Splicing factor SRSF1 controls distinct molecular programs in regulatory and effector T cells implicated in systemic autoimmune disease

2022 ◽  
Vol 141 ◽  
pp. 94-103
Author(s):  
Michael F. Cassidy ◽  
Zachary T. Herbert ◽  
Vaishali R. Moulton
Keyword(s):  
T Cells ◽  
Autoimmune Disease ◽  
Effector T Cells ◽  
Splicing Factor ◽  
Systemic Autoimmune Disease

scholarly journals CD4+CD25+ T Cells Prevent the Development of Organ-Specific Autoimmune Disease by Inhibiting the Differentiation of Autoreactive Effector T Cells

2005 ◽  
Vol 175 (11) ◽  
pp. 7135-7142 ◽  
Author(s):  
Richard J. DiPaolo ◽  
Deborah D. Glass ◽  
Karen E. Bijwaard ◽  
Ethan M. Shevach
Keyword(s):  
T Cells ◽  
Autoimmune Disease ◽  
Effector T Cells ◽  
Organ Specific

Murine systemic autoimmune disease induced by mercuric chloride (HgCl2): Hg-specific helper T-cells react to antigen stored in macrophages

1993 ◽  
Vol 15 (2) ◽  
pp. 151-161 ◽  
Author(s):  
Malgorzata Kubicka-Muranyi ◽  
Olaf Behmer ◽  
Markus Uhrberg ◽  
Hanne Klonowski ◽  
Joachim Bister ◽  
...  
Keyword(s):  
T Cells ◽  
Autoimmune Disease ◽  
Mercuric Chloride ◽  
Helper T Cells ◽  
Systemic Autoimmune Disease

scholarly journals Mannose Treatment: A Promising Novel Strategy to Suppress Inflammation

2021 ◽  
Vol 12 ◽  
Author(s):  
Wei Zhang ◽  
Hao Cheng ◽  
Yuanyuan Gui ◽  
Qipeng Zhan ◽  
Si Li ◽  
...  
Keyword(s):  
T Cells ◽  
Autoimmune Disease ◽  
High Glucose ◽  
Inflammatory Diseases ◽  
Effector T Cells ◽  
Discovery Process ◽  
Fructose Intake ◽  
Novel Strategy ◽  
Inflammatory Macrophages ◽  
Regulatory Functions

High glucose and fructose intake have been proven to display pro-inflammatory roles during the progression of inflammatory diseases. However, mannose has been shown to be a special type of hexose that has immune regulatory functions. In this review, we trace the discovery process of the regulatory functions of mannose and summarize some past and recent studies showing the therapeutic functions of mannose in inflammatory diseases. We conclude that treatment with mannose can suppress inflammation by inducing regulatory T cells, suppressing effector T cells and inflammatory macrophages, and increasing anti-inflammatory gut microbiome. By summarizing all the important findings, we highlight that mannose treatment is a safe and promising novel strategy to suppress inflammatory diseases, including autoimmune disease and allergic disease.

scholarly journals Nucleosome-Specific Regulatory T Cells Engineered by Triple Gene Transfer Suppress a Systemic Autoimmune Disease

2004 ◽  
Vol 173 (3) ◽  
pp. 2118-2125 ◽  
Author(s):  
Keishi Fujio ◽  
Akiko Okamoto ◽  
Hiroyuki Tahara ◽  
Masaaki Abe ◽  
Yi Jiang ◽  
...  
Keyword(s):  
T Cells ◽  
Autoimmune Disease ◽  
Gene Transfer ◽  
Regulatory T Cells ◽  
Systemic Autoimmune Disease

Impaired thymic negative selection causes autoimmune graft-versus-host disease

Blood ◽  
2003 ◽  
Vol 102 (2) ◽  
pp. 429-435 ◽  
Author(s):  
Takanori Teshima ◽  
Pavan Reddy ◽  
Chen Liu ◽  
Debra Williams ◽  
Kenneth R. Cooke ◽  
...  
Keyword(s):  
T Cells ◽  
Autoimmune Disease ◽  
Mhc Class Ii ◽  
Graft Versus Host Disease ◽  
Negative Selection ◽  
Class Ii ◽  
Systemic Autoimmune Disease ◽  
Host Disease ◽  
Graft Versus Host ◽  
Autoreactive T Cell

AbstractAnimal models with impaired thymic negative selection do not always cause autoimmune diseases despite the development of an autoreactive T-cell repertoire. We investigated the requirements for the de velopment of systemic autoimmune disease by using bone marrow chimeras that lacked expression of major histocompatibility complex (MHC) class II on thymic antigen-presenting cells (APCs), leading to impaired negative selection. We found that impaired negative selection mediated by absence of MHC class II, but not MHC class I, permitted the development of systemic autoimmune disease that is indistinguishable from acute graft-versus-host disease (GVHD). Thymectomy prevented disease, confirming the causal association of the thymus with its development. Adoptive transfer of CD4+ T cells caused GVHD in secondary hosts only when they were irradiated, and cotransfer of peripheral CD4+ and CD8+ T cells from naive mice prevented the disease. These results demonstrate that impaired thymic negative selection can cause lethal autoimmune disease indistinguishable from acute GVHD in the context of a proinflammatory milieu when peripheral regulatory mechanisms are absent.

scholarly journals Rheumatoid Arthritis: Pathogenic Roles of Diverse Immune Cells

2022 ◽  
Vol 23 (2) ◽  
pp. 905
Author(s):  
Sunhee Jang ◽  
Eui-Jong Kwon ◽  
Jennifer Jooha Lee
Keyword(s):  
Rheumatoid Arthritis ◽  
T Cells ◽  
Autoimmune Disease ◽  
Immune Cells ◽  
Cartilage Destruction ◽  
Systemic Autoimmune Disease ◽  
Pannus Formation ◽  
Systemic Complications ◽  
Tissue Proliferation ◽  
Novel Therapeutic

Rheumatoid arthritis (RA) is a chronic, systemic autoimmune disease associated with synovial tissue proliferation, pannus formation, cartilage destruction, and systemic complications. Currently, advanced understandings of the pathologic mechanisms of autoreactive CD4+ T cells, B cells, macrophages, inflammatory cytokines, chemokines, and autoantibodies that cause RA have been achieved, despite the fact that much remains to be elucidated. This review provides an updated pathogenesis of RA which will unveil novel therapeutic targets.

scholarly journals Autoimmune disease in mice due to integration of an endogenous retrovirus in an apoptosis gene.

1993 ◽  
Vol 178 (2) ◽  
pp. 461-468 ◽  
Author(s):  
J Wu ◽  
T Zhou ◽  
J He ◽  
J D Mountz
Keyword(s):  
T Cells ◽  
Autoimmune Disease ◽  
T Cell Development ◽  
Cdna Probe ◽  
Endogenous Retrovirus ◽  
Complete Sequence ◽  
Endogenous Retroviruses ◽  
Systemic Autoimmune Disease ◽  
Polymerase Chain ◽  
Apoptosis Gene

The MRL-lpr/lpr mouse strain is a model of systemic autoimmune disease. In this model, intrinsic defects of intrathymic T cell development include defective deletion of self-reactive T cells and expression of endogenous retroviruses. Defective deletion of self-reactive T cells in the thymus has been proposed to be due to germline mutation in the Fas apoptosis gene. Using different fragments of a Fas cDNA probe, we determined that the lpr/lpr mutation is a 5.3-kb insertion of DNA within the second intron of the Fas gene. cDNA corresponding to this region was then derived from thymic RNA from MRL-lpr/lpr and MRL- +/+ mice using the polymerase chain reaction. All thymic RNA samples from MRL-lpr/lpr mice yielded a unique product that was 168 bp larger than that of MRL- +/+ mice. Complete sequence analysis indicated that this inserted sequence had 98% homology with a sequence from the 3' long terminal repeat of the early transposon (ETn). RNA analysis indicated higher expression of ETn RNA in the thymus of MRL-lpr/lpr than MRL- +/+ mice. The interdependence of ETn expression and abnormal Fas expression was then analyzed in a CD2-Fas transgenic mouse model in which a full-length murine Fas cDNA under the regulation of the CD2 promoter and enhancer was used to correct defective Fas expression in T cells of MRL-lpr/lpr mice. In these mice, reduced thymic ETn expression was observed, confirming that high ETn expression is related to abnormal Fas expression. These results establish a link between endogenous retrovirus expression, abnormal Fas expression, and autoimmune disease.

Sign in / Sign up

Export Citation Format

Share Document