of bacterial pathogenesis and subvert it as a delivery system for vaccines. For example, the outer membrane fimbrial proteins of Salmonella typhimurium have a key role in the binding of these bacteria to M cells. It might be possible to use these fimbrial proteins or, ultimately, just their binding motifs, as targeting agents for vaccines. A related strategy to encourage the uptake of mucosal vaccines by M cells is to encapsulate antigens in particulate carriers that are taken up selectively by M cells.

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Small spasms mid back generic ponstel 500 mg line, soluble immune complexes that form when antigen is in excess can be deposited in and damage small blood vessels spasms lower left abdomen buy cheapest ponstel. Immune modulation is a general term encompassing various alterations in an immune response muscle relaxant homeopathic buy ponstel 500mg amex. The immune response is the response made by the host to defend itself against a pathogen spasms shoulder purchase 500mg ponstel. Immune response (Ir) genes are genetic polymorphisms that control the intensity of the immune response to a particular antigen. An immune response (Ir) gene defect is usually, but not always, due to failure to bind an immunogenic peptide, so that no T-cell response is observed. It has been proposed that most tumors that arise are detected and eliminated by immune surveillance mediated by lymphocytes specific for tumor antigens. There is little evidence for the efficacy of this proposed process, but it remains an important concept in tumor immunology. The immune system is the name used to describe the tissues, cells, and molecules involved in adaptive immunity, or sometimes the totality of host defense mechanisms. Immunization is the deliberate provocation of an adaptive immune response by introducing antigen into the body. Immunobiology is the study of the biological basis for host defense against infection. Immunoblotting is a common technique in which proteins separated by gel electrophoresis are blotted onto a nitrocellulose membrane and revealed by the binding of specific labeled antibodies. Immunodeficiency diseases are a group of inherited or acquired disorders in which some aspect or aspects of host defense are absent or functionally defective. Immunodiffusion is the detection of antigen or antibody by the formation of an antigen:antibody precipitate in a clear agar gel. Immunoelectrophoresis is a technique in which antigens are first separated by their electrophoretic mobility and are then detected and identified by immunodiffusion. Immunofluorescence is a technique for detecting molecule using antibodies labeled with fluorescent dyes. The bound fluorescent antibody can be detected by microscopy, or by flow cytometry depending on the application being used. Indirect immunofluorescence uses antiimmunoglobulin antibodies labeled with fluorescent dyes to detect the binding of a specific unlabeled antibody. There are three ways of detecting molecules in tissues: immunofluorescent microscopy that reveals the presence of any molecule against which you have a specific antibody; immunohistochemistry, in which one links an enzyme that produces a change in a molecule that is visible under the microscope; and immunoelectronmicroscopy, in which different sized gold particles are linked to antibodies and detected as bound gold particles. Any molecule that can elicit an adaptive immune response on injection into a person or animal is called an immunogen. In practice, only proteins are fully immunogenic because only proteins can be recognized by T lymphocytes. Immunogenetics now refers to the genetic analysis, by any technique, of molecules important in immunology. Many proteins are partly or entirely composed of protein domains known as immunoglobulin domains or Ig domains because they were first described in antibody molecules. The immunoglobulin domain consists of a sandwich of two b sheets held together by a disulfide bond and called the immunoglobulin fold. Domains less closely related to the canonical Ig domains are sometimes also called immunoglobulin-like domains. The immunoglobulin repertoire, also known as the antibody repertoire, is the total variety of immunoglobulin molecules in the body of an individual. Many proteins involved in antigen recognition and cellcell interaction in the immune system and other biological systems are members of a protein family called the immunoglobulin superfamily, or Ig superfamily, because their shared structural features were first defined in immunoglobulin molecules. All members of the immunoglobulin superfamily have at least one immunoglobulin or immunoglobulin-like domain. The detection of antigens in tissues by means of visible products produced by the degradation of a colorless substrate by antibody-linked enzymes is called immunohistochemistry.

We have already seen that there are two different kinds of antigen receptor: the surface immunoglobulin of B cells spasms throughout body discount ponstel 250 mg overnight delivery, and the smaller antigen receptor of T cells knee spasms pain generic 250 mg ponstel amex. These surface receptors are adapted to recognize antigen in two different ways: B cells recognize antigen that is present outside the cells of the body spasms early pregnancy generic ponstel 250mg on line, where muscle relaxant essential oils buy ponstel online now, for example, most bacteria are found; T cells, by contrast, can detect antigens generated inside infected cells, for example those due to viruses. The major pathogen types confronting the immune system and some of the diseases that they cause. The effector mechanisms that operate to eliminate pathogens in an adaptive immune response are essentially identical to those of innate immunity. Indeed, it seems likely that specific recognition by clonally distributed receptors evolved as a late addition to existing innate effector mechanisms to produce the present-day adaptive immune response. We begin by outlining the effector actions of antibodies, which depend almost entirely on recruiting cells and molecules of the innate immune system. Antibodies, which were the first specific product of the adaptive immune response to be identified, are found in the fluid component of blood, or plasma, and in extracellular fluids. Because body fluids were once known as humors, immunity mediated by antibodies is known as humoral immunity. These are highly variable from one molecule to another, providing the diversity required for specific antigen recognition. The stem of the Y, which defines the class of the antibody and determines its functional properties, takes one of only five major forms, or isotypes. Each of the five antibody classes engages a distinct set of effector mechanisms for disposing of antigen once it is recognized. The stem can take one of only a limited number of forms and is known as the constant region. It is the region that engages the effector mechanisms that antibodies activate to eliminate pathogens. The simplest and most direct way in which antibodies can protect from pathogens or their toxic products is by binding to them and thereby blocking their access to cells that they might infect or destroy. This is known as neutralization and is important for protection against bacterial toxins and against pathogens such as viruses, which can thus be prevented from entering cells and replicating. Binding by antibodies, however, is not sufficient on its own to arrest the replication of bacteria that multiply outside cells. In this case, one role of antibody is to enable a phagocytic cell to ingest and destroy the bacterium. This is important for the many bacteria that mare resistant to direct recognition by phagocytes; instead, the phagocytes recognize the constant region of the antibodies coating the bacterium. The coating of pathogens and foreign particles in this way is known as opsonization. Unbound toxin can react with receptors on the host cell, whereas the toxin:antibody complex cannot. The right panels show activation of the complement system by antibodies coating a bacterial cell. The third function of antibodies is to activate a system of plasma proteins known as complement. The complement system, which we shall discuss in detail in Chapter 2, can also be activated without the help of antibodies on many microbial surfaces, and therefore contributes to innate as well as adaptive immunity. The pores formed by activated complement components directly destroy bacteria, and this is important in a few bacterial infections. However, the main function of complement, like that of the antibodies themselves, is to coat the surface of pathogens and enable phagocytes to engulf and destroy bacteria that they would otherwise not recognize. Antibodies of different isotypes are found in different compartments of the body and differ in the effector mechanisms that they recruit, but all pathogens and particles bound by antibody are eventually delivered to phagocytes for ingestion, degradation, and removal from the body. The complement system and the phagocytes that antibodies recruit are not themselves antigen-specific; they depend upon antibody molecules to mark the particles as foreign. Antibodies coating an antigen render it recognizable as foreign by phagocytes (macrophages and neutrophils), which then ingest and destroy it; this is called opsonization. Bound antibodies form a receptor for the first protein of the complement system, which eventually forms a protein complex on the surface of the bacterium that, in some cases, can kill the bacterium directly. T cells are needed to control intracellular pathogens and to activate B-cell responses to most antigens. Pathogens are accessible to antibodies only in the blood and the extracellular spaces. However, some bacterial pathogens and parasites, and all viruses, replicate inside cells where they cannot be detected by antibodies.

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The chain is larger than the chain and contains binding sites for divalent cations that may be important in signaling muscle relaxant 16 purchase 250 mg ponstel with amex. Several structural families of adhesion molecules play a part in lymphocyte migration spasms early pregnancy buy ponstel 250mg cheap, homing spasms back ponstel 250mg online, and cell-cell interactions; most have already been introduced in muscle relaxant indications buy ponstel 500 mg mastercard. It is suspected to have a major role in interactions between dendritic cells and T cells. The initial interaction of T cells with antigen-presenting cells is mediated by cell-adhesion molecules. As they migrate through the cortical region of the lymph node, naive T cells bind transiently to each antigenpresenting cell they encounter. Perhaps because of this synergy, the precise role of each adhesion molecule has been difficult to distinguish. It would not be surprising if there were enough redundancy in the molecules mediating T-cell adhesive interactions to enable immune responses to occur in the absence of any one of them; such molecular redundancy has been observed in other complex biological processes. This conformational change is the same as that induced by signaling through chemokine receptors during the migration of leukocytes to sites of infection (see Section 2-20), although its mechanism is not known. The association can persist for several days, during which time the naive T cell proliferates and its progeny, which also adhere to the antigenpresenting cell, differentiate into armed effector T cells. Most T-cell encounters with antigen-presenting cells do not, however, result in recognition of an antigen. In these encounters, the T cells must be able to separate efficiently from the antigen-presenting cells so that they can continue to migrate through the lymph node, eventually leaving via the efferent lymphatic vessels to reenter the blood and continue circulating. Dissociation, like stable binding, may also involve signaling between the T cell and the antigenpresenting cells, but little is known of its mechanism. Transient adhesive interactions between T cells and antigen-presenting cells are stabilized by specific antigen recognition. Both specific ligand and co-stimulatory signals provided by an antigen-presenting cell are required for the clonal expansion of naive T cells. By contrast, ligation of the T-cell receptor and coreceptor does not, on its own, stimulate naive T cells to proliferate and differentiate into armed effector T cells. The antigen-specific clonal expansion of naive T cells requires a second, or co-stimulatory, signal. Activation of naive T cells requires a second signal (arrow 2), the co-stimulatory signal, to be delivered by the same antigen-presenting cell. The best-characterized co-stimulatory molecules are the structurally related glycoproteins B7. We will call them the B7 molecules from here on, as functional differences between the two have yet to be defined. The B7 molecules are homodimeric members of the immunoglobulin superfamily that are found exclusively on the surfaces of cells that can stimulate T-cell proliferation. Their role in co-stimulation has been demonstrated by transfecting fibroblasts that express a T-cell ligand with genes encoding B7 molecules and showing that the fibroblasts could then stimulate the clonal expansion of naive T cells. Although other molecules have been reported to costimulate naive T cells, so far only the B7 molecules have been shown definitively to provide costimulatory signals for naive T cells in normal immune responses. Once a naive T cell is activated, however, it expresses a number of proteins that contribute to sustaining or modifying the co-stimulatory signal that drives clonal expansion and differentiation. Thus antigen-presenting cells engage in a co-stimulatory dialogue with T cells that recognize the antigens they display. Antigen-presenting cells are activated to express B7 molecules on detecting the presence of infection through receptors of the innate immune system. The requirement for the simultaneous delivery of antigen-specific and co-stimulatory signals by one cell in the activation of naive T cells means that only such activated antigen-presenting cells, principally the dendritic cells that migrate into lymphoid tissue after being activated by binding and ingesting pathogens, can initiate T-cell responses. This is important, because not all potentially self-reactive T cells are deleted in the thymus; peptides derived from proteins made only in specialized cells in peripheral tissues might not be encountered during negative selection of thymocytes. Self-tolerance could be broken if naive autoreactive T cells could recognize self antigens on tissue cells and then be co-stimulated by an antigen-presenting cell, either locally or at a distant site. Thus, the requirement that the same cell presents both the specific antigen and the co-stimulatory signal is important in preventing destructive immune responses to self tissues. Indeed, antigen binding to the T-cell receptor in the absence of co-stimulation not only fails to activate the cell, it instead leads to a state called anergy, in which the T cell becomes refractory to activation by specific antigen even when the antigen is subsequently presented to it by a professional antigen-presenting cell. Dendritic cells, macrophages, and B cells differ in their selectivity of antigen uptake, their antigen-processing properties, and their co-stimulatory and migratory behavior, and thus have distinctive functions in initiating T-cell responses.