Like no other text, it combined an experimental emphasis with extensive pedagogical features to help students grasp basic concepts. Now in a thoroughly updated new edition, Kuby Immunology remains the only undergraduate introduction to immunology written by teachers of the course. In the Kuby tradition, authors Jenni Punt, Sharon Stranford, Patricia Jones, and Judy Owen present the most current topics in an experimental context, conveying the excitement of scientific discovery, and highlight important advances, but do so with the focus on the big picture of the study of immune response, enhanced by unsurpassed pedagogical support for the first-time learner. Punt, Stranford, Jones, and Owen bring an enormous range of teaching and research experiences to the text, as well as a dedication to continue the experiment-based, pedagogical-driven approach of Janis Kuby.
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Peter C. Doherty Rolf M. Zinkernagel Australia Switzerland Role of major histocompatibility complex in antigen recognition by by T cells Initially, a different serum component was thought to be responsible for each activity, but during the s, mainly through the efforts of Elvin Kabat, a fraction of serum first called gamma-globulin now immunoglobulin was shown to be responsible for all these activities.
The active molecules in the immunoglobulin fraction are called antibodies. Because immunity was mediated by antibodies contained in body fluids known at the time as humors , it was called humoral immunity.
In , even before the discovery that a serum component could transfer immunity, Elie Metchnikoff demonstrated that cells also contribute to the immune state of an animal. He observed that certain white blood cells, which he termed phagocytes, were able to ingest phagocytose microorganisms and other foreign material. Noting that these phagocytic cells were more active in animals that had been immunized, Metchnikoff hypothesized that cells, rather than serum components, were the major effector of immunity.
The active phagocytic cells identified by Metchnikoff were likely blood monocytes and neutrophils see Chapter 2. It was later shown that both are correct—immunity requires both cellular and humoral responses. It was difficult to study the activities of immune cells before the development of modern tissue culture techniques, whereas studies with serum took advantage of the ready availability of blood and established biochemical techniques.
Because of these technical problems, information about cellular immunity lagged behind findings that concerned humoral immunity. In a key experiment in the s, Merrill Chase succeeded in transferring immunity against the tuberculosis organism by transferring white blood cells between guinea pigs. This demonstration helped to rekindle interest in cellular immunity. With the emergence of improved cell culture techniques in the s, the lymphocyte was identified as the cell responsible for both cellular and humoral immunity.
The controversy about the roles of humoral and cellular immunity was resolved when the two systems were shown to be intertwined, and that both systems were necessary for the immune response. Early Theories Attempted to Explain the Specificity of the Antibody— Antigen Interaction One of the greatest enigmas facing early immunologists was the specificity of the antibody molecule for foreign material, or antigen the general term for a substance that binds with a specific antibody.
Around , Jules Bordet at the Pasteur Institute expanded the concept of immunity by demonstrating specific immune reactivity to nonpathogenic substances, such as red blood cells from other species. Serum from an animal inoculated previously with material that did not cause infection would react with this material in a specific manner, and this reactivity could be passed to other animals by transferring serum from the first.
The work of Karl Landsteiner and those who followed him showed that injecting an animal with almost any organic chemical could induce production of antibodies that would bind specifically to the chemical. These studies demonstrated that antibodies have a capacity for an almost unlimited range of reactivity, including responses to compounds that had only recently been synthesized in the laboratory and had not previously existed in nature.
In addition, it was shown that molecules differing in the smallest detail could be distinguished by their reactivity with different antibodies. Two major theories were proposed to account for this specificity: the selective theory and the instructional theory. The earliest conception of the selective theory dates to Paul Ehrlich in Borrowing a concept used by Emil Fischer in to explain the interaction between an enzyme and its substrate, Ehrlich proposed that binding of the receptor to an infectious agent was like the fit between a lock and key.
Ehrlich suggested that interaction between an infectious agent and a cell-bound receptor would induce the cell to produce and release more receptors with the same specificity.
In the s and s, the selective theory was challenged by various instructional theories, in which antigen played a central role in determining the specificity of the antibody molecule. According to the instructional theories, a particular antigen would serve as a template around which antibody would fold.
The antibody molecule would thereby assume a configuration complementary to that of the antigen template. This concept was first postulated by Friedrich Breinl and Felix Haurowitz about and redefined in the s in terms of protein folding by Linus Pauling.
The instructional theories were formally disproved in the s, by which time information was emerging about the structure of DNA, RNA, and protein that would offer new insights into the vexing problem of how an individual could make antibodies against almost anything. In the s, selective theories resurfaced as a result of new experimental data and, through the insights of Niels Jerne, David Talmadge, and F.
Macfarlane Burnet, were refined into a theory that came to be known as the clonalselection theory. According to this theory, an individual lymphocyte expresses membrane receptors that are specific for a distinct antigen. This unique receptor specificity is determined before the lymphocyte is exposed to the antigen. Binding of antigen to its specific receptor activates the cell, causing it to proliferate into a clone of cells that have the same immunologic specificity as the parent cell.
The clonalselection theory has been further refined and is now accepted as the underlying paradigm of modern immunology. The Immune System Includes Innate and Adaptive Components Immunity—the state of protection from infectious disease —has both a less specific and more specific component.
The less specific component, innate immunity, provides the first line of defense against infection. Most components of innate immunity are present before the onset of infection and constitute a set of disease-resistance mechanisms that are not specific to a particular pathogen but that include cellular and molecular components that recognize classes of molecules peculiar to frequently encountered pathogens.
Phagocytic cells, such as macrophages and neutrophils, barriers such as skin, and a variety of antimicrobial compounds synthesized by the host all play important roles in innate immunity. In contrast to the broad reactivity of the innate immune system, which is uniform in all members of a species, the specific component, adaptive immunity, does not come into play until there is an antigenic challenge to the organism.
The major agents of adaptive immunity are lymphocytes and the antibodies and other molecules they produce. In general, most of the microorganisms encountered by a healthy individual are readily cleared within a few days by defense mechanisms of the innate immune system before they activate the adaptive immune system.
Innate Immunity Innate immunity can be seen to comprise four types of defensive barriers: anatomic, physiologic, phagocytic, and inflammatory Table The skin and the surface of mucous membranes are included in this category because they are effective barriers to the entry of most microorganisms. The epidermis contains several layers of tightly packed epithelial cells. The outer epidermal layer consists of dead cells and is filled with a waterproofing protein called keratin. The dermis, which is composed of connective tissue, contains blood vessels, hair follicles, sebaceous glands, and sweat glands.
The sebaceous glands are associated with the hair follicles and produce an oily secretion called sebum. Sebum consists of lactic acid and fatty acids, which maintain the pH of the skin between 3 and 5; this pH inhibits the growth of most microorganisms. A few bacteria that metabolize sebum live as commensals on the skin and sometimes cause a severe form of acne. One acne drug, isotretinoin Accutane , is a vitamin A derivative that prevents the formation of sebum.
Breaks in the skin resulting from scratches, wounds, or abrasion are obvious routes of infection. The skin may also be penetrated by biting insects e. The protozoan that causes malaria, for example, is deposited in humans by mosquitoes when they take a blood meal. Similarly, bubonic plague is spread by the bite of fleas, and Lyme disease is spread by the bite of ticks. The conjunctivae and the alimentary, respiratory, and urogenital tracts are lined by mucous membranes, not by the dry, protective skin that covers the exterior of the body.
These Summary of nonspecific host defenses Type.
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