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1.
Xu-yan Yang Hui-ying Wang Xiao-ying Zhao Li-juan Wang Qing-hua Lv Qing-qing Wang 《Journal of clinical immunology》2013,33(4):767-774
Purpose
T-helper (Th) cells abnormalities are considered to be associated with the pathogenesis of Systemic lupus erythematosus (SLE). Recently, The Th22 cells have been identified and implicated in the pathogenesis of autoimmune diseases such as Rheumatoid arthritis (RA), although therir role in Systemic lupus erythematosus (SLE) remains unclear. The present study intends to investigate their roles in SLE.Methods
Clinical data were collected in 65 SLE patients and 30 healthy controls. The patients were divided into active and inactive groups. CD4+IFN-γ?IL-17?IL-22+Tcells (Th22 cells),CD4+ IFN-γ?IL-22?IL-17+T cells (Th17 cells),and CD4+ IFN-γ+ (Th1 cells) were assayed by flow cytometry. Serum interleukin-22 (IL-22) and IL-17 levels were measured by enzyme-linked immunosorbent assay.Results
The main observation focused on increased Th22 cells in patients with sole lupus skin disease and decreased Th22 cells in patients with sole lupus nephritis. Likewise, concentrations of serum IL-22 were increased in patients with sole lupus skin disease, and decreased in patients with sole lupus nephritis. Additionally, there was a positive correlation between the percentage of Th22 cells and IL-22 production. The percentage of Th17 cells or concentration of serum IL-17 correlated positively with Systemic Lupus Erythematosus Disease Activity Index (SLEDAI).Conclusion
Th22 seems to be a more significant index to predict the tissue involvement of SLE than Th17, although Th17 may play a role in the activity of SLE. 相似文献2.
Zhang L Li JM Liu XG Ma DX Hu NW Li YG Li W Hu Y Yu S Qu X Yang MX Feng AL Wang GH 《Journal of clinical immunology》2011,31(4):606-614
Background
T-helper (Th) 22 and Th17 cells are implicated in the pathogenesis of autoimmune diseases. The roles of Th22 cells in the pathophysiology of rheumatoid arthritis (RA) remain unsettled.Materials and Methods
CD4+IFN???IL17?IL-22+ T cells (Th22 cells), CD4+IFN???IL-22?IL17+ T cells (pure Th17 cells), CD4+IL17+ T cells (Th17 cells), and CD4+IFN??+ T cells (Th1 cells) in RA, osteoarthritis patients, and healthy controls were examined by flow cytometry. Plasma IL-22 and IL-17 levels were examined by enzyme-linked immunosorbent assay.Results
Th22 cells, pure Th17 cells, Th17 cells, and interleukin-22 were significantly elevated in RA patients compared with osteoarthritis and healthy controls, but there were no significant differences regarding Th1 cells and interleukin-17. Th22 cells showed a positive correlation with interleukin-22 as well as pure Th17 cells or Th17 cells in RA patients. Additionally, the percentages of Th22 cells, pure Th17 cells as well as Th17 cells correlated positively with both C-reactive protein levels and 28-joints disease activity score.Conclusion
Together, our results indicated a possible role of Th22 pure Th17 cells and Th17 cells in RA, and blockade of the interleukin-22 may be a reasonable therapeutic strategy for RA. 相似文献3.
Ester Rosári Raphaelli Dal Ben Carine Hartmann do Prado Talita Siara Almeida Baptista Moisés Evandro Bauer Henrique Luiz Staub 《Journal of clinical immunology》2013,33(4):876-879
Introduction
CD4+CD25+Foxp3+ regulatory T (Treg) cell dysfunction has been documented in various autoimmune disorders, but not in antiphospholipid syndrome (APS) so far.Methods
In this cross-sectional study, we aim to investigate CD4+CD25+Foxp3+ Treg cells, CD3+CD19? T cells and CD3?CD19+ B cells in patients with primary APS and healthy controls. Cell subtypes were immunophenotyped using specific monoclonal antibodies (anti-CD3 CY5, anti-CD4 FITC, anti-CD25, anti-Foxp3, anti-CD19 PE) and flow cytometry.Results
Twenty patients with APS and 20 age- and sex-matched controls were studied. The percentage of total lymphocytes, activated Th cells (CD4+CD25+), Treg cells and CD3?CD19+ B cells were found significantly lower in APS patients as compared to controls (all p?<?0.05).Conclusion
A dysfunction in CD4+CD25+Foxp3+ Treg cells may represent one of the mechanisms leading to autoimmunity in APS patients. The decreased number of CD3?CD19+ B cells of APS patients warrants further elucidation. 相似文献4.
Biagio Di Micco Marilena Lepretti Lidia Rota Ilaria Quaglia Paola Ferrazzi Gianluca Di Micco Pierpaolo Di Micco 《Journal of translational medicine》2007,5(1):1-7
Background
Alefacept (anti-CD2) biological therapy selectively targets effector memory T cells (Tem) in psoriasis vulgaris, a model Type 1 autoimmune disease.Methods
Circulating leukocytes were phenotyped in patients receiving alefacept for moderate to severe psoriasis.Results
In all patients, this treatment caused a preferential decrease in effector memory T cells (CCR7- CD45RA-) (mean 63% reduction) for both CD4+ and CD8+ Tem, while central memory T cells (Tcm) (CCR7+CD45RA-) were less affected, and naïve T cells (CCR7+CD45RA+) were relatively spared. Circulating CD8+ effector T cells and Type 1 T cells (IFN-γ-producing) were also significantly reduced.Conclusion
Alefacept causes a selective reduction in circulating effector memory T cells (Tem) and relative preservation of central memory T cells (Tcm) in psoriasis. 相似文献5.
Ferreyra Solari NE Inzaugarat ME Baz P De Matteo E Lezama C Galoppo M Galoppo C Cherñavsky AC 《Journal of clinical immunology》2012,32(3):611-621
Background
Nonalcoholic steatohepatitis (NASH) is a chronic inflammatory liver disease influenced by risk factors for the metabolic syndrome. In adult patients, NASH is associated with an altered phenotype and functionality of peripheral immune cells, the recruitment of leukocytes and intrahepatic activation, and an exacerbated production of reactive oxygen species (ROS) and cytokines. It remains unclear if the previously described differences between pediatric and adult nonalcoholic fatty liver diseases also reflect differences in their pathogenesis.Aims
We aimed to investigate the phenotype and functionality of circulating immune cells and the potential contribution of liver infiltrating leukocytes to the immunological imbalance in pediatric NASH.Results
By a real-time PCR-based analysis of cytokines and immunohistochemical staining of liver biopsies, we demonstrated that the hepatic microenvironment is dominated by interferon-gamma (IFN-γ) but not interleukin-4 and is infiltrated by a higher number of CD8+ cells in pediatric NASH. The number of infiltrating neutrophils positively correlated with ROS generation by peripheral polymorphonuclear cells. By a flow cytometric analysis of peripheral blood lymphocytes, a distinctive increase in CD8+ CD45RO and CD8+ CD45RA subpopulations and an increased production of IFN-γ by CD4+ and CD8+ cells were shown. The production of ROS following PMA stimulation was augmented in circulating neutrophils but not in monocytes.Conclusion
In sum, the distinctive phenotype and functionality of infiltrating and circulating cells suggest that the role of innate cells is coupled to a Th1-polarized immune response in pediatric NASH. 相似文献6.
Sonia Néron Ph.D. Gilles Boire Nathalie Dussault Claudia Racine Artur J. de Brum-Fernandes Serge C?té Annie Jacques 《Archivum immunologiae et therapiae experimentalis》2009,57(6):447-458
Introduction
Aberrant signaling within and between B and T cells, considered to be central in systemic lupus erythematosus (SLE), could depend on enhanced CD40-CD154 activation. As a result, autoreactive B cells, normally anergic, differentiate and secrete antibodies attacking several normal tissues. Thus restorating B cell homeostasis might help control this disease. In this study, two facets of SLE B cells were investigated, namely their in vitro response to CD40-CD154 and the effect of treatment with human immunoglobulins for intravenous use (IVIg).Materials and Methods
Blood samples from SLE patients and healthy volunteers were obtained and used to isolate B cells, which were activated through CD40 in the presence or absence of IVIg. The phenotype, proliferation, and differentiation of the SLE B cells were determined and compared with those of control B cells using flow cytometry and standard ELISA.Results
In this model, CD40-activated SLE B cells, as control B cells, proliferated and differentiated and were characterized by the emergence of CD19loCD38++CD138+CD27++ cells. IVIg treatment of the CD40-activated SLE B cells resulted in higher differentiation, characterized by increased secretion rates of IgG and IgM, as reported previously for control B cells.Conclusions
Taken as a whole, such accelerated differentiation of CD40-activated B cells suggests that IVIg may participate in re-equilibration of the antibody repertoire by replacing pathological antibodies by de novo harmless antibodies. 相似文献7.
Gaël Mouillot Maryvonnick Carmagnat Laurence Gérard Jean-Luc Garnier Claire Fieschi Nicolas Vince Lionel Karlin Jean-François Viallard Roland Jaussaud Julien Boileau Jean Donadieu Martine Gardembas Nicolas Schleinitz Felipe Suarez Eric Hachulla Karen Delavigne Martine Morisset Serge Jacquot Nicolas Just Lionel Galicier Dominique Charron Patrice Debré Eric Oksenhendler Claire Rabian 《Journal of clinical immunology》2010,30(5):746-755
Background
Common variable immunodeficiency (CVID) is a heterogeneous disorder characterized by recurrent infections and defective immunoglobulin production.Methods
The DEFI French national prospective study investigated peripheral T-cell and B-cell compartments in 313 CVID patients grouped according to their clinical phenotype, using flow cytometry.Results
In patients developing infection only (IO), the main B-cell or T-cell abnormalities were a defect in switched memory B cells and a decrease in naive CD4+ T cells associated with an increase in CD4+CD95+ cells. These abnormalities were more pronounced in patients developing lymphoproliferation (LP), autoimmune cytopenia (AC), or chronic enteropathy (CE). Moreover, LP and AC patients presented an increase in CD21low B cells and CD4+HLA-DR+ T cells and a decrease in regulatory T cells.Conclusion
In these large series of CVID patients, the major abnormalities of the B-cell and T-cell compartments, although a hallmark of CVID, were only observed in half of the IO patients and were more frequent and severe in patients with additional lymphoproliferative, autoimmune, and digestive complications. 相似文献8.
TCRαβ+CD3+CD4?CD8? “double negative” (DN) T cells comprise a small subset of mature peripheral T cells. The origin and function of DN T cells are somewhat unclear and discussed controversially. While DN T cells resemble a rare and heterogeneous T cell subpopulation in healthy individuals, numbers of TCRαβ+ DN T cells are expanded in several inflammatory conditions, where they also exhibit distinct effector phenotypes and infiltrate inflamed tissues. Thus, DN T cells may be involved in systemic inflammation and tissue damage in autoimmune/inflammatory conditions, including SLE, Sjögren's syndrome, and psoriasis. Here, the current understanding of the origin and phenotype of DN T cells, and their role in the instruction of immune responses, autoimmunity and inflammation will be discussed in health and disease. 相似文献
9.
Xu WH Zhang AM Ren MS Zhang XD Wang F Xu XC Li Q Wang J Din BS Wu YB Chen GH 《Journal of clinical immunology》2012,32(5):975-983
Objective
Myasthenia gravis (MG) is a CD4+ T cell-dependent autoimmune disease, and close attention has been paid to the role of CD4+CD25+Treg cells (Tregs). Previous results regarding Tregs in MG patients have been conflicting. The discrepancy was partly ascribed to selecting different Treg-associated molecules in defining Tregs. Therefore, we considered it necessary to find a reliable index for assessing the immunologic state in MG patients and explore the effect of IS on them.Methods
We adopted flow cytometric techniques to measure the numbers and frequencies of Tregs in peripheral blood taken from 57 patients and 91 age-matched healthy donors, and we also analyzed FOXP3 mean fluorescence intensity on Tregs.Results
The number and frequency of Tregs in peripheral blood of MG patients significantly decreased, together with down-regulation of FOXP3 expression. There was dynamic change of Treg cell level and the inverse relationship with clinical symptom, suggesting that the immunologic disorder in MG patients was related to peripheral Tregs population. Meanwhile, CD4+CD25+FOXP3+Helios+T cells might be activated Tregs, rather than nTregs. Moreover, the number and frequency of CD4+CD25+FOXP3+Helios+T cells significantly decreased in MG patients, indicating that the reduction of the activated Tregs population might be a critical contributor to the pathogenesis of MG.Conclusions
The significant reduction of the peripheral Tregs population in MG patients might be responsible for the immunologic disorders in MG patients. IS such as GC took its effect possible by increasing the population size, and the underlying mechanism should be further investigated. 相似文献10.
Paul Eggleton Lorna W. Harries Giada Alberigo Paul Wordsworth Nick Viner Richard Haigh Suzanne Donnelly Hugh W. Jones Ian C. Chikanza Thomas W. E. O’Conner Alasdair E. R. Thomson Paul G. Winyard 《Journal of clinical immunology》2010,30(5):649-658
Introduction
Systemic lupus erythematosus (SLE) and rheumatoid arthritis have complex genetic traits, but in both autoimmune diseases, dysfunctional apoptosis appears to play a part in disease pathology. This study examined the levels of in vitro apoptosis in lymphocytes from healthy, rheumatoid arthritis (RA) and SLE individuals and related observed differences to their lymphocyte apoptosis gene profiles.Materials and Methods
Lymphocytes were assessed for cell death by nuclear pyknosis and DNA fragmentation. Control, SLE and RA apoptosis gene profiles were obtained by quantitative real-time polymerase chain reaction (QRT-PCR) analysis.Results and Discussion
The mean levels of pyknosis in RA and SLE freshly isolated lymphocytes were significantly higher than in control lymphocytes. Ninety-three apoptosis genes were analysed by QRT-PCR of mRNA from RA, SLE and healthy lymphocytes. We identified significant differences (p?<?0.05) in the expression of the same 11 of 93 and two of 93 apoptotic genes in individual SLE and RA patients tested as compared with controls.Conclusion
We propose that similarly altered expression of specific apoptotic regulatory genes (e.g., the death effector domain-containing DNA-binding protein and apoptosis-associated speck-like protein containing a CARD) occurs in the lymphocytes of individual patients with SLE or RA that may influence the extent and rate of spontaneous apoptosis in these autoimmune conditions. 相似文献11.
Sudhir Kumar Chauhan Vikas Vikram Singh Richa Rai Madhukar Rai Geeta Rai 《Journal of clinical immunology》2014,34(4):491-503
Purpose
Systemic lupus erythematosus (SLE) patients have anti-nuclear autoantibodies directed against dsDNA and RNA-associated antigens (extractable nuclear antigens; ENA). In this study, we investigated the differences in microRNA (miRNA) expression and its biological implications in SLE patients with distinct autoantibody specificities.Methods
The SLE patients were grouped into three subsets based on the type of autoantibodies present in their sera (anti-ENA+ group with autoantibodies against ENA alone; anti-dsDNA+ group having autoantibodies against dsDNA only, and anti-ENA+dsDNA+ group having autoantibodies to both dsDNA and ENA). Global miRNA expression profiling was done for each of these three groups using TaqMan® low density miRNA arrays.Results
We report that different sets of miRNAs are dysregulated in SLE patients with different autoantibody specificities. Further, Ingenuity pathway analysis (IPA) software revealed specific biological pathways that were targeted by miRNAs dysregulated in different SLE subsets. Molecules involved in cell cycle and cytoskeleton remodeling were the prime targets of miRNAs dysregulated in anti-ENA+ patients whereas miRNAs dysregulated in anti-dsDNA+ patients were found to be implicated in multiple cytokine signaling pathways. IPA analysis of gene targets of miRNAs commonly dysregulated in all three SLE subsets identified several metabolic-, hormone-, and interferon-related pathways to be affected.Conclusion
The differential miRNA expression in patients with distinct autoantibodies is suggestive of different regulatory mechanisms operating among them. Based on these observations, we are hopeful that this ‘sub-grouping’ approach could be used to identify other defective processes associated with varying disease manifestations in SLE and may be considered when designing therapeutic interventions. 相似文献12.
Nils Hofmann Nina Lachnit Michael Streppel Brigitte Witter Wolfram F Neiss Orlando Guntinas-Lichius Doychin N Angelov 《BMC immunology》2002,3(1):11-13
Background
T-cells extravasation and CNS parenchyma infiltration during autoimmune neurodegenerative disease can be evoked by local antigen presenting cells. Studying the chemoattracting potential of spinal perivascular macrophages (SPM) during experimental allergic encephalomyelitis (EAE), we observed numerous infiltrates of densely-packed mononuclear cells. Apart from the poor spatial and optical resolution, no differentiation between the resident SPM (mabs ED1+, ED2+) and the just recruited monocytes/macrophages (mab ED1+) was possible.Results
This is why we labeled SPM by injections of different fluoresecent dyes into the lateral cerebral ventricle before induction of active EAE. Within an additional experimental set EAE was induced by an intraperitoneal injection of T-cells specifically sensitized to myelin basic protein (MBP) and engineered to express the green fluorescent protein (GFP). In both experiments we observed a strong activation of SPM (mabs OX6+, SILK6+, CD40+, CD80+, CD86+) which was accompanied by a consistently increased expression of ICAM-1, VCAM-1, and the chemokines MCP-1 and MIP-1α.Conclusion
These observations indicate that SPM play a role in promoting lymphocyte extravasation. 相似文献13.
Autoimmune hepatitis (AIH), a severe hepatopathy characterized by hypergammaglobulinaemia, autoantibodies and interface hepatitis, is occasionally associated with systemic autoimmune manifestations [systemic lupus erythematosus (SLE); mixed connective tissue disease (MCTD)]. In both AIH and SLE/MCTD numerical and/or functional impairment of regulatory T-cells (T-regs) is believed to favour autoimmunity. To investigate whether immune-tolerance breakdown profiles differ in patients with AIH and SLE/MCTD, isolated AIH or systemic autoimmunity, we studied phenotypic and functional features of T-regs in 10 patients with AIH-SLE/MCTD, 22 with AIH, 12 with SLE and 20 healthy subjects. Compared to health, CD4posCD25pos cells were decreased in number and expressed high levels of the CD127 activation marker in all three disease groups; in AIH-SLE/MCTD and in SLE they displayed low levels of FOXP3. In AIH-SLE/MCTD, they also contained a high proportion of IFNγ positive cells, indicating a Th1 profile. Similarly, in AIH-SLE/MCTD, CD4posCD25posCD25high T-regs were reduced in number and contained an increased proportion of activated CD127pos and IFNγpos cells. Such skewing towards a Th1 profile was also present at effector level, as a high frequency of IFNγ-producing cells was observed within AIH-SLE/MCTD CD4posCD25neg responder cells. Impairment in suppressor function both of CD4posCD25pos cells and CD4posCD25posCD127neg T-regs was observed in all three autoimmune conditions, but while addition of CD4posCD25posCD127neg T-regs decreased CD4posCD25neg responder cell proliferation in healthy subjects and partially in AIH patients, it had no effect in AIH-SLE/MCTD and SLE patients.In conclusion, in AIH-SLE/MCTD T-regs display a distinctive phenotypic and functional signature, characterized by marked activation, elevated IFNγ production and by a profound impairment of suppressive function, suggesting that multiple autoimmune manifestations may derive from a complex defect of immune-regulation. 相似文献
14.
Kamya P Tsoukas CM Boulet S Routy JP Thomas R Côté P Boulassel MR Lessard B Kaul R Ostrowski M Kovacs C Tremblay CL Bernard NF 《AIDS research and therapy》2011,8(1):20-7
Background
Elite controllers (EC) are a rare subset of HIV infected individuals who control viral load below 50 copies/ml of plasma without treatment.Methods
Thirty four EC were studied. The slope of CD4 count change was available for 25 of these subjects. We assessed immune activation by measuring the percent of CD38+HLA-DR+CD8+ T cells in the EC group and comparing it with that in 24 treatment-naïve HIV disease progressors and 13 HIV uninfected healthy controls.Results
Compared to HIV uninfected subjects, EC had higher percentages of CD38+HLA-DR+CD8+ T cells (p < 0.001) that was lower than that observed in progressors (p < 0.01). Fifteen of 25 EC had a slope of CD4 count change that was not significantly different from 0 while 3 had a positive and 7 a negative CD4 count slope. Immune activation did not distinguish EC subsets with stable/increasing versus declining CD4 counts.Conclusions
Elevated immune activation in ECs is not associated with a faster rate of CD4 decline 相似文献15.
Jolly M Pickard AS Mikolaitis RA Cornejo J Sequeira W Cash TF Block JA 《International journal of behavioral medicine》2012,19(2):157-164
Background
Systemic lupus erythematosus (SLE), a multisystemic disease of young women may be disfiguring and affect physical and emotional health. Body image literature in SLE is scant and controversial.Purpose
We compared body image-related quality of life in subjects with (n?=?87) and without (n?=?78) SLE and determined its correlates using the body image quality of life inventory (BIQLI).Method
The tool was self-administered to consenting individuals. Demographic information along with disease activity and damage assessments for SLE patients were obtained. T test, chi square test, correlational, and regression analyses were used to make comparisons.Results
Mean age (±SD) were 42.4?±?13.1 and 38.7?±?13.2?years for SLE and non-SLE subjects, respectively. Mean (±SD) BIQLI scores were significantly worse in SLE than non-SLE subjects: 19.9?±?33.2 and 41.6?±?24.8 (p?=?0.001). In SLE, BIQLI scores correlated inversely with overall damage, irreversible cutaneous damage, alopecia, and self-reported depression, and directly with age and health status.Conclusion
Body image in SLE is poor, and effective interventions may be directed at cutaneous disease activity, damage, and depression. 相似文献16.
Nechvatalova J Pikulova Z Stikarovska D Pesak S Vlkova M Litzman J 《Journal of clinical immunology》2012,32(3):441-448
Introduction
Selective deficiency IgA (IgAD) is the most common primary abnormality of immunoglobulin production with unknown pathophysiology. It is genetically related to common variable immunodeficiency (CVID), where besides IgA also IgG and frequently IgM serum levels are decreased. In this study we focused on determination of B-lymphocyte developmental stages and searching for similarities between CVID and IgAD.Materials and Methods
Using flow cytometry we determined major lymphocyte subpopulations and B-lymphocyte subsets: na?ve (CD27-IgD+), marginal zone cells (CD27+IgD+), class-switched memory cells (CD27+IgD-), ??double-negative?? B cells (CD27-IgD-), transitional cells (IgM++CD38++), plasmablasts (CD38+++IgM+ or IgM-), and CD21lowCD38low cells in 80 patients with IgAD, 48 patients with CVID, and 80 control persons.Results
Compared to healthy controls, a decrease in the absolute number and frequency of CD4+ cells (both?0.001) was observed in IgAD patients. A decrease in the frequency of switched memory cells (P?0.001), transitional cells (P?=?0.035) as well as plasmablasts (P?0.001) and an increase in the CD21lowCD38low subset (P?=?0.007) was observed in IgAD patients compared to control persons. No significant differences were observed in the remaining B-cell developmental subsets. A decrease in CD27+IgD- (<0.4% of peripheral blood lymphocytes), frequently observed in CVID patients and also previously reported in IgAD, was found in only five patients (6%) with IgAD, two of them being first-degree relatives of CVID patients.Conclusion
Our results show a decrease of terminally differentiated B-lymphocyte subsets in patients with IgAD, similar as previously found in patients with CVID, but these results are less expressed than in CVID patients. 相似文献17.
Keigo Ikeda Kunihiro Hayakawa Maki Fujishiro Mikiko Kawasaki Takuya Hirai Hiroshi Tsushima Tomoko Miyashita Satoshi Suzuki Shinji Morimoto Naoto Tamura Kenji Takamori Hideoki Ogawa Iwao Sekigawa 《BMC immunology》2017,18(1):41
Background
We previously reported that JAK–STAT-pathway mediated regulation of IFN-regulatory factor genes could play an important role in SLE pathogenesis. Here, we evaluated the efficacy of the JAK inhibitor tofacitinib (TOFA) for controlling IFN signalling via the JAK–STAT pathway and as a therapeutic for SLE.Results
We treated NZB/NZW F1 mice with TOFA and assessed alterations in their disease, pathological, and immunological conditions. Gene-expression results obtained from CD4+ T cells (SLE mice) and CD3+ T cells (human SLE patients) were measured by DNA microarray and qRT-PCR. TOFA treatment resulted in reduced levels of anti-dsDNA antibodies, decreased proteinuria, and amelioration of nephritis as compared with those observed in control animals. Moreover, we observed the rebalance in the populations of naïve CD4+ T cells and effector/memory cells in TOFA-treated mice; however, treatment with a combination of TOFA and dexamethasone (DEXA) elicited a stronger inhibitory effect toward the effector/memory cells than did TOFA or DEXA monotherapy. We also detected decreased expression of several IFN-signature genes Ifit3 and Isg15 in CD4+ from SLE-prone mice following TOFA and DEXA treatment, and IFIT3 in CD3+ T cells from human patients following immunosuppressant therapy including steroid, respectively.Conclusion
Modulation of type I IFN signalling via JAK–STAT inhibition may exert a beneficial effect in SLE patients, and our results suggest that TOFA could be utilised for the development of new SLE-specific therapeutic strategies.18.
19.
Zohreh Tatari-Calderone Milica Stojakovic Ramita Dewan Gama Le Bouder Dragana Jankovic Stanislav Vukmanovic 《BMC immunology》2012,13(1):1-11