scholarly journals ROLE OF MUCOSAL-ASSOCIATED INVARIANT T CELLS IN SYSTEMIC LUPUS ERYTHEMATOSUS

2021 ◽  
Vol 44 (2) ◽  
pp. 511-524
Author(s):  
rehab mekkawy ◽  
Omnia El-badawy ◽  
Helal F. Hetta ◽  
Doaa K. Abd El-hafez ◽  
Khaled M. Hassanein
Keyword(s):  
Systemic Lupus Erythematosus ◽  
T Cells ◽  
Lupus Erythematosus ◽  
Systemic Lupus ◽  
Invariant T Cells

scholarly journals Role of Mucosal-Associated Invariant T Cells in Systemic Lupus Erythematosus

2021 ◽  
Vol 0 (0) ◽  
pp. 0-0
Author(s):  
Rehab Mekkawy ◽  
Omnia El-badawy ◽  
Helal Hetta ◽  
Doaa Abd El-hafez ◽  
Khaled Hassanein
Keyword(s):  
Systemic Lupus Erythematosus ◽  
T Cells ◽  
Lupus Erythematosus ◽  
Systemic Lupus ◽  
Invariant T Cells

scholarly journals Leptin promotes systemic lupus erythematosus by increasing autoantibody production and inhibiting immune regulation

2016 ◽  
Vol 113 (38) ◽  
pp. 10637-10642 ◽  
Author(s):  
Elaine V. Lourenço ◽  
Aijing Liu ◽  
Giuseppe Matarese ◽  
Antonio La Cava
Keyword(s):  
Systemic Lupus Erythematosus ◽  
T Cells ◽  
New Zealand ◽  
Renal Disease ◽  
Lupus Erythematosus ◽  
Cellular Level ◽  
Presentation Of Self ◽  
Systemic Lupus ◽  
Autoantibody Production

Leptin is an adipocytokine that plays a key role in the modulation of immune responses and the development and maintenance of inflammation. Circulating levels of leptin are elevated in systemic lupus erythematosus (SLE) patients, but it is not clear whether this association can reflect a direct influence of leptin on the propathogenic events that lead to SLE. To investigate this possibility, we compared the extent of susceptibility to SLE and lupus manifestations between leptin-deficient (ob/ob) and H2-matched leptin-sufficient (wild-type, WT) mice that had been treated with the lupus-inducing agent pristane. Leptin deficiency protected ob/ob mice from the development of autoantibodies and renal disease and increased the frequency of immunoregulatory T cells (Tregs) compared with leptin-sufficient WT mice. The role of leptin in the development of SLE was confirmed in the New Zealand Black (NZB) × New Zealand White (NZW)F1 (NZB/W) mouse model of spontaneous SLE, where elevated leptin levels correlated with disease manifestations and the administration of leptin accelerated development of autoantibodies and renal disease. Conversely, leptin antagonism delayed disease progression and increased survival of severely nephritic NZB/W mice. At the cellular level, leptin promoted effector T-cell responses and facilitated the presentation of self-antigens to T cells, whereas it inhibited the activity of regulatory CD4 T cells. The understanding of the role of leptin in modulating autoimmune responses in SLE can open possibilities of leptin-targeted therapeutic intervention in the disease.

scholarly journals The Role ofγδT Cells in Systemic Lupus Erythematosus

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Meng Wu ◽  
Jinhua Yang ◽  
Xiaofeng Li ◽  
Junwei Chen
Keyword(s):  
Systemic Lupus Erythematosus ◽  
T Cells ◽  
Autoimmune Disease ◽  
Lupus Erythematosus ◽  
Systemic Lupus ◽  
Multiple Organs ◽  
Minor Population ◽  
Neuronal Tissues ◽  
A Minor

Systemic lupus erythematosus (SLE) is an autoimmune disease that is characterized by the overproduction of autoantibodies against an array of nuclear and cytoplasmic antigens and affects multiple organs, such as the skin, joints, kidneys, and neuronal tissues. T cells have been recognized as important players in the development of SLE due to their functions in cytokine secretion, antigen presentation, and supporting B cells for antibody production.γδT cells are a minor population of T cells that play important roles in infection and tumor-associated disease. In recent years, the role ofγδT cells in autoimmune diseases has been investigated. In this review, we discussed the role ofγδT cells in the pathogenesis of SLE.

Regulatory T cells in systemic lupus erythematosus (SLE); Role of peptide tolerance

2012 ◽  
Vol 11 (9) ◽  
pp. 611-614 ◽  
Author(s):  
Priya Sawla ◽  
Awlad Hossain ◽  
Bevra H. Hahn ◽  
Ram P. Singh
Keyword(s):  
Systemic Lupus Erythematosus ◽  
T Cells ◽  
Regulatory T Cells ◽  
Lupus Erythematosus ◽  
Systemic Lupus

Role of Stem Cell-Like Memory T Cells in Systemic Lupus Erythematosus

2018 ◽  
Vol 70 (9) ◽  
pp. 1459-1469 ◽  
Author(s):  
Ye Ji Lee ◽  
Ji Ah Park ◽  
Hyunmi Kwon ◽  
Youn Soo Choi ◽  
Kyeong Cheon Jung ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
T Cells ◽  
Stem Cell ◽  
Lupus Erythematosus ◽  
Memory T Cells ◽  
Systemic Lupus

scholarly journals THU0221 EVIDENCE FOR A PATHOGENIC ROLE OF EXTRA-FOLLICULAR, IL-10 PRODUCING CCR6+B-HELPER T-CELLS IN SYSTEMIC LUPUS ERYTHEMATOSUS

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 337-337
Author(s):  
M. Gerosa ◽  
F. Facciotti ◽  
P. Larghi ◽  
R. Bosotti ◽  
C. Vasco ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
T Cells ◽  
B Cells ◽  
Disease Activity ◽  
B Cell ◽  
Lupus Erythematosus ◽  
Helper T Cells ◽  
Systemic Lupus ◽  
Pathogenic Role

Background:IL-10 plays a key role in systemic lupus erythematosus (SLE) pathogenesis, promoting B-cell response. IL10 is mainly secreted by regulatory T-cells, but follicular helper T-cells (TFH), also produce it. We previously identified a subset of CCR6+IL-7R+T-cells in human tonsils providing IL-10-dependent B-cell help. These CCR6+T-cells were able to produce IL-10, inducing IgG production.Objectives:to investigate a possible role of CD4+CCR6+IL7R+T-cells in SLE pathogenesis.Methods:37 patients fulfilling the ACR criteria for SLE have been included. Disease activity was assessed by 2k-SLEDAI. PBMC were analyzed by flow cytometry, using specific lineage markers. CCR6+IL7R+T-cells purified from total PBMC of SLE patients or healthy donors (HD) were co-cultured with autologous CD20+B-cells. IL-10, Il-17, total IgG and anti-dsDNA antibodies titers in patients serum and culture supernatants were assessed by ELISA. Embedded sections of lymph nodes from 8 SLE patients were analyzed by immunofluorescence (IF).Results:IL10 levels were significantly higher in SLE patients (Fig 1A). CD4+CCR6+IL7R+T-cells were significantly increased in SLE, in particular in those with higher disease activity and higher IL10 levels. CD4+CCR6+IL7R+T-cells levels associated with anti-dsDNA positivity. CCR6+IL7R+T-cells of SLE patients induced production of IgG and anti-dsDNA IgG (in anti-dsDNA + patients) from autologous B-cells, providing spontaneous help for autoantibody productionex vivo(Fig 1B-C). The IF study of lymph nodes of SLE patients showed that IL-10-producing CCR6+T-cells were highly abundant and co-localized with B-cells at follicle margins.Fig 1Conclusion:our study revealed a novel population of extra-follicular B-helper T-cells, which produce IL-10 and could play a prominent pathogenic role in SLE. Further studies will clarify if this potentially pathogenic cell population might represent a possible future therapeutic target.References:[1]Facciotti F. J Allergy Clin Immunol. 2016; Geginat J. Semin Immunol. 2019; Tsokos GC. Nat Rev Rheumatol. 2019Tab 1:SLE patients characteristics(n=37)DemographicsFemale/Male, n37/5Age, years, median (IQR)44 (38-49)Disease duration, years, median (IQR)19 (11-26)Lab testsANA86%*anti-dsDNA (%)46% medium/high titre41%Disease activity and clinical manifestations SLEDAI-2K, median (min-max)3.5 (0-24) Moderate/high activity19%Ongoing therapyPrednisone dose mg/day, median (IQR)7,5 mg (2,5 – 20)hydroxychloroquine78%Immunosuppressants87%Fig 2Disclosure of Interests: :Maria Gerosa: None declared, Federica Facciotti: None declared, Paola Larghi: None declared, Roberto Bosotti: None declared, Chiara Vasco: None declared, Nicola Gagliani: None declared, Chiara Cordiglieri: None declared, Elsa Rottoli: None declared, Alessandra Emiliana Penatti: None declared, Lorenza Maria Argolini: None declared, Bhavna Karnani: None declared, Yasushi Kobayashi: None declared, Mauro Bombaci: None declared, Jan Piet Van Hamburg: None declared, Roberta Gualtierotti: None declared, Stefano Gatti: None declared, Sara Torretta: None declared, Lorenzo Pignataro: None declared, Sander W. Tas: None declared, Roberto Caporali Consultant of: AbbVie; Gilead Sciences, Inc.; Lilly; Merck Sharp & Dohme; Celgene; Bristol-Myers Squibb; Pfizer; UCB, Speakers bureau: Abbvie; Bristol-Myers Squibb; Celgene; Lilly; Gilead Sciences, Inc; MSD; Pfizer; Roche; UCB, Sergio Abrignani: None declared, Massimiliano Pagani: None declared, Fabio Grassi: None declared, Pier Luigi Meroni: None declared, Richard Flavell: None declared, Jens Geginat: None declared

scholarly journals SH3BP2 Deficiency Ameliorates Murine Systemic Lupus Erythematosus

2021 ◽  
Vol 22 (8) ◽  
pp. 4169
Author(s):  
Kyoko Kawahara ◽  
Tomoyuki Mukai ◽  
Masanori Iseki ◽  
Akiko Nagasu ◽  
Hajime Nagasu ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
T Cells ◽  
Dendritic Cells ◽  
Lupus Erythematosus ◽  
Renal Involvement ◽  
Adaptor Protein ◽  
Systemic Lupus ◽  
Murine Systemic Lupus Erythematosus

Background: The adaptor protein Src homology 3 domain-binding protein 2 (SH3BP2) is widely expressed in immune cells. It controls intracellular signaling pathways. The present study was undertaken to investigate the role of SH3BP2 in a murine systemic lupus erythematosus model. Methods: For the lupus model, we used Faslpr/lpr mice. Clinical and immunological phenotypes were compared between Faslpr/lpr and SH3BP2-deficient Faslpr/lpr mice. Splenomegaly and renal involvement were assessed. Lymphocyte subsets in the spleen were analyzed by flow cytometry. To examine the role of SH3BP2 in specific cells, B cell-specific SH3BP2-deficient lupus mice were analyzed; T cells and bone marrow-derived dendritic cells and macrophages were analyzed in vitro. Results: SH3BP2 deficiency significantly reduced lupus-like phenotypes, presented as splenomegaly, renal involvement, elevated serum anti-dsDNA antibody, and increased splenic B220+CD4−CD8− T cells. Notably, SH3BP2 deficiency in B cells did not rescue the lupus-like phenotypes. Furthermore, SH3BP2 deficiency did not substantially affect the characteristics of T cells and macrophages in vitro. Interestingly, SH3BP2 deficiency suppressed the differentiation of dendritic cells in vitro and reduced the number of dendritic cells in the spleen of the lupus-prone mice. Conclusions: SH3BP2 deficiency ameliorated lupus-like manifestations. Modulating SH3BP2 expression could thus provide a novel therapeutic approach to autoimmune diseases.

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