Critical role of interleukin (IL)-17 in inflammatory and immune disorders: An updated review of the evidence focusing in controversies

Morales, José María García Ruiz de; Puig, Lluís; Daudén, E.; Cañete, Juan D.; Pablos, José L.; Martín, Antonio Olveira; Juanatey, Carlos González; Adán, Alfredo; Montalbán, Xavier; Borruel, Natalia; Ortí, Guillermo; Holgado-Martín, Esther; García-Vidal, Carolina; Vizcaya-Morales, Cynthia; Martín-Vázquez, Víctor; González-Gay, Miguel Á.

doi:10.1016/j.autrev.2019.102429

Cited by 244 publications

(198 citation statements)

References 167 publications

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“…For instance, ILC-derived IL-22 seems to protect against genotoxic stress in the colon [ 133 ], whereas IL-22 derived from Th17 cells has been shown to play a pathogenic role in colorectal cancer [ 134 ]. Of note, co-production of IL-17 appears to have a major role in the resolution of inflammation and overall tissue damage, particularly in chronic inflammatory settings [ 135 ]. Likewise, the different cellular sources of IL-22BP induce contrasting outcomes in disease settings.…”

Section: Discussionmentioning

confidence: 99%

Microbiota-Dependent Effects of IL-22

Sabihi

Böttcher

Pelczar

et al. 2020

Cells

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Cytokines are important contributors to immune responses against microbial and environmental threats and are of particular importance at epithelial barriers. These interfaces are continuously exposed to external factors and thus require immune components to both protect the host from pathogen invasion and to regulate overt inflammation. Recently, substantial efforts have been devoted to understanding how cytokines act on certain cells at barrier sites, and why the dysregulation of immune responses may lead to pathogenesis. In particular, the cytokine IL-22 is involved in preserving an intact epithelium, maintaining a balanced microbiota and a functioning defense system against external threats. However, a tight regulation of IL-22 is generally needed, since uncontrolled IL-22 production can lead to the progression of autoimmunity and cancer. Our aim in this review is to summarize novel findings on IL-22 and its interactions with specific microbial stimuli, and subsequently, to understand their contributions to the function of IL-22 and the clinical outcome. We particularly focus on understanding the detrimental effects of dysregulated control of IL-22 in certain disease contexts.

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Section: Discussionmentioning

confidence: 99%

Microbiota-Dependent Effects of IL-22

Sabihi

Böttcher

Pelczar

et al. 2020

Cells

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“…Among them, IL-17 in the CS5 and CS6 groups were significantly lower than that in other groups. Similar to IL-8, IL-17 is a class of pro-inflammatory cytokines [48,49]. After the intermittent and mild cold stimulation ended, the low expression level of IL-17 was also a manifestation of cold adaptation in broilers.…”

Section: Discussionmentioning

confidence: 99%

Effect of Intermittent and Mild Cold Stimulation on the Immune Function of Bursa in Broilers

Liu

Xue

et al. 2020

Animals

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Cold stress causes growth performance to decrease and increases production costs. Cold adaptation can enhance immune function and alleviate the negative impact caused by the stress condition. The study investigated the effect of intermittent and mild cold stimulation on the immune function of the bursa of Fabricius in broilers. A total of 400 healthy one-day-old broilers were divided into the control group (CC) and cold stimulation (CS) groups. The CC group was raised at a conventional raising temperature of broilers, while the CS groups were raised at 3°C below the temperature of the CC for three-, four-, five-, or six-hour periods at one-day intervals from 15 to 35 days of age (D35), denoted CS3, CS4, CS5, and CS6, respectively. Subsequently, they were raised at 20°C from 36 to 49 days of age (D49). The expression levels of TLRs, cytokines, and AvBDs were determined to access the immune function of bursa in broilers. After 21-day IMCS (at D36), the expression levels of TLR1, TLR15 and TLR21, interleukin (IL)-8, and interferon (IFN)-γ, as well as AvBD8 in CS groups, were lower than those in CC (p < 0.05). The expression levels of TLR3, TLR4 and TLR7, were decreased in the CS3, CS5, and CS6 groups (p < 0.05), but there were no significant differences in both the CC and CS4 groups (p > 0.05). When the IMCS ended for 14 days (at D49), the expression levels of TLR2, TLR3, TLR5, TLR7, TLR15, and TLR21, and IL-8, as well as AvBD2, AvBD4 and AvBD7 in CS groups, were lower than those in CC (p < 0.05). In addition to CS4, the expression levels of TLR1, IFN-γ, and AvBD8 in CS3, CS5, and CS6 were still lower than those in CC (p < 0.05). We concluded that the intermittent and mild cold stimulation could regulate immunoreaction by modulating the production of TLRs, cytokines, and AvBDs in the bursa, which could help broilers adapt to low ambient temperature and maintain homeostasis.

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“…In fact, while healthy human skin contains just a few Th17 cells, their concentration is highly increased in psoriasis and other inflammatory disorders [100]. The IL-17 family of cytokines consists of 6 proteins (IL-17A to IL-17F), with IL-17A and IL-17F being mainly produced by Th17 cells [101].…”

Section: Adamtsl5mentioning

confidence: 99%

The Brain–Skin Connection and the Pathogenesis of Psoriasis: A Review with a Focus on the Serotonergic System

Martins¹,

Ascenso²,

Ribeiro³

et al. 2020

Cells

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Psoriasis is a common non-communicable chronic immune-mediated skin disease, affecting approximately 125 million people in the world. Its pathogenesis results from a combination of genetic and environmental factors. The pathogenesis of psoriasis seems to be driven by the interaction between innate immune cells, adaptive immune cells and keratinocytes, in a process mediated by cytokines (including interleukins (IL)-6, IL-17 and IL-22, interferon and tumor necrosis factor) and other signaling molecules. This leads to an inflammatory process with increased proliferation of epidermal cells, neo-angiogenesis and infiltration of dendritic cells in the skin. Dysfunctional de novo glucocorticoid synthesis in psoriatic keratinocytes and the skin microbiome have also been suggested as mediators in the pathogenesis of this disease. To understand psoriasis, it is essential to comprehend the processes underlying the skin immunity and neuroendocrinology. This review paper focuses on the skin as a neuroendocrine organ and summarizes what is known about the skin immune system, the brain–skin connection and the role played by the serotonergic system in skin. Subsequently, the alterations of neuroimmune processes and of the serotonergic system in psoriatic skin are discussed, as well as, briefly, the genetic basis of psoriasis.

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Critical role of interleukin (IL)-17 in inflammatory and immune disorders: An updated review of the evidence focusing in controversies

Cited by 244 publications

References 167 publications

Microbiota-Dependent Effects of IL-22

Microbiota-Dependent Effects of IL-22

Effect of Intermittent and Mild Cold Stimulation on the Immune Function of Bursa in Broilers

The Brain–Skin Connection and the Pathogenesis of Psoriasis: A Review with a Focus on the Serotonergic System

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