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Human serum sickness: a prospective analysis of 35 patients treated with equine anti-thymocyte globulin for bone marrow failure Medicine (Baltimore) 1988 symptoms 0f heart attack cyklokapron 500 mg cheap. Serum sickness and acute renal failure after streptokinase therapy for myocardial infarction Clin medicine ball exercises generic cyklokapron 500mg with amex. An essential role for macrophage migration inhibitory factor in the tuberculin delayed-type hypersensitivity reaction J 400 medications cheap 500 mg cyklokapron mastercard. Immunoregulatory mechanisms involved in elicitation of allergic contact hypersensitivity Immunol treatment hyperkalemia cyklokapron 500 mg line. Processing of urushiol (poison ivy) hapten by both endogenous and exogenous pathways for presentation to T cells in vitro J. Required early complement activation in contact sensitivity with generation of local C5-dependent chemotactic activity, and late T cell interferon gamma: a possible initiating role of B cells J. Autoimmunity and Transplantation Introduction to Chapter 13 Autoimmune responses are directed against self antigens Responses to alloantigens and transplant rejection Self-tolerance and its loss References to Chapter 13 Introduction to Chapter 13. We have learned in preceding chapters that the adaptive immune response is a critical component of host defense against infection and therefore essential for normal health. Unfortunately, adaptive immune responses are also sometimes elicited by antigens not associated with infectious agents, and this may cause serious disease. These responses are essentially identical to adaptive immune responses to infectious agents; only the antigens differ. In Chapter 12, we saw how responses to certain environmental antigens cause allergic diseases and other hypersensitivity reactions. In this chapter we will examine responses to two particularly important categories of antigen: responses to self tissue antigens, called autoimmunity, which can lead to autoimmune diseases characterized by tissue damage; and responses to transplanted organs that lead to graft rejection. We will examine these disease processes and the mechanisms that lead to the undesirable adaptive immune responses that are their root cause. Autoimmune disease occurs when a specific adaptive immune response is mounted against self antigens. The normal consequence of an adaptive immune response against a foreign antigen is the clearance of the antigen from the body. Virus-infected cells, for example, are destroyed by cytotoxic T cells, whereas soluble antigens are cleared by formation of immune complexes of antibody and antigen, which are taken up by cells of the mononuclear phagocytic system such as macrophages. When an adaptive immune response develops against self antigens, however, it is usually impossible for immune effector mechanisms to eliminate the antigen completely, and so a sustained response occurs. The consequence is that the effector pathways of immunity cause chronic inflammatory injury to tissues, which may prove lethal. The mechanisms of tissue damage in autoimmune diseases are essentially the same as those that operate in protective immunity and in hypersensitivity diseases. Autoimmune diseases can be grouped in the same way as hypersensitivity reactions, according to the type of immune response and the mechanism by which it damages tissues. The immunopathological mechanisms are as illustrated for the hypersensitivity reactions in. Some additional autoimmune diseases in which the antigen is a cellsurface receptor, and the pathology is due to altered signaling, are listed later in. Several immunopathogenic mechanisms operate in parallel to cause many autoimmune diseases. This is illustrated in the case of rheumatoid arthritis, which appears in more than one category of immunopathological mechanism. There are four types of hypersensitivity reaction mediated by immunological mechanisms that cause tissue damage. Adaptive immune responses are initiated by the activation of antigen-specific T cells, and it is believed that autoimmunity is initiated in the same way. T-cell responses to self antigens can inflict tissue damage either directly or indirectly. Autoimmune responses are a natural consequence of the open repertoires of both Bcell and T-cell receptors, which allow them to recognize any pathogen. Although these repertoires are purged of most receptors that bind with high affinity to self antigens encountered during development, they still include receptors of lower affinity reactive to some self antigens. Transient autoimmune responses are common, but it is only when they are sustained and cause lasting tissue damage that they attract medical attention.
Sperm entering the epididymis show weak treatment 4 high blood pressure cyklokapron 500mg with visa, random movement symptoms 4 weeks order cyklokapron 500mg with amex, and for the most part they are incapable of fertilization; spermatozoa from the distal epididymis show strong treatment 5th metatarsal shaft fracture order cyklokapron 500 mg with amex, unidirectional motility and are capable of fertilization treatment 2nd degree burn cyklokapron 500 mg on line. Sperm are slowly propelled through the long ductus epididymidis by peristaltic contractions of its muscular walls. During their passage through the epididymis, spermatozoa show continued differentiation of the acrosome and sperm head, as well as progressive increase in the fertilizing capacity. Sperm require the environment provided by the epididymis to become physiologically mature and viable. Although the maturation process is androgen-dependent, how the various segments of the epididymis control and regulate the physiologic maturation of spermatozoa is unknown. Because of its thick muscular wall, it can contract forcibly and, in coordination with the wall of the ductus deferens, empty stored sperm into the prostatic urethra. During ejaculation, the primary accessory sex glands contribute successively to the seminal fluid. The bulbourethral and intraepithelial urethral glands secrete fluids that lubricate the urethra during sexual arousal and erection of the penis. At the onset of ejaculation, muscular tissue of the prostatic stroma contracts, discharging the secretory product into the prostatic urethra. Sperm and their suspending fluids are expelled from the distal ductus epididymidis and ductus deferens. The last component added to the ejaculate is the viscous secretion of the seminal vesicles. This secretion is rich in fructose, an important energy source for the active, motile spermatozoa. Seminal vesicles also secrete prostaglandins in high concentration, that stimulate contractions within the female reproductive tract that aid in moving spermatozoa to the site of fertilization (ampulla of the oviduct). The final phase of physiologic maturation of spermatozoa is capacitation and occurs in the female reproductive tract, substantially increasing the number of spermatozoa that are capable of fertilization. Testosterone and its metabolites are vital for the male reproductive system to develop properly and to maintain normal structure and function. Testosterone levels are high during in utero development and produce the male phenotype. Testosterone levels rise steeply at puberty, plateau in the adult and slowly decline in old age. It is through this feedback system that normal testosterone levels are maintained. Although not genital organs, the mammary glands are important accessory organs of the female reproductive system. For the first 10 or 11 years of life, the reproductive organs remain immature and growth parallels that of the body generally. During the 2 to 3 years prior to the first menstrual period, the generative organs increase in size, the breasts enlarge, and pubic and axillary hair appears. Following the first menses and thereafter throughout the reproductive period, the ovaries, oviducts, uterus, vagina, and mammary glands undergo cyclic changes in function and structure associated with the menstrual cycle and pregnancy. During menopause, the cycles become irregular and eventually cease; in the postmenopausal period the reproductive organs atrophy. Elastic fibers are associated mainly with blood vessels and otherwise are rare in the cortex. Scattered throughout the cortical tissue are the ovarian follicles, whose size varies with their stage of development. Immediately beneath the surface epithelium, the connective tissue of the cortex is less cellular and more compact, forming a dense layer called the tunica albuginea. The stroma of the medulla consists of a loose connective tissue that is less cellular than that of the cortex and contains many elastic fibers and smooth muscle cells. Numerous large, tortuous blood vessels, lymphatics, and nerves also are present in the medulla. At puberty, the human ovary contains 300,000 to 400,000 ova embedded in the cortical stroma, but only a few reach maturity and are ovulated. During the menstrual cycle, several follicles (15-25) begin to grow and develop, but only one attains full maturity; the rest degenerate. The size of the follicle and the thickness of the epithelial envelope vary with the stage of development. During their growth, the follicles undergo a sequence of changes in which primordial, primary, secondary, and mature follicles can be distinguished.
Cardiac muscle develops from mesenchyme (the myoepithelial mantle) that envelops the endocardial tube of the embryonic heart medicine mountain scout ranch cyklokapron 500 mg otc. With the synthesis of myofilaments symptoms melanoma generic cyklokapron 500mg without a prescription, the cells elongate and become myoblasts medicine misuse definition generic cyklokapron 500mg mastercard, which soon begin rhythmic contractions treatment lice generic 500mg cyklokapron. Cell division continues into postnatal life but subsequently gives way to hypertrophy as the means of further growth. The sites of desmosomal unions between cells transform into the intercalated discs. Formation of Ttubules characterizes the final stage of development of mammalian cardiac muscle. The tubules arise from invaginations of the sarcolemma late in the prenatal period. Smooth muscle arises from the mesenchyme at various sites in the embryo where smooth muscle ordinarily will occur in the adult. The undifferentiated cells in these areas continue to divide until they become confluent, after which individual cells, the myoblasts, differentiate. The myoblasts elongate and take on the fusiform shape characteristic of adult smooth muscle cells; early in development the myoblasts resemble fibroblasts. The cytoplasm contains abundant free ribosomes, granular endoplasmic reticulum, and mitochondria, and Golgi complexes are prominent. Few filaments are present initially, but as the smooth muscle cell develops, bundles of thin filaments appear in association with dense bodies. Concomitant with the appearance of filaments, cytoplasmic organelles decrease in number. Attachment plaques along the cell membrane, plasmalemmal vesicles, and a external lamina appear at the same time or a little later than the thick filaments. In the newborn, myofilaments are small and usually restricted to the cytoplasm at the edge of the cell. Granular endoplasmic reticulum and Golgi elements are prominent and extend throughout the cell. The smooth muscle of the iris is commonly thought to be derived from cells near the margin of the optic cup and therefore is of ectodermal origin. Summary Nerve impulses reaching the myoneural junctions of skeletal muscle cells cause release of acetylcholine contained within the synaptic vesicles. This neurotransmitter diffuses across the synaptic trough, the surface area of which is greatly increased by the junctional folds. Acetylcholine causes depolarization of the sarcolemma at the motor end-plate, from which an excitation wave (action potential) sweeps over the surface of the muscle fiber and, by means of the T-system, is delivered to all the myofibrils throughout the fiber. At the triads, the impulse is passed to the sarcoplasmic reticulum, causing release of calcium ions from the terminal cisternae. Free calcium ions activate the myosin-actin interaction through the intervention of tropomyosin and troponin. Troponin acts as a calcium receptor that, in the presence of increased calcium ion, is thought to cause conformational changes in the tropomyosin, bringing about the interaction of myosin and actin. As the actin filaments slide past the myosin filaments to penetrate more deeply between them, the length of each sarcomere is reduced, resulting in an overall shortening of each myofibril and thus of each fiber. The tension generated is transmitted in succession to the sarcolemma, the external lamina, the connective tissue sheath, and then to a tendon or other muscle attachment. Muscle spindles serve as stretch receptors and coordinate the degree of muscle contraction with the strength of the stimulus. Tendon organs sense the stresses produced by the muscle contractions and prevent them from becoming excessive. The function of skeletal muscle depends on the precise alignment of actin and myosin filaments within each myofibril. A complex skeleton of accessory proteins (myomesin, -actinin, desmin, titin) supports the myofilaments, maintains their alignment, and holds them in register to each other. Intermediate filaments of the cytoskeleton (desmin) link adjacent myofibrils and maintain their register as well as linking them to the lateral aspects of the sarcolemma.
Antibody levels and effector T-cell activity gradually decline after an infection is cleared medications pancreatitis order cyklokapron 500 mg on line. Reinfection at later times leads to symptoms stomach ulcer buy discount cyklokapron 500 mg rapid increases in antibody and effector T cells owing to symptoms 5 days past ovulation cheap cyklokapron 500mg immunological memory symptoms strep throat discount 500 mg cyklokapron overnight delivery, and infection can be mild or even inapparent. Resolution of an infection is accompanied by the death of most of the effector cells and the generation of memory cells. When an infection is effectively repelled by the adaptive immune system, two things occur. The first is the removal of most of the effector cells, as part of the restoration of tissue integrity. The immune system has well-developed mechanisms for getting rid of cells that have outlasted their usefulness. Most unwanted effector cells die by apoptosis, a process used by all multicellular eukaryotic organisms to remove unwanted cells. The actions of effector cells remove the specific stimulus that originally recruited them. The dying cells are rapidly cleared by macrophages, which recognize the membrane lipid phosphatidylserine. This lipid is normally found only on the inner surface of the plasma membrane, but in apoptotic cells it rapidly redistributes to the outer surface, where it can be recognized by specific receptors on phagocytes. Thus, not only does the ending of infection lead to the removal of the pathogen, it also leads to the loss of most of the pathogen-specific effector cells. However, some of the effector cells are retained, and these provide the raw material for memory T-cell and B-cell responses. These are crucially important to the operation of the adaptive immune system, as we will argue in Chapter 15. The memory T cells, which we will consider at the end of this chapter, are retained virtually forever. However, the mechanisms underlying the decision to induce apoptosis in the majority of effector cells and retain only a few are not known. It seems likely that the answer will lie in the cytokines produced by the environment or by the T cells themselves. The adaptive immune response is required for effective protection of the host against pathogenic microorganisms. The response of the innate immune system to pathogens helps initiate the adaptive immune response, as interactions with these pathogens lead to the production of cytokines and the activation of dendritic cells to activated antigenpresenting cell status. The antigens of the pathogen are transported to local lymphoid organs by these migrating antigen-presenting cells and presented to antigen-specific naive T cells that continuously recirculate through the lymphoid organs. T-cell priming and the differentiation of armed effector T cells occur here on the surface of antigenloaded dendritic cells, and the armed effector T cells either leave the lymphoid organ to effect cell-mediated immunity in sites of infection in the tissues, or remain in the lymphoid organ to participate in humoral immunity by activating antigen-binding B cells. Ideally, the adaptive immune response eliminates the infectious agent and provides the host with a state of protective immunity against reinfection with the same pathogen. The immune system may be viewed as an organ that is distributed throughout the body to provide host defense against pathogens wherever these may enter or spread. Within the immune system, a series of anatomically distinct compartments can be distinguished, each of which is specially adapted to generate a response to pathogens present in a particular set of body tissues. The previous part of the chapter illustrated the general principles underlying the initiation of an adaptive immune response in the compartment comprising the peripheral lymph nodes and spleen. This is the compartment that responds to antigens that have entered the tissues or spread into the blood. Two further distinct compartments are those of the body cavities (peritoneum and pleura) and the skin. The first is that immune responses induced within one compartment are largely confined in expression to that particular compartment. The second is that lymphocytes are restricted to particular compartments by expression of homing receptors that are bound by ligands, known as addressins, that are specifically expressed within the tissues of the compartment. We will illustrate the concept of compartmentalization of the immune system by considering the mucosal immune system. They are thin and permeable barriers to the interior of the body because of their physiological activities in gas exchange (the lungs), food absorption (the gut), sensory activities (eyes, nose, mouth, and throat), and reproduction (uterus and vagina). The necessity for permeability of the surface lining these sites creates obvious vulnerability to infection and it is not surprising that the vast majority of infectious agents invade the human body through these routes.
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