The most important thing in the immune system is the recognition of self and non-self. When a pathogen enters the body, the immune system receives a signal for an immune response. Part of that response is the production of IL-17, which provides a defense mechanism for the body. The research question for this study is: What are the effects of IL-17 on host defense against bacterial pathogens?
Bacteria can enter any part of the body, and the immune system will respond to them, but malfunction in the system can lead to various diseases such as autoimmune and infectious diseases. The immune system is divided into two parts: the innate immune system, which is a general system to protect the body, and the adaptive immune system, which protects the body by producing antibodies and memory cells.
Interleukins are essential components of the innate and adaptive immune system. They are specialized cytokines produced by activated macrophages and lymphocytes, and they are responsible for signaling between different cells of the immune system.
Proinflammatory cytokines produced by T-cells are the interleukins-17. IL-17 is responsible for the initiation and maturation of neutrophils, which are very important in the immune system against pathogens. IL-17 plays an important role in mammalian host defense against a wide range of pathogens.
IL-17 also contributes to the development of inflammatory reactions because it induces the expression of proinflammatory cytokines such as TNF-α, interleukin-1β, interleukin-6, and chemokines.
IL-17 is produced by different T cells, including TH17 cells and NK T cells. The rapid activation of NK T cells to release IL-17A may represent an important innate mechanism for recruiting neutrophils in response to bacterial infection, particularly at mucosal surfaces. Interleukin-17 has an orchestrating function in the mammalian immune response against bacteria, particularly for neutrophils.
Interleukin-17 may also play a role in chronic infections and autoimmune diseases.
The immune system is able to distinguish between self and non-self substances (such as bacteria). When bacteria are detected in the body, the immune system generates actions against them, killing them. Part of this response is the production of interleukin-17, which provides a defense mechanism to the body. The main question in this study is what the effects of interleukin-17 are on immunity when pathogenic bacteria enter the body.
Bacteria can enter any part of the body, and the immune system responds to the bacteria that enter the body. If it does not function properly, it can lead to various diseases such as autoimmune and infectious diseases. The immune system consists of two parts: the innate immune system and the adaptive immune system. The innate immune system works very generally to protect the body, while the adaptive immune system specifically responds to a pathogen, including through the formation of antibodies and memory cells.
List of abbreviations
- Cadmium Cluster of distinction
- FGF fibroblast growing factor
- IL interleukin
- K. pneumoniae Klebsiella pneumoniae
- MHC Major Histocompatibility composite
- NK Natural Killer
- TNF Tumor mortification factor
How bacteria enter the human organic structure
Bacterias can come in the organic structure via tegument, oral cavity, etc. The organic structure consists of many bacteriums that some born with these are commensals bacteriums.
The antigen acknowledgment is non the organic structure ‘s first line of defence. Simple barriers such as the tegument and the epithelial surfaces are the organic structure ‘s first line of defence ; they do n’t hold specific or unconditioned protective systems, which limit the entry of potentially invasive beings. For illustration fatty acids produced by the tegument are toxic to many beings.
Through the production of antibacterial proteins ( colicins ) , commensal bacteriums can restrict the pathogen invasion.
The acknowledgment of bacterial constituents is the organic structure ‘s 2nd line of defence.
There are several ways to acknowledge the beings who enter the tissues, for illustration the old phylogenetically mechanisms the antigen-specific receptors of either B cells or T cells.[ 1 ]
The immune system
The map of the immune system is protection for the organic structure against infectious beings (pathogens). The immune system is divided into two parts: the adaptive immune system (specific immune system) and the innate system (non-specific immune system).
The origins of all cells in the immune system are from the bone marrow. The most important thing for the immune system is self and non-self recognition. Any cell that does not have a marker based on the major histocompatibility complex (MHC) will be attacked because it is a non-self cell. Cells prime the adaptive immune system against the pathogen which results in the production of protective antibodies and cytotoxic T cells.
The interaction between the innate and the adaptive systems leads to control of the pathogen within several days. Disorder in the system can cause serious problems, like when your immune system attacks the body’s healthy cells by “error”. This is called an autoimmune disease. 
The Innate and the Adaptive Immune Systems
When a pathogen enters the body, the immune system gets a signal for an immune response. The innate immune system has to be activated first; this response is rapid. Then, the innate immune system activates the adaptive system, and this will produce antibodies. The production of antibodies is a specific immune response of the adaptive immune system. The innate immune system is a natural system that a person is born with, and it is the first line of defense.
There are some differences between the innate and the adaptive immune systems, such as:
- The action time of the innate system is in hours, and the action time of the adaptive system is in days.
- The cell types of the innate system are macrophages, neutrophils, and dendritic cells, while those of the adaptive system are T and B cells.
- Receptors of the innate system are fixed in the genome, but in the adaptive system, the rearrangement of genes is necessary.
- The adaptive system has immunological memory, which means that when a person gets the same infection for the second time, the immune system reacts more quickly, but the innate system does not have immunological memory.
The innate system consists of:
- Tissue cells: to produce antimicrobial proteins.
- Mast cells: to promote an inflammation reaction.
- Platelets: responsible for clotting and promoting an inflammation reaction.
- Natural killer cells: for protection against tumor cells and viruses.
- Phagocytes: these are monocytes, macrophages (which eat the bacteria and present it to the adaptive immune system), and granulocytes. The first function is to clear bacteria and dead cells, and the second function is to present antigens to the adaptive immune system. 
The adaptive immune system has two categories of response: cell-mediated response and antibody response. The antibody response is the first category response of the adaptive system, and it is responsible for the activation of B-cells to secrete antibodies. These antibodies are proteins called Ig. In the blood, the antibodies circulate and bind to antigens. The antibody-antigen binding will block the binding of pathogens on the host cell receptor.
The second category response of the adaptive system is cell-mediated response. This response is responsible for the activation of T-cells. When they are activated, they will respond directly against unusual antigens that are presented on the surface of the host cell. In some instances, signal molecules will be produced by T-cells that will activate macrophages, which are able to destroy the bugs. Then, the adaptive system makes memory cells for the second time of the same infection. That means that the body is immune to an infection and can kill the sources but without symptoms. 
Autoimmune diseases are multifactorial processes affecting the deregulation of multiple constituents of the immune system, including the innate and adaptive immune systems.
The interaction of multiple constituents of the immune system is necessary for clinically manifest autoimmune disease.
Strong innate immune responses carry a limited hazard to excite an autoimmune disease, as long as they are ephemeral. Such unconditioned signals are necessary for pathogen clearance, preventing infectious disease and immunopathology. Long-term activation of the innate immune system can interrupt peripheral tolerance or ignorance.
Autoimmune diseases occur when the body’s healthy cells lack some receptors needed to be recognized as the body’s own cells/substances. Missing these receptors will trigger the two major parts of the immune system, which will cause the B and T lymphocytes to attack these cells.
Interleukins (IL) are specialized cytokines that identify the influences of the functions of lymph cells. These proteins act as the primary signaling response between cells of the immune system and are produced by diverse cells, including lymph cells, scavenger cells, and endothelial cells.
Interleukins are an indispensable mechanism of both adaptive and innate responses in mammals. The term “interleukin” is used to exemplify cytokines generally produced by leukocytes, which take action on leukocytes in a specific manner.
Identification of IL-17
Interleukin-17 (synonymous with IL-17A) was discovered in 1995/96 as a pro-inflammatory cytokine formed by T cells. IL-17 was shown to stimulate and mature neutrophils, an indication of its function in the acute mechanisms in host defense. This result indicated very early the relationship between IL-17 and neutrophil biology. It was discovered under the name of CTLA-8, a gene product without a clear function.
IL-17 is a paradigm molecule for an entire family of IL-17 cytokines. It is now believed to be formed primarily by a specific separation of CD4 cells, named Th-17 cells. IL-17 is found at the line of innate and acquired immunity. There is growing evidence that IL-17 signaling might be helpful in a diversity of diseases, including asthma, multiple sclerosis, and rheumatoid arthritis.
The IL-17 family and its receptors
IL-17 is the founding member of the IL-17 family, which includes IL-17A-F. Th17 cells were first discovered in the mouse with the production of IL-17A, and they also produced a list of other pro-inflammatory cytokines, including IL-17F, IL-22, TNF, IL-6. The primary receptor for IL-17, named IL-17R, was described in 1995/96 when IL-17 was discovered.
L-17F, IL-22, TNF, IL-6. The primary receptor for IL-17 named IL-17R was described in 1995/96 when IL-17 was discovered.[ 12 ]
Il-17″ should be written as “IL-17” throughout the text to follow proper capitalization rules.
IL-17 was identified chiefly as a gnawer complementary DNA transcript named cytotoxic T-lymphocyte-associated antigen 8. IL-17 is now the prototypic member of a household of cytokines that besides includes IL-17B, IL-17C, IL-17D, and IL-17F, which were discovered utilizing homology-based cloning (Table 1). IL-17E (now renamed IL-25) was identified individually but is no longer regarded as a member of the IL-17 household because of its functional function as an eosinophil-promoting cytokine .
Like the IL-17 cytokine household, IL-17 receptors form a unique household including IL-17 receptor RA-E. IL-17 stimulates a receptor compound consisting of IL-17RA and IL-17RC. IL-17RA, which is also the founding member of this household, is a type I transmembrane protein consisting of a 293 amino acid extracellular sphere, a 21 amino acid transmembrane sphere, and a 521 amino acid cytoplasmic tail. Besides IL-17RA and IL-17RC, three additional IL-17 receptors have been established; these are IL-17RB, IL-17RD, and IL-17RE, but their particular functional features remain to be identified .
Until now, six IL-17 household cytokines (IL-17A-IL-17F) and five members of the IL-17 receptor household (IL-17RA-IL-17RE) have been identified. The various receptor composites through which each ligand induces signaling are shown. The receptor for IL-17D and the ligand for IL-17RD and IL-17RA-IL-17RD are unknown .
IL-17 is a homodimeric glycoprotein consisting of 155 amino acids and has a molecular weight of 35 kDa. Among the accurate members of the IL-17 household, IL-17F has the greatest degree of structural and functional homology with IL-17. Since IL-17 and IL-17F are both homodimers, it is not unexpected that there is now evidence that mouse and human CD4 cells can produce an IL-17-IL-17F heterodimer also with similar proinflammatory properties.
Mouse and rat, in addition to bovine and swine IL-17, are structurally the same as human IL-17, particularly concerning the structure of the cysteine residues forming the canonical pseudo-knot crease. The molecular structure of IL-17 is among several mammalian species compatible with IL-17, playing a significant role in the mammalian immune system .
Th17, the cellular origin of IL-17
The most recent step was the discovery in 2006 of the cellular origin of IL-17. IFN-I? was identified as a shaper of Th1 cells, and IL-4 of Th2 cells. The origin of IL-17 was different, and these cells were named Th17. In the mouse, this new division was identified by the expression of the repressive effect of IFN-I? on IL-17 production in mouse models of autoimmune diseases .
IL-17 in host defense
Even though the certification of the engagement of IL-17 in human host defense is still incomplete, experimental studies in mice provide wide and convincing evidence that IL-17 plays an important role in mammalian host defense against a broad range of pathogens. For example, it has been reported that patients with a lack of the IL-12p40 subunit, leading to a combined absence of IL-12 and IL-23, or with a lack of IL-12 R b1, leading to IL-12 and IL-23 signaling impairments, are more susceptible to mycobacterial disease and infections with nontyphoidal Salmonellae.
These results also provide support for an involvement of IL-17 because the deficiency of IL-23 is likely to lead to a lower release of IL-17 protein and an inadequate differentiation and maturation of Th-17 cells. Animal models of infection with Gram-negative and Gram-positive bacteria, in addition to Mycoplasma pneumoniae and certain Protozoa, do suggest that IL-17 contributes to host defense against these bugs through its promoting effects on neutrophil recruitment and activation and the subsequent improved clearance of the pathogens. In addition, IL-17 upregulates the expression of antimicrobial molecules, such as β-defensins, in the lung, skin, and intestine. 
IL-17 in antibacterial host defense
The protective effects of IL-17 in host defense against bacterial pathogens were first verified by Kolls and co-workers in studies that compared the exposure of IL-17 receptor-deficient and control mice to K. pneumoniae. After intranasal infection, IL-17 receptor-deficient mice have increased numbers of recoverable bacteria in the lung, increased bacterial dissemination into the spleen, and reduced overall survival.
The increased exposure of IL-17 receptor-deficient mice to K. pneumoniae was directly associated with delayed neutrophil recruitment and decreased expression levels of granulocyte colony-stimulating factor and macrophage-inflammatory protein-2 in the lungs within the first 12-24 hours after infection. 
Even though TH1 and TH2 cells give protection against intracellular bugs and roundworms, respectively, TH17 cells have been implicated in the defense against certain bacteria and fungi. In addition to their helpful roles in the control of pathogens, TH subset effector responses can also induce pathology. In mice, the importance of IL-17 in conferring protection against pulmonary bacterial infections was verified after intranasal challenge with Klebsiella pneumoniae.
In the absence of functional IL-17RA signaling, infected animals displayed increased bacterial dissemination and mortality when compared with their wild-type counterparts. The role of TH17 cells in this model was supported by Happel et al., who showed increased susceptibility to disease in IL-23p19- and IL-23p40-deficient mice but reduced bacterial burden after administration of IL-17A. 
Beneficial and damaging roles for TH17 effector cytokines in the course of pulmonary immune responses. Bacterial and fungal infections in the lung trigger generation of TH1 cells, TH17 cells, γδ T cells, and NKT cells, which secrete a panel of pro-inflammatory cytokines. IL-17A and related cytokines play an important role in inducing mobilization and activation of neutrophils, which contribute to pathogen clearance.
In line with the expected effector function of IL-17A, the increased exposure of IL-17RA-deficient mice to bacterial infection correlated with reduced chemokine production and dysfunctional neutrophil recruitment to the site of infection. 
Bacteria can enter the organic structure via the skin, mouth, etc. Simple barriers such as the skin and epithelial surfaces are the organic body’s first line of defense. They do not have specific or unconditional protective systems, which limit the entry of potentially invasive organisms. The acknowledgment of bacterial constituents is the organic body’s second line of defense.
The most important thing in the immune system is self and non-self acknowledgment. The immune system is divided into the adaptive immune system and the innate system. The innate immune system activates the adaptive system, and this will produce antibodies. The innate immune system is a natural system that a person is born with, and it is the first line of defense.
The adaptive immune system has two categories of response: cell-mediated response and antibody response. The antibody-antigen binding will block the binding of pathogens on the host cell receptor. The second category response of the adaptive system is cell-mediated response. This response is responsible for the activation of T-cells.
The increasingly more research on IL-17 biology during the past 15 years has provided compelling confirmation that IL-17 has an orchestrating function in the mammalian immune response against bacteria, in particular for neutrophils. IL-17 might also be pathogenically important in chronic inflammatory and autoimmune disorders.
Contrasting the relatively well-studied IL-17 and IL-17F, the potential role of other IL-17 family members in host defense against bacterial infections remains largely unknown.
Many studies over the last decade have given IL-17 a unique function in the location of the inflammatory response. This cytokine is produced mainly by T cells rather than by macrophages or other cells of the innate immune system and therefore, it is believed to play an important role in the inflammatory events triggered by the adaptive or memory immune system.
Th17 cells play important roles in host defense against infection with extracellular bacterial pathogens by recruiting acute inflammatory cells into local sites of infection. As a result, the discovery that Th17 cells provide protection against extracellular bacterial fills a gap in immunity to a function of pathogens not previously covered by the Th1 or Th2 lineages and furthers understanding of host defense.
In addition to host defense, plenty of experimental evidence supports a pathological role for Th17 cells during numerous systemic and organ-specific autoimmune diseases. Accumulating evidence demonstrates that Th17 cells also provide protective effects during infection with more traditional intracellular pathogens.
The anecdote of IL-17 and Th17 separation is a new stimulation of the role of some T cells in chronic inflammation and extracellular matrix destruction. A list of diseases has been associated with IL-17, but the final presentation of its part to disease pathogenesis is still missing. Tools are now being organized to test these concepts in the hospital.
In conclusion, IL-17 is produced by different types of T cells, as well as TH17 cells and NK T cells that are involved in the initiation and effecter stage of a variety of immune responses. The rapid activation of NK T cells to release IL-17 might represent an important innate mechanism for the recruitment of neutrophils in response to bacterial infection, in particular at mucosal surfaces.
Depending on the timing, tissue, and local microenvironment, IL-17-secreting cells appear to play both positive and detrimental roles in lung immunity and disease. Future studies on humans will shed more light on the more specific immunological and infectious role of IL-17 in higher primates and are required.