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For queries regarding Research Topics, Editorial Board applications, and journal development, please contact immunology frontiersin. Fees Article types Author guidelines Review guidelines Submission checklist Contact editorial office Submit your manuscript Editorial board. About Frontiers Research Topics. During the encounter, if some damage in the house occurs, that is just like a hypersensitivity reaction. Now, if the security guard becomes dishonest and corrupt, it starts damaging the house like autoimmune diseases, where the immune system is defective.
The above example shows that nature is present everywhere and has a similar system at a micro-level in our body and macro-level in our surroundings. This is defined as the study of molecules, cells, organs, and the system responsible for the recognition and disposal of nonself foreign substances. The function of the immune system is to recognize the nonself from the self to defend the body from the nonself.
Immunology is one of the most developing medical sciences. The following are some of its recent advances:. The immune system is the defensive system of our body and has two types: specific and non-specific.
This immunity protects us from various pathogens and is the first line of defense. Non-specific immunity takes place through the following means:. This immunity protects us from various specific pathogens and has a specific response for a particular antigen. Specific immunity takes place through the following means:. Let us look at an example of specific immunity. The following figure shows a child infected with smallpox and later recovering.
During this process, the immune system recognized R smallpox, produced specific S antibodies, and kept memory M of the antigen; this RSM process is the backbone of the immune system. Afterward, whenever smallpox infects this child again, the specific immunity will notice that it is the same antigen and produce an exaggerated immune response, not allowing the infection; but exposure to other viruses antigens will not show such specific immunity but will instead result in repeating the RSM process.
Fig 2: Recognition, specificity, and memory of the specific immunity. 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 — 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. Table 1 summarizes the non-specific host-defense mechanisms for each of these barriers. 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. Summary of non-specific host-defense mechanisms for barriers of innate immunity [ 1 ].
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. IgE antibodies are also associated with allergic reactions see Table 2. Therefore, an imbalance of Th2 cytokine production is associated with the development of atopic allergic conditions.
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 ].
Major functions of human Ig antibodies [ 5 ]. 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.
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