scholarly journals Analysis of Sodium Chloride Intake and Treg/Th17 Lymphocytes in Healthy Individuals and Patients with Rheumatoid Arthritis or Systemic Lupus Erythematosus

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Marlen Vitales-Noyola ◽  
Esther Layseca-Espinosa ◽  
Lourdes Baranda ◽  
Carlos Abud-Mendoza ◽  
Perla Niño-Moreno ◽  
...  

We assessed different immune parameters in patients with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) with low (LSI) and high (HSI) sodium intake. Thirty-eight patients with RA, thirty-seven with SLE, and twenty-eight healthy subjects were studied and classified as LSI or HSI. Levels and suppressive function of CD4+CD25+Foxp3+ and CD4+CD69+Foxp3− Treg cells were determined by flow cytometry in blood samples. Levels and in vitro differentiation of Th17 cells were also assessed. Similar levels of CD4+CD25+Foxp3+ and CD4+CD69+Foxp3− Treg cells were observed in LSI and HSI patients or controls. However, a positive correlation was detected between sodium intake and levels of CD4+CD25+Foxp3+ Treg cells in SLE and a negative association between CD4+CD69+Foxp3− Treg cells and sodium intake in RA. No other significant associations were detected, including disease activity and sodium intake. Moreover, the suppressor activity of CD4+CD25+Foxp3+ and CD4+CD69+Foxp3− Treg cells was similar in LSI and HSI patients or controls. The levels and in vitro differentiation of Th17 cells were also similar in LSI and HSI individuals. Our results suggest that, in the population studied (Mexican mestizo), the level of sodium intake is not apparently associated with different relevant immune parameters in healthy subjects or patients with SLE or RA.

2014 ◽  
Vol 44 (2) ◽  
pp. 267-267 ◽  
Author(s):  
Chiara Tani ◽  
Dario D’Aniello ◽  
Niccolò Possemato ◽  
Andrea Delle Sedie ◽  
Davide Caramella ◽  
...  

2012 ◽  
Vol 2012 ◽  
pp. 1-5 ◽  
Author(s):  
Alessia Alunno ◽  
Elena Bartoloni ◽  
Onelia Bistoni ◽  
Giuseppe Nocentini ◽  
Simona Ronchetti ◽  
...  

Pathogenic mechanisms underlying the development of systemic lupus erythematosus (SLE) are very complex and not yet entirely clarified. However, the pivotal role of T lymphocytes in the induction and perpetuation of aberrant immune response is well established. Among T cells, IL-17 producing T helper (Th17) cells and regulatory T (Treg) cells represent an intriguing issue to be addressed in SLE pathogenesis, since an imbalance between the two subsets has been observed in the course of the disease. Treg cells appear to be impaired and therefore unable to counteract autoreactive T lymphocytes. Conversely, Th17 cells accumulate in target organs contributing to local IL-17 production and eventually tissue damage. In this setting, targeting Treg/Th17 balance for therapeutic purposes may represent an intriguing and useful tool for SLE treatment in the next future. In this paper, the current knowledge about Treg and Th17 cells interplay in SLE will be discussed.


2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 1073.1-1073
Author(s):  
F. Natalucci ◽  
F. Ceccarelli ◽  
T. Colasanti ◽  
G. Olivieri ◽  
A. I. Celia ◽  
...  

Background:Joint involvement represents one of the most frequent features in patients affected by Systemic Lupus Erythematosus (SLE). This manifestation is characterized by a great heterogeneity in phenotype and severity: the application of more sensitive imaging techniques identified an erosive damage in about 25% of patients (1). This damage has been associated with autoantibodies, such as anti-citrullinated (ACPA) and anti-carbamylated proteins (antiCarP), previously identified in patients Rheumatoid Arthritis (RA) patients. Recently, homocysteinylated alpha 1 antitrypsin (Hcy-1A1AT) has been identified as a new antigenic target of autoantibodies in seronegative RA patients: in detail, anti-homocysteinylated alpha 1 antitrypsin (anti – HATA) antibodies have been identified in 75.7% of patients (2).Objectives:In the present study, we aimed at determining the prevalence of anti – HATA in a cohort of SLE patients.Methods:We evaluated patients affected by SLE according to the 1997 ACR criteria. Demographic, clinical, and laboratory data were collected in a standardized computerized electronically filled form. Each subject underwent peripheral blood sample collection. Hcy-A1AT was obtained by in vitro modification of native A1AT and used as antigens by ELISA to test the presence of anti–HATA in sera obtained from enrolled subjects. Finally, we investigated the presence of ACPA and Rheumatoid Factor (RF) commercial ELISA kits and of anti-CarP (home-made ELISA) by a home-made ELISA in SLE patients’ sera. As control, we enrolled 40 patients affected by Osteoarthritis (OA) and 41 healthy subjects (HS).Results:The present analysis included 88 SLE patients (M/F 6/82 median age 47 years (IQR 17), median disease duration 156 months (IQR 180). Joint involvement was observed in 75 SLE patients (85.2%): in detail, 65 patients referred arthritis and the remaining 10 inflammatory arthralgias. We identified the presence of anti–HATA IgG in 38 SLE patients (43.2%). This prevalence was significantly higher in comparison with OA and HS subjects [15.0% (p<0.001) and 0% (p<0.0001), respectively; Figure 1A]. Focusing on the SLE cohort, no differences were observed between patients with and without joint involvement in anti–HATA IgG prevalence (41.3% versus 34.7%, respectively; p=0.34). However considering SLE patients according to the presence of arthralgia and arthritis, the prevalence of anti-HATA was significantly higher in patients with arthritis in comparison with those patients with arthralgias (46.1% versus 11.1%, p=0.02; figure 1B). Finally, no significant association between anti-HATA and the other tested autoantibodies (RF, ACPA, anti-CarP) was found.Conclusion:We evaluated the prevalence of anti-HATA in a cohort of SLE patients. The prevalence of these autoantibodies was significantly higher in SLE patients than in OA patients and in HS. The association with arthritis suggests a possible role for anti-HATA as biomarkers of SLE-related joint involvement.References:[1]Ceccarelli F. Perricone C. Cipriano E. et al. Joint involvement in systemic lupus erythematosus: From pathogenesis to clinical assessment. Seminar in Arthritis and Rheumatism, 47(1), 53 – 64.[2]Colasanti T. Sabatinelli D. Mancone et al. Homocysteinylated alpha 1 antitrypsin as an antigenic target of autoantibodies in seronegative rheumatoid arthritis patients. Journal of Autoimmunity 2020 Sep;113:102470.Disclosure of Interests:None declared


2021 ◽  
Vol 9 (A) ◽  
pp. 169-176
Author(s):  
Azizah Retno Kustiyah ◽  
Agung Putra ◽  
Taufiqurrachman Nasihun ◽  
Rajesh Ramasamy

BACKGROUND: Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by altered T-cell population homeostasis, including Th1 and Th17 populations. Mesenchymal stem cell (MSC)-induced i-Treg in SLE milieu can suppress Th17 cell populations; however, Th1 cell population status as a response to the Th17 decrease remains unclear. Therefore, improving SLE flare by suppressing Th17 and constantly controlling Th1 under normal level through MSCs administration is crucial. AIM: This study aimed to investigate the role of MSCs in suppressing Th17 cell populations and controlling Th1 to a normal level by in vitro coculturing MSCs with PBMC from SLE patients.. METHODS: This study used a post-test control group design. MSCs were obtained from human umbilical cord blood and characterized according to their surface antigen expression and multilineage differentiation capacities. PBMCs isolated from SLE patients were divided into five groups: Sham, control, and three treatment groups. The treatment groups were treated by coculturing MSCs to PBMCs with a ratio of 1:10, 1:25, and 1:40 for 72 h incubation. Th1 and Th17 cells were analyzed by flow cytometry. RESULTS: This study showed that there was no significance difference of the percentages of Th1 cells on all treatment groups. On the other hand, the percentages of Th17 were significantly decreased on T1 group. Interestingly, there was also significant decrease of Th1-like Th17 cells population on T1 group. CONCLUSIONS: MSCs may suppress Th17 and control Th1 to a normal level by in vitro coculturing MSCs with PBMC from SLE.


2017 ◽  
Vol 44 (1) ◽  
pp. 412-422 ◽  
Author(s):  
Ning An ◽  
Yanwen Chen ◽  
Chao Wang ◽  
Chen Yang ◽  
Zhi-hong Wu ◽  
...  

Background: Imbalanced cellular immunity is critical to the pathogenesis of systemic lupus erythematosus (SLE). Recently, autophagy has emerged as a key homeostatic mechanism in T lymphocytes. This study was conducted to explore the impact of autophagy on the Th17/ regulatory T (Treg) immune imbalance in SLE. Methods: Peripheral Th17 and Treg cells from newly diagnosed patients with SLE and healthy controls were detected by flow cytometry. Additionally, the effects of chloroquine (CQ) autophagic inhibition on the Th17/Treg immune response were investigated in vitro. In addition, hydroxychloroquine (HCQ) treatment of the Th17/Treg immune response and the disease progression of lupus MRL/lpr mice were studied in vivo. Results: Compared with healthy controls, both peripheral Th17 and Treg cells of patients with SLE exhibited activated autophagy, resulting in a heightened Th17 proinflammatory response and diminished Treg immunosuppression. Furthermore, in vitro experiments indicated that CQ autophagic inhibition effectively rebalanced the Th17/Treg immune responses in patients with SLE. In vivo studies of MRL/lpr mice similarly confirmed that HCQ treatment decisively inhibited the autophagy of Th17/Treg cellular subsets, restoring the immune balance, lowering the serum levels of inflammatory cytokines and autoantibodies, and improving renal histopathology. Conclusion: Activated autophagy contributed to the Th17/Treg immune imbalance in SLE, and chloroquine autophagic inhibition rebalanced Th17/ Treg-mediated immunity and ameliorated SLE.


2014 ◽  
Vol 44 (2) ◽  
pp. 261-266 ◽  
Author(s):  
Tani Chiara ◽  
D’aniello Dario ◽  
Possemato Niccolò ◽  
Delle Sedie Andrea ◽  
Caramella Davide ◽  
...  

1991 ◽  
Vol 37 (10) ◽  
pp. 1691-1695 ◽  
Author(s):  
A M Teppo ◽  
K Metsärinne ◽  
F Fyhrquist

Abstract We present a double-antibody radioimmunoassay for determining human interleukin-6 (IL-6) in biological fluids. The detection limit of the assay is 20 ng/L (B0 - 2 SD). Bound radioactivity in the range of 30% to 90% of the B0 counts corresponds to IL-6 concentrations of 100 to 14,000 ng/L. Analytical recovery of IL-6 added to EDTA-treated plasma averaged 25% more than that added to serum. The plasma concentration of IL-6 was therefore approximately 85 ng/L more than the concentration in simultaneously drawn serum. The mean serum concentration of IL-6 in 45 healthy subjects was 83 ng/L (range 20-290 ng/L), in 20 patients with multiple myeloma 303 ng/L, in 20 patients with rheumatoid arthritis 234 ng/L, and in 13 patients with systemic lupus erythematosus 183 ng/L. Markedly increased (greater than 3000 ng/L) concentrations of IL-6 were found in sera of patients with meningococcus meningitis and infectious peritonitis.


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