File Name: innate and adaptive immunity .zip
- Research Area
- Innate and Adaptive Immunity
- Difference between Innate and Adaptive Immunity
- An introduction to immunology and immunopathology
Metrics details. Beyond structural and chemical barriers to pathogens, the immune system has two fundamental lines of defense: innate immunity and adaptive immunity.
Innate immunity is the first immunological mechanism for fighting against an intruding pathogen. It is a rapid immune response, initiated within minutes or hours after aggression, that has no immunologic memory. Adaptive immunity, on the other hand, is antigen-dependent and antigen-specific; it has the capacity for memory, which enables the host to mount a more rapid and efficient immune response upon subsequent exposure to the antigen.
There is a great deal of synergy between the adaptive immune system and its innate counterpart, and defects in either system can provoke illness or disease, such as inappropriate inflammation, autoimmune diseases, immunodeficiency disorders and hypersensitivity reactions.
This article provides a practical overview of innate and adaptive immunity, and describes how these host defense mechanisms are involved in both heath and illness.
There are continuous advances in our current understanding of the immune system and how it functions to protect the body from infection. Given the complex nature of this subject, it is beyond the scope of this article to provide an in-depth review of all aspects of immunology.
Rather, the purpose of this article is to provide medical students, medical residents, primary-care practitioners and other healthcare professionals with a basic introduction to the main components and function of the immune system and its role in both health and disease. This article will also serve as a backgrounder to the immunopathological disorders discussed in the remainder of this supplement.
The immune system refers to a collection of cells, chemicals and processes that function to protect the skin, respiratory passages, intestinal tract and other areas from foreign antigens, such as microbes organisms such as bacteria, fungi, and parasites , viruses, cancer cells, and toxins.
Innate immunity represents the first line of defense to an intruding pathogen. It is an antigen-independent non-specific defense mechanism that is used by the host immediately or within hours of encountering an antigen. Adaptive immunity, on the other hand, is antigen-dependent and antigen-specific and, therefore, involves a lag time between exposure to the antigen and maximal response.
The hallmark of adaptive immunity is the capacity for memory which enables the host to mount a more rapid and efficient immune response upon subsequent exposure to the antigen. Innate and adaptive immunity are not mutually exclusive mechanisms of host defense, but rather are complementary, with defects in either system resulting in host vulnerability or inappropriate responses [ 1 , 2 , 3 ]. Innate immunity can be viewed as comprising four types of defensive barriers: anatomic skin and mucous membrane , physiologic temperature, low pH and chemical mediators , endocytic and phagocytic, and inflammatory.
Cells and processes that are critical for effective innate immunity to pathogens that evade the anatomic barriers have been widely studied. Innate immunity to pathogens relies on pattern recognition receptors PRRs which allow a limited range of immune cells to detect and respond rapidly to a wide range of pathogens that share common structures, known as pathogen associated molecular patterns PAMPs.
Examples of these include bacterial cell wall components such as lipopolysaccharides LPS and double-stranded ribonucleic acid RNA produced during viral infection. An important function of innate immunity is the rapid recruitment of immune cells to sites of infection and inflammation through the production of cytokines and chemokines small proteins involved in cell—cell communication and recruitment. Cytokine production during innate immunity mobilizes many defense mechanisms throughout the body while also activating local cellular responses to infection or injury.
Key inflammatory cytokines released during the early response to bacterial infection are: tumour necrosis factor TNF , interleukin 1 IL-1 and interleukin 6 IL These cytokines are critical for initiating cell recruitment and the local inflammation which is essential for clearance of many pathogens. They also contribute to the development of fever.
Dysregulated production of such inflammatory cytokines is often associated with inflammatory or autoimmune disease, making them important therapeutic targets. The complement system is a biochemical cascade that functions to identify and opsonize coat bacteria and other pathogens. It renders pathogens susceptible to phagocytosis, a process by which immune cells engulf microbes and remove cell debris, and also kills some pathogens and infected cells directly.
The phagocytic action of the innate immune response promotes clearance of dead cells or antibody complexes and removes foreign substances present in organs, tissues, blood and lymph. It can also activate the adaptive immune response through the mobilization and activation of antigen-presenting cells APCs discussed later [ 1 , 3 ]. Numerous cells are involved in the innate immune response such as phagocytes macrophages and neutrophils , dendritic cells, mast cells, basophils, eosinophils, natural killer NK cells and innate lymphoid cells.
Phagocytes are sub-divided into two main cell types: neutrophils and macrophages. Both of these cells share a similar function: to engulf phagocytose microbes and kill them through multiple bactericidal pathways. In addition to their phagocytic properties, neutrophils contain granules and enzyme pathways that assist in the elimination of pathogenic microbes.
Unlike neutrophils which are short-lived cells , macrophages are long-lived cells that not only play a role in phagocytosis, but are also involved in antigen presentation to T cells see Fig.
Characteristics and function of cells involved in innate immunity [ 1 , 3 , 4 ]. Dendritic cells also phagocytose and function as APCs, initiating the acquired immune response and acting as important messengers between innate and adaptive immunity.
Mast cells and basophils share many salient features with each other, and both are instrumental in the initiation of acute inflammatory responses, such as those seen in allergy and asthma. Unlike mast cells, which generally reside in the connective tissue surrounding blood vessels and are particularly common at mucosal surfaces, basophils reside in the circulation. Eosinophils are granulocytes that possess phagocytic properties and play an important role in the destruction of parasites that are often too large to be phagocytosed.
Along with mast cells and basophils, they also control mechanisms associated with allergy and asthma. Natural killer NK cells play a major role in the rejection of tumours and the destruction of cells infected by viruses. Destruction of infected cells is achieved through the release of perforins and granzymes proteins that cause lysis of target cells from NK-cell granules which induce apoptosis programmed cell death [ 4 ]. Innate lymphoid cells ILCs play a more regulatory role.
Depending on their type i. The main characteristics and functions of the cells involved in the innate immune response are summarized in Fig. The development of adaptive immunity is aided by the actions of the innate immune system, and is critical when innate immunity is ineffective in eliminating infectious agents. Adaptive immune responses are the basis for effective immunization against infectious diseases. The cells of the adaptive immune system include: antigen-specific T cells, which are activated to proliferate through the action of APCs, and B cells which differentiate into plasma cells to produce antibodies.
T cells derive from hematopoietic stem cells in bone marrow and, following migration, mature in the thymus. These cells express a series of unique antigen-binding receptors on their membrane, known as the T-cell receptor TCR.
Each T cell expresses a single type of TCR and has the capacity to rapidly proliferate and differentiate if it receives the appropriate signals. As previously mentioned, T cells require the action of APCs usually dendritic cells, but also macrophages, B cells, fibroblasts and epithelial cells to recognize a specific antigen.
The MHC protein displays fragments of antigens peptides when a cell is infected with an intracellular pathogen, such as a virus, or has phagocytosed foreign proteins or organisms [ 2 , 3 ]. T cells have a wide range of unique TCRs which can bind to specific foreign peptides. During the development of the immune system, T cells that would react to antigens normally found in our body are largely eliminated.
T cells are activated when they encounter an APC that has digested an antigen and is displaying the correct antigen fragments peptides bound to its MHC molecules. The opportunities for the right T cells to be in contact with an APC carrying the appropriate peptide MHC complex are increased by the circulation of T cells throughout the body via the lymphatic system and blood stream and their accumulation together with APCs in lymph nodes.
Clonal expansion of cytotoxic T cells produces effector cells which release substances that induce apoptosis of target cells. Upon resolution of the infection, most effector cells die and are cleared by phagocytes. However, a few of these cells are retained as memory cells that can quickly differentiate into effector cells upon subsequent encounters with the same antigen [ 2 , 3 ]. Adaptive immunity: T-cell and B-cell activation and function.
These cells have no cytotoxic or phagocytic activity, and cannot directly kill infected cells or clear pathogens. Once activated, Th cells release cytokines that influence the activity of many cell types, including the APCs that activate them. Th1-derived cytokines also contribute to the differentiation of B cells to make opsonizing antibodies that enhance the efficiency of phagocytes.
An inappropriate Th1 response is associated with certain autoimmune diseases. The Th2 response is characterized by the release of cytokines IL-4, 5 and 13 which are involved in the development of immunoglobulin E IgE antibody-producing B cells, as well as the development and recruitment of mast cells and eosinophils that are essential for effective responses against many parasites.
In addition, they enhance the production of certain forms of IgG that aid in combatting bacterial infection. As mentioned earlier, mast cells and eosinophils are instrumental in the initiation of acute inflammatory responses, such as those seen in allergy and asthma. Th17 cells have been more recently described. They are characterized by the production of cytokines of the IL family, and are associated with ongoing inflammatory responses, particularly in chronic infection and disease.
Like cytotoxic T cells, most Th cells will die upon resolution of infection, with a few remaining as Th memory cells [ 2 , 3 ].
T reg cells limit and suppress immune responses and, thereby, may function to control aberrant responses to self-antigens and the development of autoimmune disease. T reg cells may also help in the resolution of normal immune responses, as pathogens or antigens are eliminated. B cells arise from hematopoietic stem cells in the bone marrow and, following maturation, leave the marrow expressing a unique antigen-binding receptor on their membrane.
Unlike T cells, B cells can recognize antigens directly, without the need for APCs, through unique antibodies expressed on their cell surface. The principal function of B cells is the production of antibodies against foreign antigens which requires their further differentiation [ 2 , 3 ]. Under certain circumstances, B cells can also act as APCs. When activated by foreign antigens to which they have an appropriate antigen specific receptor, B cells undergo proliferation and differentiate into antibody-secreting plasma cells or memory B cells see Fig.
These cells can be called upon to respond quickly by producing antibodies and eliminating an antigen upon re-exposure. Plasma cells, on the other hand, are relatively short-lived cells that often undergo apoptosis when the inciting agent that induced the immune response is eliminated. However, these cells produce large amounts of antibody that enter the circulation and tissues providing effective protection against pathogens.
Given their function in antibody production, B cells play a major role in the humoral or antibody-mediated immune response as opposed to the cell-mediated immune response, which is governed primarily by T cells [ 2 , 3 ]. Antibody-mediated immunity is the branch of the acquired immune system that is mediated by B-cell-antibody production. Local Th cells secrete cytokines that help the B cell multiply and direct the type of antibody that will be subsequently produced.
Some cytokines, such as IL-6, help B-cells to mature into antibody-secreting plasma cells. The secreted antibodies bind to antigens on the surface of pathogens, flagging them for destruction through complement activation, opsonin promotion of phagocytosis and pathogen elimination by immune effector cells.
Upon elimination of the pathogen, the antigen—antibody complexes are cleared by the complement cascade see Fig. IgG antibodies can be further subdivided into structurally distinct subclasses with differing abilities to fix complement, act as opsonins, etc. The major classes of antibodies have substantially different biological functions and recognize and neutralize specific pathogens.
Antibodies play an important role in containing virus proliferation during the acute phase of infection. However, they are not generally capable of eliminating a virus once infection has occurred.
Once an infection is established, cell-mediated immune mechanisms are most important in host defense against most intracellular pathogens. Cell-mediated immunity does not involve antibodies, but rather protects an organism through [ 2 ]:. The activation of antigen-specific cytotoxic T cells that induce apoptosis of cells displaying foreign antigens or derived peptides on their surface, such as virus-infected cells, cells with intracellular bacteria, and cancer cells displaying tumour antigens;.
The activation of macrophages and NK cells, enabling them to destroy intracellular pathogens; and. Cell-mediated immunity is directed primarily at microbes that survive in phagocytes as well as those that infect non-phagocytic cells. This type of immunity is most effective in eliminating virus-infected cells and cancer cells, but can also participate in defending against fungi, protozoa, cancers, and intracellular bacteria.
Innate and Adaptive Immunity
Defense against microbes is mediated by the early reactions of innate immunity and the later responses of adaptive immunity. Figure 1, 2; Table 1. Innate immunity also called natural or native immunity provides the early line of defense against microbes. It consists of cellular and biochemical defense mechanisms that are in place even before infection and are poised to respond rapidly to infections. The mechanisms of innate immunity are specific for structures that are common to groups of related microbes and may not distinguish fine differences between microbes.
Metrics details. Beyond structural and chemical barriers to pathogens, the immune system has two fundamental lines of defense: innate immunity and adaptive immunity. Innate immunity is the first immunological mechanism for fighting against an intruding pathogen. It is a rapid immune response, initiated within minutes or hours after aggression, that has no immunologic memory. Adaptive immunity, on the other hand, is antigen-dependent and antigen-specific; it has the capacity for memory, which enables the host to mount a more rapid and efficient immune response upon subsequent exposure to the antigen. There is a great deal of synergy between the adaptive immune system and its innate counterpart, and defects in either system can provoke illness or disease, such as inappropriate inflammation, autoimmune diseases, immunodeficiency disorders and hypersensitivity reactions.
Clinical and Basic Immunodermatology pp Cite as. The skin immune system is the complex network of cells that are able to mount an immune response in the skin. The immune response can be divided into innate and adaptive arms. This is highly relevant to both systemic immunity, as well as immunity in the skin. The innate immune system responds rapidly to microbial insults, but is thought to have no memory or specificity. The adaptive immune system, composed of B lymphocytes and T lymphocytes, requires more time to respond to a threatening challenge to the host, but is responsible for long-lasting memory and specificity, and the development of an effector pool of lymphocytes for humoral or cell mediated immunity. Virtually all cells that reside in the skin play some role in the function of the skin immune system.
Synopsis: In this lecture we will review basic concepts in immunology, including the cells of the immune system, the innate and adaptive immune responses.
Difference between Innate and Adaptive Immunity
What happen if foreign invader attack the body to the second time in innate immunity? How innate immunity will response? An Ag can specifically bind to an Ab molecule. An Ag i.
An introduction to immunology and immunopathology
As mentioned in Unit 5, the body has two immune systems: innate immunity and adaptive immunity. Unit 5 dealt with innate immunity. In Unit 6 we will cover adaptive immunity. Let's first again briefly compare acquired and innate immunity. Innate immunity is an antigen-nonspecific defense mechanisms that a host uses immediately or within several hours after exposure to almost any microbe.
1-5. Most infectious agents induce inflammatory responses by activating innate immunity
NCBI Bookshelf. New York: Garland Science; The macrophages and neutrophils of the innate immune system provide a first line of defense against many common microorganisms and are essential for the control of common bacterial infections. However, they cannot always eliminate infectious organisms, and there are some pathogens that they cannot recognize. The lymphocytes of the adaptive immune system have evolved to provide a more versatile means of defense which, in addition, provides increased protection against subsequent reinfection with the same pathogen. The cells of the innate immune system, however, play a crucial part in the initiation and subsequent direction of adaptive immune responses, as well as participating in the removal of pathogens that have been targeted by an adaptive immune response.
In Silico Immunology pp Cite as. Innate immune responses recognise generic targets on pathogens using germline encoded receptors, whereas adaptive immune responses recognise specific targets using randomly generated receptors which have an essentially unlimited recognition repertoire. Interactions between innate and adaptive forms of immune recognition are increasingly being recognised as essential for the effective functioning of the immune response. Examples given here demonstrate the advantages of integrating pre-programmed recognition rapid response using widely distributed receptors with random repertoire recognition open repertoire for specific recognition of novel targets, with memory. The interactions between innate and adaptive immunity are many, complex, and bidirectional, with innate mechanisms being instrumental in the initiation of adaptive responses, and controlling the type of adaptive response induced; innate effector mechanisms are also recruited in the effector phase of adaptive responses. The challenge is now to abstract the essential components of the innate-adaptive interaction in order to utilise this concept in alternative contexts. Unable to display preview.