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Role Of Cytokines In Autoimmune Disorders

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Role Of Cytokines In Autoimmune Disorders Question: Discuss about the Role of Cytokines in Autoimmune Disorders.     Answer: Introduction Basically, the identification of critical roles that cytokines play in autoimmune and many inflammatory diseases has resulted in an improved treatment of these diseases (Abbas et al., 2014). The autoimmune illness is inclusive of rheumatoid arthritis (RA), (MS), psoriasis, systemic lupus erythematosus sclerosis, systemic sclerosis (SS), Crohn’s disease (CD), and type-1 diabetes. These bring about many different characteristics associated with ill health. Autoimmune diseases occur when the immune system attacks the body because it confuses it for something foreign (Egwuagu et al., 2015). Being the main cause of mortality as well as morbidity in the industrialized world, they affect about 3 to 8% of the world’s population. The occurrence of autoimmunity is felt due to reduced self-tolerance associated with the immune system, and this involves a couple of molecules that are different (Noack & Miossec 2014).            There exists a lifelong gap in the knowledge about the causative agents that act as the contributors to the initiation of these diseases, whether viral or bacterial pathogens (Abbas et al., 2014).  Bacterial infections have been found to be the cause of such infections encompassing systemic lupus erythematosus (SLE), rheumatoid arthritis, and psoriasis. There is a need for further clarification concerning the pathogenesis of autoimmune process even though significant progress has been noted in the growth of latest mode of treatment (Noack & Miossec 2014). Despite displaying the same features, the autoimmune diseases have pathogenic and clinical overlaps that include RA, SLE, SS, and psoriasis that have common chronic inflammatory joint diseases. In particular, SS and SLE share cardiac pathologies that are comparable (Siebert, 2015). Evidently, inflammatory chemokines are scientifically known to take part in the pathogenesis of the above diseases where a majority of them have been discovered recently and widely declared that factors such as the environment, immunity, and genes are the main contributors to a rise in autoimmunity (Egwuagu et al., 2015). Cytokines are a large group of peptides, proteins, and glycoproteins that are secreted by the cells and are also inclusive of chemokines, tumor necrosis factor, interleukins, lymphokines, interferons, growth factors, and adipokines.  They have a fundamental role in the pathogenesis of these sicknesses through various ways that includes the regulation of inflammation and angiogenesis (Raphael et al., 2015).   However, there is a need to gain a whole comprehension of the molecules tangled in autoimmune diseases, proteome techniques, and functional genome as briefly described. IL-12 related associates perform a core role. In occasions where there is an existence of inflammatory cytokine interferon (IFN), available antigen-presenting cells (APCs) produce interleukin (IL)-12, that later leads to a differentiation of CD4+ T cells transformation to IFN- -secreting T helper type 1cells (Sun et al., 2015). On the other hand, it has the capability of making the IL-4 to cause the CD4+ T cells to preferably progress into IL-4- and IL-5- that later makes IL-13- to result in Th2 cells. However, convincing proof exists for the biologically known third effector CD4+ of a trail in autoimmunity. The Th17 T cells enhance the production of IL-17A as well as IL-17F. These are the two of the cytokines whose production is neither by Th1 or Th2 CD4+ T cells (Noack & Miossec 2014). A mishmash of the transforming growth factor (TGF) -1 as well as IL-6, together with IL-23 results in the generation of the CD4+T cell subtypes (Raphael et al., 2015). After IL-23 stimulation, this modern kind of T cells yields a variety of inflammatory mediators that are inclusive of tumor necrosis factor (Teng et al., 2015). According to the existing knowledge, it emerges that IL-17-producing T cells are the ones responsible for a number of the inflammatory as well as autoimmune responses that were at one time attributed to Th1 cells (Raphael et al., 2015). Out of these, CD, TNF-α in RA, psoriasis, and IL-6/IL-6R in RA have been demonstrated widely to be of clinical importance (Moudgil, 2015). A review of the biological aspects of IL-21 as well as its function in the course of pathogenesis of the related autoimmune sicknesses has been done recently. It was found that a sequence of autoimmune models IL-21 played an exclusively non-redundant role in autoimmunity and seemed to be a typical modulator, specifically for the adaptive immune response that is associated with self-tissue in chronic illnesses such as type-1 diabetes, MS, RA, and SLE (Abbas et al., 2014). Rheumatoid Arthritis Primarily, this disease is detected as a result of prolonged irritation of the joints that lead to decreased movement and these later results to the emergence of key disabilities in most of the reported cases (Siebert, 2015). The joints’ synovial tissues form the major marks of this disease, although its nature can be systemic because it has an impact on the genes and patterns of proteins in the peripheral blood. Evidently, IL-17, IL-23, and IL-27 play a critical part in pathogenesis of RA (Abbas, Litchman & Pillai, 2014).  A study conducted in IL12/p35 and IL23/p19 knocks out CIA model in mice, one of the conforming mouse models of human RA. Consequently, the result was that IL-23 is important in autoimmune inflammation of joints (Floss, 2015). Naturally, IL-27 constitutes a family of IL-12. It plays a crucial role in the initial initiation of Th1 comebacks (Chong et al., 2014). IL-27 joins with a receptor that comprises of WSX-1/TCCR as well as gp130. These are significant in serving as a collective signal transduction receptor that is designated specifically for IL-6 (Teng et al., 2015). In general, IL-27 leads to anti-inflammation, and it is therefore considered to be a suppressor of autoimmunity (Prinz &priller, 2017). IL-10 regulates the production of the proinflammatory cytokine in RA synovial tissues. Being a potential anti-inflammatory cytokine, its protein and mRNA were detected in joints of people with the disease (Sun et al., 2015). Evidently, potent anti-inflammatory cytokine has been found to foster the regulation of RA and OA. To add on, the counterbalancing of endogenously produced IL-10 in the RA synovial membrane cultures resulted in a significant increase in the protein levels of proinflammatory cytokines tumor linked to necrosis factor alpha (TNF-alpha) and IL-1 (Sun et al., 2015). Recently, the biological contribution of IL-7 in RA has been identified (Teng et al., 2015). There is an increasing level of IL-7 as well as IL-15 mRNA coupled with protein expression from the synovial tissue cells of RA patients (Siebert, 2015). The role of IL-7 in synovial tissue of RA patients is to induce variation of CD14+ to form giant, multinucleated, and bone-resorbing cells. Additionally, the vital role played by ThIL-7 can take part in the chronic inflammation associated with the destruction of joints through T-cell interceded initiation of osteoclasts (Sun et al., 2015).   Multiple Sclerosis (MS) Primarily, MS refers to an inflammatory demyelinating illness that is chronic in nature and affects the nervous system (CNS), especially the white matter. In multiple sclerosis, the protective sheath (myelin) is attacked by the immune. As a result, it causes problems to the brain and the whole body at large (Maddur et al., 2012). Eventually, permanent damage may occur due to the deterioration of the nerves. Signs and symptoms of this disease may arise in a different manner, and this depends on the intensity of the damage and which nerve has been attacked (Nyirenda et al., 2015). Many neurological symptoms may be observed including epilepsy, aphasia, muscle weakness, visual problems, difficulties with coordination, and balance as well as changes in sensation. IFN- plays a vital part in multiple sclerosis. As such, elevated heights of IFN have shown through studies that allergic encephalomyelitis (EAE) as well as individuals treated with IFN- was lethal to multiple sclerosis (Maddur et al., 2012). Evidently, genetic polymorphisms embodied in the IFNG gene are associated in a way with MS. Besides, researchers have declared that IL-23/Th17 trail takes part in EAE. In a manner, this pathway is of great importance in human beings (Nyirenda et al., 2015). Systemic lupus erythematosus (SLE) SLE can be described as a chronic disease which may alternate with periods of negligible symptoms. Most of the individuals with the disease may live a normal lifestyle after treatment (Maddur et al., 2012). It has a strong background related to genetic makeup, and 80% of patients are female. Patients may have skin lesions where the most common are the malar rash. SLE may also affect internal organs including heart, kidney, lungs, CNS, and joints (Prinz & Priller, 2017). Other symptoms of abnormalities are observed in the blood including deficiency of thrombocytopenia, lymphopenia, leucopenia, and complement (C4, C1q, and C2). Genes belonging to the functional groups of apoptosis, DNA repair or replication, and cell cycle regulation refer to the genes that are known to play roles in LE, such as Fc fragment, cytochrome c, immunoglobulin G, CD22, and p53. There is also evidence that immunosuppressive treatment in SLE can lead to a detrimental impact on the pathway and molecules that take part in the pathogenesis of LE (Floss, 2015). Cumulatively, lupus expresses a common characteristic that includes the upfront regulation of IL-1 members (Sun et al., 2015). Psoriasis This can be described as an inflammatory skin disease where there are a reasonable number of patients who suffer from a joint ailment. Psoriasis can be considered as a complex disease that involves coronary artery as well as the heart (Sun et al., 2015). There is a specific auto-antigen that has not been identified during the study of patients bearing this inflammatory disease. Without a doubt, IL-23/Th17 pathway plays an important role of psoriasis skin inflammation where it bears the growth of pro-inflammatory, IL-17-secreting CD4+ memory cells (Moudgil, 2015). Psoriasis plays a role in mediating epidermal skin thickening (acanthosis), as it is through the Th17 cytokine that enhances the intermediation of IL-23-inducing acanthosis. Finally, IL-23- can lead to the swelling of the ears that can decrease in IL-22-/- in the case of a particular study using mice (Sun et al., 2015). Systemic sclerosis (SSc) SSc is an autoimmune disease which is multisystem and can be detected due to the skin schlerosis. Internal organs may also be affected including heart, liver, lungs, and gastrointestinal tract. COL7A1 and COL18A1 have been described as putative biomarkers in early stages of SSc (Maddur et al., 2012).  Coagulation system, fibroblasts, T-cells, and B-cells together with the endothelial cells are involved in the pathogenesis of SSc. Their role is minor in this disease because only a trace of them is detected.   Type I Diabetes Primarily, the contribution of cytokines found in the pathogenesis of autoimmune diabetes (type I diabetes) was demonstrated using models. These functions include; the pathogenic role of IL-27, the plasticity of the subsets of T cells, and the protective contribution of IL-35 (Moudgil, 2015). This is also described as the influence of cytokines on rendering the effector T cells intractable to the suppression by Treg. This is the function of effector T cells that enhances the balance between IL-2 and IL-21, especially in infection vulnerability (Floss, 2015). Myocarditis More precisely, the role of this disease is in the initiation of an autoimmune disease (Rose, 2012). It is evidenced that the role of cytokines is normally at various phases of myocarditis progression, whereby CB3 activates the fabrication of innate cytokines that later triggers cardiac inflammation. In a way, a succeeding upsurge of Th2 as well as Th1 coordinates the autoimmune sensitivity against cardiac myosin. Th17 responsiveness enhances the mediation of dilated cardiomyopathy (Isono et al., 2014). Ideally, the comparative input of Th1 versus Th17 leads to the contrasting properties of IL-12 versus IFN-g, and of IL-4. It also results in IL-13 and the dichotomy of functionality in certain cytokines in the progression of the disease (Chong et al., 2014). Thyroiditis Mainly, this is one of the commonest autoimmune diseases that are organ-specific (Ganesh et al., 2011). As such, the role played by the cytokines in the autoimmune thyroiditis, particularly in a stage where the disease manifests itself as Hashimoto’s thyroiditis, is viewed as a disorder that is associated with hypothyroidism (Trovato et al., 2015). There is a significant contribution to Th1, Th2, as well as Th17 responses to the process of the disease in HT and Graves’ disease (Isono et al., 2014). Naturally, the significant contribution of granulocyte macrophage colony-stimulating factor (GMCSF) is in the expansion of CD8a-dendritic cells (DCs) and also in the maintenance DCs in a semi-mature phenotype. As such, this leads in turn to the segregation as well as the expansion of IL-10- that produces Treg. It is evidenced that Treg are useful in the prevention and suppression of tentative autoimmune thyroiditis (EAT). Furthermore, IL-10 is known to suppress EAT through the inhibition of the costimulatory pathways. On the same note, it also plays a part in preventing the apoptosis of thyrocytes (Trovato et al., 2015). Also, contradictory effects of various cytokines include; regulatory and pro-inflammatory response. These cytokines include TNFa, IL-2, IL-7, and IL-1b (Moudgil, 2015). Uveitis Uveitis is one of the causative agents of blindness in the developed nations (Caspi et al., 2014). The diseases include uveoretinitis, retinitis, and retinopathy. Evidently, autoimmune inflammation is thought to be the most crucial component of uveitis’ process. The protective function of early IFN-g/IL-12 response in EAU has been highlighted, together with the double contribution of Th2 response as well as other cytokines (Teng et al., 2015).   Crown’s Head Disease Crohn’s disease (CD) refers to a chronic inflammatory disorder, and it occurs throughout the gastrointestinal tract. Its characteristics are the episodes of relapse and remission. Despite being prevalent in North America and Europe, CD is being observed in developing countries due to westernization and industrialization (Neirath, 2014). It starts as an inflammatory process that in most cases affects terminal ileum and often leads to progressive as well as permanent bowel damage. A complication that occurs includes the structuring disease that is associated with symptoms related to bowel obstruction and penetrating disease that involves abscess and fistula formation (Sun et al., 2015). Ideally, Tumor Necrosis Factor-alpha has been proven to be directly associated with cytotoxic impacts to the intestinal mucosa in Crohn’s head disease together with ulcerative colitis. Primarily, it also donates to the systemic displays that occur mostly in crown’s diseases. Anti-TNFα antibodies show a clear anti-inflammatory impact in patients with this illness. Long-term effects caused by TNFα blockage in vivo may have detrimental impacts especially in children (Egwuagu et al., 2015). Other roles of TNFα in inflammatory diseases include the pathogenic contribution in the formation of blister lesions that are integral to bullous phemphigoid. Similarly, TNFα is scientifically known to have an imperative role in the pathogenesis of RA. Furthermore, it has been noted that the variants of TNFα gene function as the markers of RA sternness (Teng et al., 2015). Without a doubt, TNFα entails the major cytokine in the development of T1D that contributes to beta cell dysfunction as well as death (Siebert, 2015). In a way, TNFα could be vital to the interruption of tolerance to self-antigens in viruses that induce diabetes. Fascinatingly, the late manifestation of TNFα in a framework can reinstate normal function of the beta cell, probably through the induction of T-cell apoptosis. As such, this is one of the contrasts that make up a regular matter with other cytokines (Neirath, 2014). In a nutshell, TNFα is suggestively known to play a deviating part in the development of EAE as well as MS, by leading to demyelination alongside fostering the chronicity of the disease (EAE) or by regulating the disease process (MS) (Neirath, 2014). Willenborg and other authors, however, have portrayed that the presence of completely opposed interpretations on the effects of TNFα in EAE can be accessed in the literature, spanning from pro-EAE to the range of anti-EAE (Moudgil, 2015). Some research works that have been done in the past indicate that EAE can be subdued by TNFα (Teng et al., 2015). The treatment of patients suffering from autoimmune illnesses has been underpinned by the utilization of anti-inflammatory drugs as well as the introduction of immunosuppression for a considerable time.   References Abbas, A. K., Lichtman, A. H., & Pillai, S. (2014). Basic immunology: functions and disorders of the immune system. Elsevier Health Sciences. Chong, W. P., Horai, R., Mattapallil, M. J., Silver, P. B., Chen, J., Zhou, R., … & Caspi, R. R. (2014). IL-27p28 inhibits central nervous system autoimmunity by concurrently antagonizing Th1 and Th17 responses. Journal of autoimmunity, 50, 12-22. Egwuagu, C. E., Yu, C. R., Sun, L., & Wang, R. (2015). Interleukin 35: Critical regulator of immunity and lymphocyte-mediated diseases. Cytokine & growth factor reviews, 26(5), 587-593. Floss, D. M., Schröder, J., Franke, M., & Scheller, J. (2015). Insights into IL-23 biology: from structure to function. Cytokine & growth factor reviews, 26(5), 569-578 Isono, F., Fujita-Sato, S., & Ito, S. (2014). Inhibiting RORγt/Th17 axis for autoimmune disorders. Drug discovery today, 19(8), 1205-1211. Liu, X., Leung, S., Fang, L., Chen, X., Guo, T., & Zhang, J. (2012). Interplay of Pathogenic TH1/TH17 Cells and Regulatory T Cells in Auto-immune Disease: A Tale of Yin and Yang. In TH17 Cells in Health and Disease (pp. 367-389). Springer New York. Maddur, M. S., Miossec, P., Kaveri, S. V., & Bayry, J. (2012). Th17 cells: biology, pathogenesis of autoimmune and inflammatory diseases, and therapeutic strategies. The American journal of pathology, 181(1), 8-18. Moudgil, K.D., 2015. Interplay among cytokines and T cell subsets in the progression and control of immune-mediated diseases. Netea, M. G., Latz, E., Mills, K. H., & O’neill, L. A. (2015). Innate immune memory: a paradigm shift in understanding host defense. Neurath, M. F. (2014). Cytokines in inflammatory bowel disease. Nature Reviews Immunology, 14(5), 329-342. Noack, M., & Miossec, P. (2014). Th17 and regulatory T cell balance in autoimmune and inflammatory diseases. Autoimmunity reviews, 13(6), 668-677. Nyirenda, M. H., Morandi, E., Vinkemeier, U., Constantin-Teodosiu, D., Drinkwater, S., Mee, M., … & Constantinescu, C. S. (2015). TLR2 stimulation regulates the balance between regulatory T cell and Th17 function: a novel mechanism of reduced regulatory T cell function in multiple sclerosis. The Journal of Immunology, 194(12), 5761-5774. Prinz, M., & Priller, J. (2017). The role of peripheral immune cells in the CNS in steady state and disease. Nature neuroscience, 20(2), 136-144. Raphael, I., Nalawade, S., Eagar, T. N., & Forsthuber, T. G. (2015). T cell subsets and their signature cytokines in autoimmune and inflammatory diseases. Cytokine, 74(1), 5-17. Schett, G., Elewaut, D., McInnes, I. B., Dayer, J. M., & Neurath, M. F. (2013). How cytokine networks fuel inflammation: toward a cytokine-based disease taxonomy. Nature medicine, 19(7), 822-824. Siebert, S., Tsoukas, A., Robertson, J., & McInnes, I. (2015). Cytokines as therapeutic targets in rheumatoid arthritis and other inflammatory diseases. Pharmacological reviews, 67(2), 280-309. Sun, L., He, C., Nair, L., Yeung, J., & Egwuagu, C. E. (2015). Interleukin 12 (IL-12) family cytokines: role in immune pathogenesis and treatment of CNS autoimmune disease. Cytokine, 75(2), 249-255. Teng, M. W., Bowman, E. P., McElwee, J. J., Smyth, M. J., Casanova, J. L., Cooper, A. M., & Cua, D. J. (2015). IL-12 and IL-23 cytokines: from discovery to targeted therapies for immune-mediated inflammatory diseases. Nature medicine, 21(7), 719-729. Trovato, M. C., Ruggeri, R. M., Scardigno, M., Sturniolo, G., Vita, R., Vitarelli, E., … & Bourdon, J. C. (2016). Immunoreactions for P53 isoforms are associated with ultrastructural proliferative profiles in benign thyroid nodules. Histology and histopathology, 31(10), 1079-1087. Wahren-Herlenius, M., & Dörner, T. (2013). Immunopathogenic mechanisms of systemic autoimmune disease. The Lancet, 382(9894), 819-831.

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