Clinical significance of TLR7/IL-23/IL-17 signaling pathway in patients with acute respiratory distress syndrome.

OBJECTIVES: To analyze the clinical significance of Toll-Like Receptor 7/Interleukin-23/Interleukin-17 (TLR7/IL-23/IL-17) signaling pathway in patients with Acute Respiratory Distress Syndrome (ARDS). METHOD: The clinical data of 85 patients with ARDS were retrospectively analyzed and set as the ARDS group, and the clinical data of 85 healthy participants during the same period were set as the healthy control group. Univariate and multivariate logistic regression were used to analyze risk the factors affecting the prognosis of ARDS patients. RESULTS: TheTLR7 mRNA expression and IL-23 and IL-17 levels in peripheral blood mononuclear cells were higher in the ARDS group than in the control group (p < 0.05). TLR7 mRNA expression, IL-23, IL-17, Surfactant Protein-D (SP-D), and Clara Cell protein-16 (CC-16) levels were the highest in the severe group, followed by the moderate group, and the lowest in the mild group, while Oxygenation Index (OI) was the lowest in the severe group, followed by the moderate group, and the highest in the mild group (p < 0.05). Multivariate logistic regression analysis found that the disease grade (severe), TLR7 mRNA expression, IL-23 level, and IL-17 level were the risk factors affecting the 28-d survival status of ARDS patients (OR > 1, p < 0.05). CONCLUSIONS: In ARDS patients, the TLR7/IL-23/IL-17 signaling pathway is activated. The expression of this pathway is closely related to the severity of the disease and the levels of lung injury markers, and it is a risk factor that may have a direct impact on the prognosis of ARDS patients.

IL-23/IL-17 axis levels in gingival crevicular fluid of subjects with periodontal disease: a systematic review.

BACKGROUND: The IL-23/IL-17 axis plays an important role in the immunopathogenesis of periodontal disease. A systematic review was conducted to synthesize all research reporting on the levels of the IL-23/IL-17 axis in gingival crevicular fluid (GCF) from subjects with gingivits, and periodontitis, compared to healthy controls. METHODS: The protocol followed the PRISMA, and Cochrane guidelines, and was registered with the Open Science Framework (OSF): https://doi.org/10.17605/OSF.IO/7495V . A search was conducted in the electronic databases PubMed/MEDLINE, Scopus, Google Schoolar, and Cochrane from November 15th, 2005, to May 10th, 2023. The quality of the studies was assessed using the JBI tool for cross-sectional studies. RESULTS: The search strategy provided a total of 2,098 articles, of which 12 investigations met the inclusion criteria. The total number of patients studied was 537, of which 337 represented the case group (subjects with gingivitis, and chronic periodontitis), and 200 represented the control group (periodontally healthy subjects). The ages of the patients ranged from 20 to 50 years, with a mean (SD) of 36,6 ± 4,2, of which 47% were men, and 53% were women. 75% of the investigations collected GCF samples with absorbent paper strips, and analyzed cytokine IL-17 levels individually. In addition, qualitative analysis revealed that there are differences between IL-23/IL-17 axis levels in subjects with chronic periodontitis, gingivitis and healthy controls. CONCLUSIONS: Thus, IL-23/IL-17 axis levels could be used in the future as a diagnostic tool to distinguish between periodontal diseases.

Clinical significance of TLR7/IL-23/IL-17 signaling pathway in patients with acute respiratory distress syndrome

Abstract Objectives: To analyze the clinical significance of Toll-Like Receptor 7/Interleukin-23/Interleukin-17 (TLR7/IL-23/IL-17) signaling pathway in patients with Acute Respiratory Distress Syndrome (ARDS). Method: The clinical data of 85 patients with ARDS were retrospectively analyzed and set as the ARDS group, and the clinical data of 85 healthy participants during the same period were set as the healthy control group. Univari-ate and multivariate logistic regression were used to analyze risk the factors affecting the prognosis of ARDS patients. Results: TheTLR7 mRNA expression and IL-23 and IL-17 levels in peripheral blood mononuclear cells were higher in the ARDS group than in the control group (p < 0.05). TLR7 mRNA expression, IL-23, IL-17, Surfactant Protein-D (SP-D), and Clara Cell protein-16 (CC-16) levels were the highest in the severe group, followed by the moderate group, and the lowest in the mild group, while Oxygenation Index (OI) was the lowest in the severe group, followed by the moderate group, and the highest in the mild group (p < 0.05). Multivariate logistic regression analysis found that the disease grade (severe), TLR7 mRNA expression, IL-23 level, and IL-17 level were the risk factors affecting the 28-d survival status of ARDS patients (OR > 1, p < 0.05). Conclusions: In ARDS patients, the TLR7/IL-23/IL-17 signaling pathway is activated. The expression of this pathway is closely related to the severity of the disease and the levels of lung injury markers, and it is a risk factor that may have a direct impact on the prognosis of ARDS patients.

The Relationship between Serum IL-17 and IL-23 Levels, and Other Disease Activity Parameters in Patients with Behçet's Disease

ABSTRACT Objective: To investigate the relationship between disease activity and the involvement of Behçet's disease (BD) and serum levels of interleukin (IL)-17 and IL-23. Methods: Sixty patients with BD and 20 healthy control group subjects were included in this study. The patients were divided into four groups according to clinical findings as follows: entero-Behçet, mucocutaneous-Behçet, neuro-Behçet and vascular-Behçet. The serum levels of the IL-17 and IL-23 levels were evaluated using enzyme-linked immunosorbent assay. Results: Of the BD patients, 15 (25%) had active disease and 45 (75%) had inactive disease. The serum levels of IL-23 and IL-17 were statistically significantly higher in the patients with BD than in the control groups (p < 0.05). A significant relationship was also observed between the disease activity, and both the erythrocyte sedimentation rate and the C-reactive protein levels (p < 0.05). The mean serum levels of IL-17 and IL-23 in patients with active disease were 0.07 ± 0.25 pg/ml and 36.0 ± 30.5 pg/ml, respectively. There was no statistically significant relationship between the disease activity and the serum levels of IL-17 and IL-23 (p > 0.05). There were also statistically significant relationships between the disease activity and uveitis, retinal vasculitis or superficial thrombophlebitis. Conclusion: No relationship was found between BD and serum levels of the IL-17 and the IL-23.

The Effect of Interleukin 23 Levels on Clinical and Laboratory Parameters of Patients with Ankylosing Spondylitis

ABSTRACT Objective: In the present study, we aimed to investigate the relationship between interleukin 23 (IL-23) and the clinical and laboratory parameters in patients with ankylosing spondylitis (AS). Ankylosing spondylitis causes structural and functional inability, particularly in the axial skeleton, and results in the inflammatory lower back pain. At the same time, we aimed to investigate the relationship between IL-23 levels and disease related variables in patients with AS. Methods: A total of 38 patients with AS (33 males and 5 females) and 42 healthy controls (32 males and 10 female) were enrolled in the study. The demographic characteristics of the participants were recorded. As laboratory findings, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and IL-23 values were noted. Bath AS Disease Activity Index, Bath AS Functional Index, Visual Analogue Scale, and AS Quality of Life scales of the patients were measured. Results: The mean age of the AS group and the control subjects was 32.4 ± 7.06 and 30.0 ± 6.24 years, respectively. The ESR, CRP and IL-23 levels were significantly higher in the AS group compared to those of the healthy controls (p < 0.001, p < 0.013, p < 0.012, respectively). There was a significant correlation between ESR, CRP, and IL-23 levels in patients with AS (r = 0.328, p = 0.030 and r = 0.392, p = 0.008, respectively). While 12 subjects (31.5%) were positive for peripheral arthritis, 26 patients were negative (68.4%). The IL-23 levels were significantly higher in the group that was positive for peripheral arthritis (p < 0.05). Conclusion: Interleukin 23 may play a role in the progression and/or pathogenesis of AS and is most likely involved in the joint problems independent of the classic inflammatory response measures.

Macrophages skew towards M1 profile through reduced CD163 expression in symptomatic apical periodontitis.

OBJECTIVES: To explore the macrophage profiles in symptomatic and asymptomatic forms of AP through phenotypic and functional analyses. MATERIAL AND METHODS: Cross-sectional study. Apical tissue/lesion samples were collected from patients with clinical diagnosis of AAP (n = 51) or SAP (n = 45) and healthy periodontal ligament (HPL) from healthy patients as controls (n = 14), all with indication of tooth extraction. Samples were digested, cells were stained for CD14, M1 (CD64, CD80), and M2 (CD163, CD206) phenotypic surface markers and analyzed by flow cytometry. Functional cytokine profiles L-6, IL-12, TNF-α, IL-23 (M1), IL-10, and TGF-ß (M2) were determined by qPCR. RESULTS: Higher macrophage M1/M2 ratio (CD64+CD80+/CD163+CD206+) along with lower CD163 mean fluorescence intensity (MFI) were found in SAP compared to AAP and controls (p < 0.05). IL-6, IL-12, TNF-α, IL-23 (M1), and IL-10 mRNA (M2) were upregulated, whereas TGF-ß mRNA (M2) was downregulated in apical lesions compared to controls. Specifically, IL-6 and IL-23 (M1) were upregulated in SAP compared with AAP and controls (p < 0.05). The data were analyzed with Kruskal-Wallis test. CONCLUSIONS: Macrophages exhibited a polarization switch towards M1 in AL. SAP exhibited a reduced M2 differentiation profile based on a reduction of CD163 expression levels in SAP over AAP. Specifically, IL-6 and IL-23 were augmented SAP over AAP, suggesting a role in the severity of apical lesions. CLINICAL RELEVANCE: Deciphering the macrophage polarization and functions in apical periodontitis can contribute to explain AP dynamics, its clinical presentation and systemic impact.

Influência da laserterapia de baixa intensidade no processo inflamatório e na imunomarcação da interleucina­23 e do fator indutor de hipóxia 1-alfa no tecido pulpar de dentes clareados / Influence of low-level laser therapy on the inflammatory process and immunolabeling of interleukin-23 and hypoxia-inducing factor 1-alpha in the pulp tissue of bleached teeth

Introdução: O uso do laser infravermelho (LIV) através da fotobiomodulação, tem demonstrado efeitos benéficos aos tecidos. Objetivos: Avaliar a influência do LIV sobre o processo inflamatório, por meio da imunomarcação da interleucina próinflamatória IL-23, e sobre a angiogênese, por meio da imunomarcação do fator induzível por hipóxia-1 alfa (HIF-1α), no tecido pulpar de dentes clareados. Materiais e métodos: Quarenta ratos Wistar foram distribuídos aleatoriamente em 4 grupos de 20 hemi-maxilas cada: Grupo Controle ­ recebeu o tratamento com o gel placebo; Grupo Cla - recebeu 30 minutos do gel clareador H2O2 a 35%; Grupo LIV ­ recebeu uma aplicação de LIV (808 nm, 30 segundos, 3J); Grupo Cla-LIV ­ imediatamente após a aplicação do H2O2 a 35%, recebeu uma aplicação de LIV, como descrito no grupo LIV. Após 2 e 30 dias (n = 10), os animais foram eutanasiados e as maxilas removidas e processadas para avaliação histológica (H.E.) e imunoistoquímica. Forma de análise: Os cortes teciduais seriados e com espessura de 5 µm corados em H.E. foram avaliados por escores atribuídos à inflamação, e a análise imunoistoquímica foi realizada através de escores atribuídos à imunomarcação. Os dados foram submetidos aos testes de Wilcoxon e Mann Whitney (p < 0,05). Resultados: Aos 2 dias, houve inflamação severa e necrose nos terços oclusal e médio do tecido pulpar no grupo Cla, diferente do grupo Cla-LIV com inflamação leve à moderada (p < 0,05). No terço cervical, houve inflamação moderada a severa no grupo Cla, e leve no grupo Cla-LIV (p < 0,05). Aos 30 dias, houve ausência de inflamação e os grupos clareados apresentaram deposição de dentina terciária. Em relação à IL-23, aos 2 dias foi observada imunomarcação severa no grupo Cla e moderada no grupo Cla-LIV (p < 0,05); aos 30 dias, houve redução na imunomarcação de IL-23 nos grupos clareados, onde o grupo Cla apresentou imunomarcação moderada, e o grupo Cla-LIV leve imunomarcação, sem diferença significante (p > 0,05). HIF-1α foi mais presente aos 2 dias no grupo Cla, sem diferença significativa com Cla-LIV (p > 0,05). Foi observada diferença entre os grupos clareados e seus respectivos controles, que não apresentaram imunomarcação (p < 0,05); aos 30 dias, o grupo Cla apresentou redução na imunomarcação para HIF-1α, enquanto o grupo Cla-LIV apresentou aumento da imunomarcação, mas a diferença permaneceu apenas entre os grupos clareados e seus controles (p > 0,05). Conclusão: O laser infravermelho minimizou o infiltrado inflamatório e a imunomarcação de IL-23 no tecido pulpar após a clareação dentária, mas não influenciou a imunomarcação de HIF-1α(AU)

Introduction: The use of infrared laser (IRL) through photobiomodulation has shown beneficial effects on tissues. Objectives: To evaluate the influence of LLL on the inflammatory process, by immunolabeling IL-23 pro-inflammatory interleukin, and on angiogenesis, by immunolabeling hif-1 alpha inducible factor (HIF-1α) in the pulp tissue of bleached teeth (HIF-1α). Materials and methods: Forty Wistar rats were randomly divided into 4 groups of 20 hemimaxilla each: control group - received treatment with placebo gel; Ble group - received 30 minutes of 35% H2O2 bleaching gel; IRL group - received one application of IRL (808 nm, 30 seconds, 3 J); Ble-IRL group - immediately after application of 35% H2O2, received an application of IRL, as described in the IRL group.. After 2 and 30 days (n = 10), the rats were euthanized and the jaws removed and processed for histological evaluation (H.E.) and immunohistochemistry. Form of analysis: Serial tissue sections with thickness of 5 µm stained in H.E. were evaluated by scores attributed to inflammation, and immunohistochemical analysis was performed by scores attributed to immunolabeling. The data were submitted to the Wilcoxon and Mann Whitney tests (P < 0.05). Results: At 2 days, there was a severe inflammation and the presence of necrosis in the occlusal and middle thirds of the pulp tissue in the Ble group, different compared to the Ble-IRL group with moderate to mild inflammation (P < 0.05). In the cervical third, there was moderate to severe inflammation in the Ble group, and mild in the Ble-IRL group (P < 0.05). At 30 days, there was absence of inflammation and bleached groups had an extensive deposition of tertiary dentin. Regarding IL-23, at 2 days was observed severe immunolabeling in the Ble group and moderate in the Ble-IRL group (P < 0.05); at 30 days, there was a reduction in IL-23 immunolabeling in the bleached groups, where Ble group had moderate immunolabeling, and Ble-IRL group had mild immunolabeling, without significant difference (P > 0.05). HIF-1α was more evident at 2 days in the Ble group, without significant difference with Ble-IRL (P > 0.05). The difference was observed between the bleached groups and their respective controls, which had no immunolabeling (P < 0.05); at 30 days, the Ble group had a reduction in HIF-1α immunolabeling, while the Ble-IRL group had an increase in immunolabeling from moderate to severe; however, the difference remained only between the bleached groups and their controls (P > 0.05). Conclusion: Infrared laser minimized the inflammatory infiltrate and IL-23 immunolabeling in the pulp tissue after dental bleaching, but did not influenced HIF-1α immunolabeling(AU)

Systemic Th17 response in the presence of periodontal inflammation

Abstract The relationship between periodontitis and the pathogenesis of other inflammatory diseases, such as diabetes, rheumatoid arthritis and obesity has been an important topic of study in recent decades. The Th17 pathway plays a significant role in how local inflammation can influence systemic inflammation in the absence of systemic pathology. Objective: To determine Th17 biased-cells in systemically healthy patients in the presence of generalized chronic periodontitis. Methodology: A total of 28 patients were recruited without systemic inflammatory pathology, which was determined by clinical history, the Health Assessment Questionnaire (HAQ) and rheumatoid factor detection. Of these patients, 13 were diagnosed as healthy/gingivitis (H/G) and 15 as generalized chronic periodontitis (GCP). Th17 (CD4+CD161+) cells and Th17IL23R+ (CD4+CD161+IL-23R+) cells were quantified by flow cytometry, based on the total cells and on the lymphocyte region, termed the "enriched population" (50,000 events for each). Results: The percentages of Th17 cells of the H/G and periodontitis groups were similar on total cells and enriched population (19 vs 21.8; p=4.134 and 19.6 vs 21.8; p=0.55). However, Th17IL23R+ cells differ significantly between periodontally healthy patients and generalized chronic periodontitis patients in both total cell (0.22% vs 0.65%; p=0.0004) and enriched populations (0.2% vs 0.75%; p=0.0266). Conclusions: GCP patients (otherwise systemically healthy) were characterized by increased Th17-proinflammatory cell phenotype positive for the IL-23 receptor in peripheral blood. The proportion of Th17 cells that are negative for the IL-23 receptor in the peripheral blood of systemically healthy patients seemed to be unaffected by the presence or absence of chronic periodontitis.

Induction of Follicular-Like CXCR5+ CD8+ T Cells by TGF-ß1/IL-23 Is Limited During HIV Infection.

Follicular CD4+ T cells are the main HIV reservoirs due to, among other factors, the low frequency of CD8+ T cells in lymphoid follicles. Follicular CXCR5+ CD8+ T cells are associated with HIV control, but their differentiation conditions are yet undefined. In this study, we explored the in vitro effect of transforming growth factor (TGF)-ß1, interleukin (IL)-12, and IL-23 on the induction of CXCR5, the follicle homing receptor, in human circulating CD8+ T cells from seronegative, and treated HIV-infected individuals. The combination of TGF-ß1 plus IL-23 induced the highest expression of CXCR5 in purified CD8+ T cells. These CXCR5+ CD8+ T cells also expressed a transcriptional and phenotypic profile similar to that of follicular CD4+ T cells, such as the upregulation of BCL6, inducible costimulator and CD40L, and downregulation of PRDM1. These cells responded in vitro to CXCL13 and had low expression of CCR7. In addition, after polyclonal stimulation, they produced IL-21, interferon-γ, and de novo perforin. However, in comparison with seronegative individuals, CD8+ T cells from HIV-infected patients had a lower response to TGF-ß1/IL-23, a defect that was restored with the blockade of the programmed cell death 1 inhibitory receptor. Thus, TGF-ß1 plus IL-23 induce follicular-like CXCR5+ CD8+ T cells in seronegative individuals, but in HIV-infected patients there is a limited response which could impair the generation of this cell population.

The rs2066808 Polymorphism Located Near the IL-23A Gene Is Associated with Premature Coronary Artery Disease in Mexican Population (GEA Study).

Interleukin-23 (IL-23) has been associated with atherosclerosis in both humans and animal models with contradictory results. This cytokine is conformed by an α p19 (encoded by IL-23A gene) and a ß p40 subunit (encoded by IL-12B gene). The aim of this study was to evaluate the association of two polymorphisms located within (rs11171806) or near (rs2066808) of the IL-23A gene with the presence of premature coronary artery disease (CAD) and with cardiometabolic parameters. The rs2066808 and rs11171806 polymorphisms were determined in 2249 Mexican individuals (1160 with premature CAD and 1089 healthy controls). Under recessive and codominant 2 models, adjusted by confounding variables, the rs2066808 polymorphism could increase the genetic risk of premature CAD (odds ratio [OR] = 4.567, 95% confidence interval [CI]: 1.03-20.24, Precessive = 0.046 and OR = 4.606, 95% CI: 1.039-20.43, Pcodominant2 = 0.044). The association of the polymorphisms with cardiovascular risk factors was evaluated separately in premature CAD patients and healthy controls. In patients, the rs2066808 polymorphism could decrease the genetic risk of hyperinsulinemia, insulin resistance, and hypoalphalipoproteinemia, and increase the genetic risk of hyperuricemia, whereas the rs11171806 polymorphism could decrease the genetic risk of hyperinsulinemia and insulin resistance. In healthy controls, the rs11171806 polymorphism could decrease the genetic risk of hyperinsulinemia. These findings suggest that the rs2066808 polymorphism located near the IL-23A gene could increase the genetic risk of premature CAD and both studied polymorphisms could be associated with some cardiometabolic parameters in premature CAD patients and in healthy controls.

Tras los pasos de la interleucina-23. su papel en la psoriasis / Following the footsteps of interleukin - 23. its role in psoriasis

Resumen: La psoriasis es una enfermedad inflamatoria crónica multisistémica con compromiso de la piel, de distribución mundial, que afecta todas las edades y a ambos sexos; dentro de su complejo origen etiológico interactúan factores genéticos, inmunológicos y ambientales. Se ha descrito que la relación de la IL-23 y los linfocitos Th17 forman un eje que está íntimamente asociado con la patogénesis de esta enfermedad. La IL-23 es producida por macrófagos y células dendríticas. Está conformada por dos subunidades: la p40, que es común para la IL-12, y la p19, que es exclusiva de la IL-23. Dado que la subunidad p19 es abundante en la piel con psoriasis, se han venido diseñando moléculas que la bloquean, y que a la fecha han mostrado eficacia clínica en el control de las lesiones en la piel. En este artículo de revisión se presenta el panorama general de la IL-23 en psoriasis y el advenimiento de las moléculas dirigidas a modificar su actividad biológica.

Summary: Psoriasis is a multisystem chronic inflammatory disease with skin involvement, worldwide distribution that affects all ages and both sexes; Genetic, immunological and environmental factors interact within its complex etiological origin. It has been described that the relationship of IL-23 and Th17 lymphocytes form an axis that is intimately associated with the pathogenesis of this disease. IL-23 is produced by macrophages and dendritic cells and is composed of two subunits, p40 which is common for IL-12, and p19 that is unique to IL-23. Since p19 is abundant in the skin with psoriasis, molecules have been designed to block it, and to date they have shown clinical efficacy in the control of skin lesions. In this review article we present the general panorama of IL-23 in psoriasis and the advent of molecules aimed at modifying its biological activity.

High IL-17 expression is associated with an unfavorable prognosis in thyroid cancer.

Previous studies have indicated that cancer may be promoted and/or exacerbated by inflammation and infection. The cytokines produced by activated innate immune cells that stimulate tumor growth and progression are considered as important components in this process. The interleukin (IL)-23/T helper (Th)17 axis, which exerts marked pro-inflammatory effects, has emerged as an important mediator in inflammation-associated cancer. Increasing clinical evidence indicates that Th17 may promote or inhibit tumor progression, however, the function of Th17 in the pathogenesis of benign and malignant thyroid neoplasms remains unclear. The present study investigated the association between the IL-23/Th17 axis and neoplastic and non-neoplastic thyroid lesions using immunohistochemistry. A total of 131 thyroid biopsy specimens were analyzed, which revealed high IL-17 and IL-23 expression in differentiated thyroid cancer and medullary thyroid cancer tissues when compared with benign lesions, including follicular thyroid adenoma and goiter tissues. Furthermore, high IL-17 expression was associated with recurrence and mortality. These results indicate that the IL-23/Th17 axis exhibits a pivotal function in the development of thyroid neoplasms.

Interleukin (IL)-23 Stimulates IFN-γ Secretion by CD56bright Natural Killer Cells and Enhances IL-18-Driven Dendritic Cells Activation.

Interleukin (IL)-23 is a member of the IL-12 family of cytokines that, as the other members of this family, is secreted by monocytes, macrophages, and dendritic cells (DC) upon recognition of bacterial, viral, and fungal components. IL-23 is critical during immunity against acute infections, and it is also involved in the development of autoimmune diseases. Although immunoregulatory effects of IL-23 on mouse natural killer (NK) cells have been described, the effect of IL-23 on human NK cells remains ill-defined. In this study, we observed that monocytes stimulated with LPS secreted IL-23 and that blockade of this cytokine during monocyte and NK cell coculture led to a diminished production of IFN-γ by NK cells. Accordingly, rIL-23-induced NK cell activation and stimulated IFN-γ production by CD56bright NK cells. This effect involved MEK1/MEK2, JNK, PI3K, mammalian target of rapamycin, and NF-κB, but not STAT-1, STAT-3, nor p38 MAPK pathways. Moreover, while NK cell-mediated cytotoxicity remained unaltered, antibody-dependent cellular cytotoxicity (ADCC) was enhanced after IL-23 stimulation. In addition, IL-23 displayed a synergistic effect with IL-18 for IFN-γ production by both CD56bright and CD56dim NK cells, and this effect was due to a priming effect of IL-23 for IL-18 responsiveness. Furthermore, NK cells pre-stimulated with IL-18 promoted an increase in CD86 expression and IL-12 secretion by DC treated with LPS, and IL-23 potentiated these effects. Moreover, IL-23-driven enhancement of NK cell "helper" function was dependent on NK cell-derived IFN-γ. Therefore, our results suggest that IL-23 may trigger NK cell-mediated "helper" effects on adaptive immunity, shaping T cell responses during different pathological situations through the regulation of DC maturation.

Elementos clave de la inmunogenética de la psoriasis: A review / Key elements of psoriasis immunogenetics / Elementos importantes da imunogenética da psoríase

La psoriasis, que afecta de 2% a 3% de la población mundial, es una de las enfermedades cutáneas más frecuentes, Se presenta en cualquier etapa de la vida. La psoriasis tipo I o temprana comienza antes de los 40 años en tanto que la tipo II es de inicio tardío, luego de los 40 años. Tiene una fuerte base genética y la probabilidad de heredarla cuando los dos padres están afectados es hasta del 50%. Se han descrito diferentes regiones de susceptibilidad asociadas a la psoriasis, que se denominan PSORS, de las que PSORS-1 es la más frecuente. PSORS-1 está en el cromosoma 6 en el que se localiza el HLA-Cw6, que es el gen hasta ahora más relacionado con la psoriasis. La función de HLA-Cw6 en la psoriasis no está completamente entendida, pero se ha asociado con la psoriasis tipo I, la psoriasis en gotas y la presentación antigénica de una gama de antígenos entre los que se encuentran los derivados de Streptococcus pyogenes. Por otra parte, algunos polimorfismos de nucleótido simple en genes que codifican para citocinas como IL-12, IL-23, TNF-α o sus receptores, se han relacionado con la inmunopatogénesis de esta enfermedad.

Psoriasis is one of the most common skin diseases, affecting 2% to 3% of the world population. It occurs at any stage of life. ''Early'' psoriasis or type I manifests before 40 years, and ''late'' psoriasis or type II, after 40 years. It has a strong genetic basis and the probability of inheriting the disease when both parents are affected is up to 50%. Different susceptibility regions associated with psoriasis, called PSORS, have been described, PSORS-1 being the most frequent one. It is in chromosome 6 and in this region HLA-Cw6 is located, which is until now the gene more associated with psoriasis. The role of HLA-Cw6 in psoriasis is not fully understood, but it has a relationship with type I psoriasis, guttate psoriasis and the presentation of an array of antigens including those derived from Streptococcus pyogenes. Furthermore, some single nucleotide polymorphisms in genes encoding cytokines such as IL-12, IL-23, TNF-α or their receptors are associated with the immunopathogenesis of the disease.

A psoríase, que afeta de 2% a 3% da população mundial, é uma das doenças cutâneas mais frequentes, Apresenta-se em qualquer etapa da vida. A psoríase tipo I ou precoce começa antes dos 40 anos enquanto a tipo II é de início tardio, depois dos 40 anos. Tem uma forte base genética e a probabilidade de herdá-la quando os dois pais estão afetados é até de 50%. Descreveram-se diferentes regiões de susceptibilidade associadas à psoríase, que se denominam PSORS, das que PSORS-1 é a mais frequente. PSORS-1 está no cromossomo 6 no que se localiza o HLA-Cw6, que é o gene até agora mais relacionado com a psoríase. A função de HLA-Cw6 na psoríase não está completamente entendida, mas se associou com a psoríase tipo I, a psoríase em gotas e a apresentação antigénica de uma gama de antígenos entre os que se encontram os derivados de Streptococcus pyogenes. Por outra parte, alguns polimorfismos de nucleótido simples em genes que codificam para citocinas como IL-12, IL-23, TNF-α ou seus receptores, relacionaram-se com a imunopatogênese desta doença.