SAT0163 Defective autophagy in T lymphocytes from patients with systemic lupus erythematosus: Potential role of anti-lymphocyte autoantibodies

2013 ◽  
Vol 71 (Suppl 3) ◽  
pp. 526.4-527
Author(s):  
C. Alessandri ◽  
M. Pierdominici ◽  
F. Conti ◽  
S. Truglia ◽  
C. Barbati ◽  
...  
2018 ◽  
Vol 38 (4) ◽  
pp. 1031-1038 ◽  
Author(s):  
Li Jin ◽  
Xuan Fang ◽  
Chao Dai ◽  
Nan Xiang ◽  
Jinhui Tao ◽  
...  

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 2021 ◽  
pp. 1-6
Author(s):  
Vanessa Ocampo-Piraquive ◽  
Inés Mondragón-Lenis ◽  
Juan G. De los Rios ◽  
Carlos A. Cañas

Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disease with various clinical manifestations, including, rarely, a form of interstitial cystitis (lupus cystitis, LC). LC can be asymptomatic and usually has discrete symptoms that improve with conventional therapies available for SLE and/or typical interstitial cystitis. A very severe and refractory form is rarely described. In this study, we present four patients with SLE and a very severe form of noninfectious cystitis refractory to the different forms of treatment described. The clinical descriptions of the cases, demographic factors, manifestations associated with SLE, and clinical and paraclinical manifestations related to cystitis, treatments, and outcomes are provided. A proposal for the pathogenesis of this condition is based on the common findings of these patients, including the fact that three were in SLE remission and all four receiving rituximab as induction and/or maintenance therapy.


2014 ◽  
Vol 2 (4) ◽  
pp. 662-667 ◽  
Author(s):  
Rada Miskovic ◽  
Aleksandra Plavsic ◽  
Jasna Bolpacic ◽  
Sanvila Raskovic ◽  
Mirjana Bogic

Vitamin D is a steroid hormone that in addition to its well known role in the metabolism of calcium and phosphorus exerts immunoregulatory properties. Data from animal studies and from prospective clinical trials on patients with rheumatoid arthritis, multiple sclerosis and type 1 diabetes point to the potential role of vitamin D as important environmental factor in the development of autoimmune diseases. Such role of vitamin D in systemic lupus erythematosus (SLE) has not yet been sufficiently studied. This review shows the sources, metabolism and mechanism of action of vitamin D, its effect on the cells of the immune system, prevalence and causes of vitamin D deficiency in patients with SLE, the link between vitamin D status and disease activity as well as recommendations for vitamin D supplementation.


2019 ◽  
Vol 200 ◽  
pp. 35-36
Author(s):  
Kunihiro Ichinose ◽  
Masataka Umeda ◽  
Tomohiro Koga ◽  
Atsushi Kawakami

2019 ◽  
Author(s):  
Audrey Lee ◽  
Vicky Cho ◽  
T. Daniel Andrews

AbstractShort tandem repeat (STR) expansions have been shown to be pathogenic in human neurological diseases, such as Huntington disease. Yet, the potential role of STRs in non-neurological diseases has yet to be fully investigated. In this study, the potential role of STR expansions in the pathogenesis of systemic lupus erythematosus (SLE) was investigated using patient genomic data and two computational tools, HipSTR and exSTRa. The length variability of STRs in 76 SLE-associated genes was compared using exome data from 271 SLE affected individuals and 158 of their unaffected relatives. We conclude that no large STR expansions associated with SLE were present in these affected individuals within the 76 genes investigated. Lack of evidence does not negate a pathogenic role for STR expansions in SLE, yet given the number of individuals included in this study, we expect that this is not a common source of pathogenesis in SLE.Significance statementThe increasing availability and decreasing cost of sequencing genomes lends itself to computational analysis, extracting information to aid diagnosis, guide treatment or discover disease mechanisms and new treatments. Computational tools have been developed to look for various types of mutations, including short tandem repeats (STRs), which has been shown to cause diseases such as Huntington disease. Limited research on the possible role of STR expansions in systemic lupus erythematosus (SLE) has been done. Here we use computational tools to compare the length of STRs in 76 SLE-associated genes in patients and their unaffected relatives. Our results did not identify any large STR expansions associated with SLE, and further research is required to gain a better understanding of this complex disease.


1999 ◽  
Vol 8 (6) ◽  
pp. 305-312 ◽  
Author(s):  
Ewa Robak ◽  
Jerzy Z. Błoński ◽  
Jacek Bartkowiak ◽  
Hanna Niewiadomska ◽  
Anna Sysa-Jędrzejowska ◽  
...  

Systemic lupus erythematosus (SLE) is a disorder with a wide range of immunological abnormalities. The results of the studies undertaken in the last decade indicated that SLE pathogenesis was mainly connected with the breakdown of the activation control of B and T cells, generating humoral or cell-mediated responses against several self-antigens of affected cells. The last studies demonstrate that the role of γδ T lymphocytes in autoimmune diseases can be especially important. Flow cytometry techniques were used to investigate the number and percentage of TCR γδ T cells and their most frequent subtypes in peripheral blood of 32 patients with SLE and 16 healthy volunteers. We also correlated TCR γδ cells number with the level of T CD3+, T CD4+, T CD8+, and NK (CD16) cells (cytometric measurements) and SLE activity (on the basis of clinical investigations). Our studies were preliminary attempts to evaluate the role of that minor T cell subpopulation in SLE. Absolute numbers of cells expressing γδ TCR in most SLE blood specimens were significantly lower than in the control group (P<0.006). However, since the level of total T cell population was also decreased in the case of SLE, the mean values of the percentage γδ T cells of pan T lymphocytes were almost the same in both analysed populations (7.1% vs 6.3%, respectively). In contrast to Vδ2+ and Vγ9+ subtypes of pan γδ T cells, Vδ3+ T cells number was higher in SLE patients (20×10 cells/μl) than in healthy control group (2×2 cells/μl) (P=0.001). However, we found no differences between the numbers of pan γδ T lymphocytes and studied their subtypes in the patients with active and inactive disease. These cell subpopulations were doubled in the treated patients with immunosuppressive agents in comparison with untreated ones; however, data were not statistically significant. Our study indicated that Vδ3+ subtype of γδ T cells seems to be involved in SLE pathogenesis; however, we accept the idea that the autoimmunity does not develop from a single abnormality, but rather from a number of different events.


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