This chapter begins with the description of adaptive immunity. It notes that the term uses the word adaptive because of the way this type of immunity allows both species and individuals to tailor-make their own set of recognition molecules, adapted to the microbes they actually encounter. In immunological language, the system displays high specificity and memory. The chapter then explores the other properties which distinguish lymphocytes from other immunological cells. It brings out the essential differences between lymphocytes and phagocytic cells. The chapter also outlines the lymphoid system, the total mass of lymphocytes in the body, then explains the fundamental part of lymphocyte function. It then considers the antigen, antigen-recognition molecules, clonal selection, and memory. The chapter concludes by discussing the regulation of adaptive immunity.
Chapter
Adaptive immunity: introduction
Chapter
Allergies and Hypersensitivity Reactions
Stephen Juris
This chapter explores the various hypersensitivity reactions that can occur, which depend on the immune system's ability to recognize foreign antigens through the action of cellular receptors. It looks at the various types of hypersensitivity reactions and describes how these responses are identical to the ways in which the body reacts to foreign pathogens. It also reviews the four types of hypersensitivity reactions which differ based on the immune response: Type I, Type II, Type III, and Type IV. The chapter points out that Type I hypersensitivity reactions are driven by allergen recognition by IgE bound to granulocytes, while Type II hypersensitivity reactions are driven by the action of soluble immunoglobulins. Type III hypersensitivity reactions are caused by inefficient clearance of soluble antigens bound as small immune complexes in the bloodstream, while Type IV hypersensitivity is an induction of the cellular arm of the adaptive immune response.
Chapter
Allergy
This chapter explains the exaggerated response to common environmental substances which we know as allergies. It acknowledges the increasing incidence of allergy disease. The chapter refers to allergy as a type I hypersensitivity reaction then recognizes IgE antibodies' two-stage reaction: induction/sensitization and reactive phases. It notes how component resolved diagnostics (CRD) can define disease eliciting components and help develop avoidance advice. Moreover, the chapter indicates allergen-specific IgG antibody testing, which helps in the diagnosis of respiratory conditions caused by chronic exposure to inhaled allergens. It clarifies how allergy diagnosis is based on clinical assessment supplemented by laboratory investigations. In addition, the chapter clarifies that quality assurance can be problematic due to no reference standards available for allergen preparation.
Chapter
The antibody response
This chapter examines how B-cells and T-cells, acting together, give rise to the production of antibody molecules: the antibody response. It begins with discussing the activation of B-cells, which occurs mainly in the lymphoid organs (the site depending on the route by which antigen arrives). The chapter then looks at the different sorts of antigen to activate B-cells in different ways, emphasizing the T-independent (Ti antigens) and T-dependent (TD). It then shifts to investigate how an immunoglobulin molecule on the surface of the B-cell switches on the intracellular mechanisms that lead to antibody formation. Next, the chapter outlines the consequences of the activation through the B-cell antigenreceptor complex. It also looks at the signals of T-cell activation, then reviews the B-cell memory and the antibody responses at mucosal surfaces.
Chapter
Antigen Recognition by T Lymphocytes
Stephen Juris
This chapter explores the important interactions between T cells and antigen-presenting cells, noting how through these interactions the adaptive immune system is able to recognize an infection. It explains the defining features of the T-cell receptor structure and shows how this allows it to be both diverse and to function in recognizing an MHC-peptide complex. It also reviews what are the molecular mechanisms of antigen processing and presentation by MHC class I and class II molecules. The chapter looks at the diversity in MHC molecules, which is a result of different MHC genes in the population. It shows that the maintenance of MHC diversity promotes organism survival in the evolutionary arms race against pathogens and causes problems for medical breakthroughs, such as tissue and hematopoietic stem cell transplantation.
Chapter
Autoimmune Diseases
Stephen Juris
This chapter explores problems that occur when tolerance to self-antigens is lost, noting that cells of the adaptive immune system undergo somatic recombination events to provide a diverse array of receptors at their surfaces. It analyses similarities between autoimmune diseases and hypersensitivity responses. While the antigens recognized in hypersensitivity reactions differ from those recognized in autoimmune, recognition prompts activation of adaptive immune responses that can be damaging and life-threatening. The chapter describes how autoimmune diseases are induced due to a lack of central or peripheral tolerance of the adaptive immune system. It highlights the failure of central and peripheral tolerance, which drives the onset of autoimmune disease and caused by both genetic and environmental factors.
Chapter
Autoimmune kidney disease
This chapter looks into autoimmune kidney diseases which could be divided between diseases associated with either antibodies to anti-neutrophil cytoplasmic antibodies (ANCA) or the glomerular basement membrane (GBM). The chapter notes vasculitis and its classifications, in terms of the following sizes: primary, secondary, and vessel. It points out that laboratory findings are necessary if we are to have direct diagnosis and treatment on ANCA-associated vasculitic syndromes, anti-GBM disease, and membranous nephropathy. In addition, the chapter refers to microscopic polyangiitis, granulomatosis with polyangiitis, eosiniphilic granulomatosis with polyangiitis, anti-GBM disease, and membranous nephropathy. The chapter notes the pathogenesis, treatment, and prognosis of renal related auto-antibodies as well. It explores the auto-antibodies in autoimmune kidney diseases.
Chapter
Autoimmune liver diseases
This chapter focuses on autoimmune liver diseases like autoimmune hepatitis (AIH), autoimmune sclerosing cholangitis (ASC), and primary biliary cirrhosis (PBC). Then, it looks at AIH, ASC, and PBC. It explains incidence, serology, and histopathology. The chapter also looks into the anti-smooth muscle antibody (SMA), anti-nuclear antibodies (ANA), anti-liver kidney microsomal antibody (LKM), anti-liver cytosol (LC 1), anti-soluble liver antigen (SLA). In addition, it explains that ASC has a disease characterized by inflammation of intra- and extrahepatic bile duct and hepatitis. PBC is the result of the destruction of the small intrahepatic bile ducts' epithelia. The chapter notes immunosuppression as a major therapeutic action. However, a therapeutic modality is required to manage bile acids when the biliary tree is involved.
Chapter
Autoimmune rheumatological disease
This chapter looks into rheumatic diseases. It looks at systemic lupus erythematosus (SLE) which is a multisystem disease affecting various organs in the body. The chapter recognizes that auto-antibodies are useful tools in the diagnosis and management of autoimmune rheumatic diseases. It presents the American College of Rheumatology's eleven diagnostic criteria. The chapter clarifies that the SLE's aetiology and auto-antibodies' role in pathogenesis remains unclear. In addition, it explores the antibodies in SLE, rheumatoid arthritis, scleroderma, Sjogren's syndrome, antiphospholid syndrome, polymyositis, and dermatomyositis. The chapter discusses auto-antibodies and anti-nuclear antibodies as well.
Chapter
Autoimmune skin disease
This chapter looks at autoimmune skin diseases such as pemphigoid and pemphigus. It notes how auto-antibodies are directed against protein at the dermal-epidermal junction in the pemphigoid, while pemphigus has auto-antibodies directed against cell junctions in the epidermis. The chapter indicates that specific auto-antibodies are associated with disruption of the skin structure leading to blistering. Biopsies or serums can demonstrate the presence of auto-antibodies as well. The chapter shows how treatment can include steroid, topic, systemic, steroid-sparing systemic immune suppression, high dose intravenous immunoglobulin, plasmapheresis in conjunction with systemic immune suppression, or monoclonal antibody therapy targeting B lymphocytes. In addition, it references other autoimmune blistering skin disorders such as dermatitis herpetiformis and toxic epidermal necrolysis.
Chapter
B cells and antibody
This chapter stresses the function of B lymphocytes (or B-cells), essentially little antibody factories, able to switch on high-rate synthesis and secretion of antibody molecules when stimulated by recognition of the right antigen. It tracks the coordinated recognition and response in B-cells, then explains the diversity of the antibody repertoire. The chapter then describes the antibody molecule and its classes and subclasses. All antibody molecules using a particular heavy-chain constant-region gene are defined as belonging to the same class. The differences between different classes are fairly major, but there are smaller differences within classes, which are referred to as subclasses. The chapter also investigates what exactly do antibodies recognize, then studies the antigenic determinant or epitope. Finally, the chapter elaborates on the affinity of the antibody-antigen bond, then emphasizes the functions of the antibody. It also considers another useful role of antibodies in the monitoring and treatment of disease.
Chapter
B-Cell-Mediated Adaptive Immunity
Stephen Juris
This chapter explores the function of B cells in the adaptive immune system. It analyses the molecular mechanisms that drive clonal selection and expansion of B cells to understand the means by which immunoglobulins act in a humoral immune response. It also notes how B cells can only become activated upon engagement of their cell-surface immunoglobulin with the antigen they are capable of recognizing. The chapter talks about the migration of B cells into secondary lymphoid tissues to monitor the presence of antigens, which is where they test for the presence of the antigen their immunoglobulin can recognize in the T-cell zone. It covers secreted immunoglobulins that have a variety of functions within the humoral adaptive immune response, including neutralization, activation of innate immune cells, protection of internal tissues, complement activation, and clearance of small immune complexes.
Chapter
Bacteria
This chapter focuses on a discussion about bacteria. It begins by looking at one part of the bacterium with a special significance for both disease and immunity: the cell wall. By providing information on bacterial classification, the chapter illustrates three types of bacterial cell wall which vary greatly in their structure: the gram-positive, mycobacterium, and the gram-negative. The chapter then moves to describe parasitic bacteria and makes a distinction between aerobic and anaerobic bacteria in certain infections. It also examines bacteria which do not fit neatly into classification. Next, the chapter examines bacterial replication, emphasizing the special features of gene expression and the method for bringing about rapid changes in genes: phase variation. The chapter also talks about the control of bacterial disease by antibiotics and the remarkable number of ways in which bacteria, far from being pathogenic, are useful and even essential to humans and animals.
Chapter
Bacterial disease and immunity
This chapter recalls the key properties of bacteria and the all-important distinction between extracellular and intracellular habitat. It reviews the immunological and therapeutic features of the most important pathogenic bacteria. The chapter begins with a discussion on staphylococcal infection, streptococcal infection, and clostridial infection. It then examines a disease of farm animals and farmers, anthrax, and other bacterial skin infections. The chapter also explicates the most important mycobacterial infection and one of the world's major health problems: tuberculosis. It then looks at respiratory infections, whooping cough, and the causes of meningitis. Next, the chapter considers some venereal diseases such as gonorrhoea and syphilis. It also considers plague, tularemia, and brucellosis, then discusses three infections: chlamydial infection, rickettsial infection, and mycoplasma infection.
Chapter
Cancer and the Immune System
Stephen Juris
This chapter investigates the interaction of the immune system with cancer cells, noting that cancer are the result of mutations within cells that affect the ability of the body to control the cell cycle and cell division. It considers proto-oncogenes and tumor suppressor genes as two key gene families that work to promote progression through the cell cycle. These are targets for mutations that can lead to the onset of cancer. It also highlights the battle that ensues between cancer cells, which aim to continue to survive and divide, and immune mechanisms, which aim to recognize and target harmful pathogens and cells. The chapter demonstrates how cancer cells avoid destruction by immune system effect or mechanisms by avoiding detection or manipulating the immune response that would normally target these cells. It talks about the recognition of the adaptive immune system of cancer cells through tumor-associated or tumor-specific antigens expressed by these cells.
Chapter
Cell-mediated responses
This chapter considers T-cell responses that do not involve B-cells and antibodies. It begins with examining the points of resemblance of the activation of macrophages by CD4 (helper) T-cells to the activation of B-cells, then explores the CD8 (cytotoxic) T-cell response. The chapter argues that both involve the selection and expansion of clones of effector cells from a tiny number of precursors and both result in the long-term survival of a population of memory cells that ensure a more vigorous secondary response to the same pathogen. The chapter analyzes how T-cells become activated for these responses. Next, the chapter highlights a more drastic approach to kill both the virus and its host-cell with the help of cytotoxic T lymphocytes (CTLs). It also elaborates on the t-cell memory and t-cell responses at mucosal surfaces.
Book
Angela Hall, Chris Scott, and Matthew Buckland
Clinical Immunology introduces the topic with an assessment of the clinical immunology laboratory. It then looks at immunoglobulins. The subject of allergies is examined next. The text contains a chapter that tackles autoimmune rheumatological disease and another chapter looks at autoimmune kidney disease. The text moves on to examine organ-specific autoimmunity. Other autoimmune diseases considered include autoimmune skin disease and autoimmune liver disease. The book also discusses neuroimmunology, flow cytometry, and primary immunodeficiency. Finally, the human immunodeficiency virus (HIV) is discussed. The book ends with a look at histocompatibility and immunogenetics.
Chapter
Complement
This chapter discusses the concept of complement, which is a vital part of the immune system. It lists ways to initiate complement activation: classical, lectin, and alternative pathways. The chapter notes the results of complement activation such as opsonization of targets, clearance of antigen-antibody complexes, inflammation, phagocyte recruitment, and formation of the membrane attack complex which can result in cell lysis. It adds how the deficiency in complement components might lead to infection susceptibility such as hereditary angioedema. The chapter explains the concentration of complement components and their functions, and shows how these could be assessed through laboratory tests. Moreover, it recognizes that most complement components, receptors, and regulators are polymorphic, some of which have several different allotypes.
Chapter
The Complement System
Stephen Juris
This chapter discusses some of the important components of the innate immune system that act to keep pathogens at bay. It highlights a key component of the innate immune system involving soluble plasma proteins: the complement system. The complement system constitutes a variety of proteins involved in recognizing and tagging foreign molecules and pathogens. The chapter points out how this family of proteins coats the surface of foreign molecules and cells, tagging them to mark them as candidates for destruction by innate immune cells. It explains how the complement system bears a remarkable similarity to the body's blood-clotting system as it involves a cascade of different proteins, each of which must be activated by cleavage via a protease to induce the next step in the process.
Chapter
Control of infectious disease: chemotherapy
This chapter examines the idea of using chemicals safely to attack microbes. It presents chemical substances which are used at four levels to kill pathogens: disinfectants, antiseptics, chemotherapy, and antibiotics. The chapter then shows that chemotherapy has been extremely successful against many bacteria, because their procaryotic structure offers several targets absent from eucaryotic cells. The chapter also elaborates on some antibacterial agents, highlighting the modern antibacterials such as the synthetic azo-dye sulphanilamide, the true antibiotics penicillin, and streptomycin. The chapter then shifts to investigate how antibiotic resistance can develop at several levels. It looks at the standard susceptibility test, biofilm, and bacterial interference. Next, the chapter analyzes the other problem with antibiotics, as with all drugs: toxicity. It then displays some of the effective drugs against eucaryotic infections.
