scholarly journals The Role of Decay Accelerating Factor in Environmentally Induced and Idiopathic Systemic Autoimmune Disease

2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Christopher B. Toomey ◽  
David M. Cauvi ◽  
Kenneth M. Pollard
Keyword(s):  
T Cell ◽  
T Cell Activation ◽  
Lupus Erythematosus ◽  
Cell Activation ◽  
T Regulatory Cells ◽  
Experimental Models ◽  
Systemic Autoimmune Disease ◽  
Regulatory Cells ◽  
Decay Accelerating Factor

Decay accelerating factor (DAF) plays a complex role in the immune system through complement-dependent and -independent regulation of innate and adaptive immunity. Over the past five years there has been accumulating evidence for a significant role of DAF in negatively regulating adaptive T-cell responses and autoimmunity in both humans and experimental models. This review discusses the relationship between DAF and the complement system and highlights major advances in our understanding of the biology of DAF in human disease, particularly systemic lupus erythematosus. The role of DAF in regulation of idiopathic and environmentally induced systemic autoimmunity is discussed including studies showing that reduction or absence of DAF is associated with autoimmunity. In contrast, DAF-mediated T cell activation leads to cytokine expression consistent with T regulatory cells. This is supported by studies showing that interaction between DAF and its molecular partner, CD97, modifies expression of autoimmunity promoting cytokines. These observations are used to develop a hypothetical model to explain how DAF expression may impact T cell differentiation via interaction with CD97 leading to T regulatory cells, increased production of IL-10, and immune tolerance.

Fetal–maternal HLA-C mismatch is associated with decidual T cell activation and induction of functional T regulatory cells

2009 ◽  
Vol 82 (2) ◽  
pp. 148-157 ◽  
Author(s):  
Tamara Tilburgs ◽  
Sicco A. Scherjon ◽  
Barbara J. van der Mast ◽  
Geert W. Haasnoot ◽  
Minke Versteeg-v.d.Voort-Maarschalk ◽  
...  
Keyword(s):  
T Cell ◽  
T Cell Activation ◽  
Cell Activation ◽  
T Regulatory Cells ◽  
Regulatory Cells

scholarly journals Delicate Role of PD-L1/PD-1 Axis in Blood Vessel Inflammatory Diseases: Current Insight and Future Significance

2020 ◽  
Vol 21 (21) ◽  
pp. 8159
Author(s):  
Priya Veluswamy ◽  
Max Wacker ◽  
Maximilian Scherner ◽  
Jens Wippermann
Keyword(s):  
T Cell ◽  
Blood Vessel ◽  
T Cell Activation ◽  
Immune Checkpoint ◽  
Cell Activation ◽  
Inflammatory Diseases ◽  
Vascular Inflammation ◽  
Experimental Models ◽  
Cell Immunity

Immune checkpoint molecules are the antigen-independent generator of secondary signals that aid in maintaining the homeostasis of the immune system. The programmed death ligand-1 (PD-L1)/PD-1 axis is one among the most extensively studied immune-inhibitory checkpoint molecules, which delivers a negative signal for T cell activation by binding to the PD-1 receptor. The general attributes of PD-L1’s immune-suppressive qualities and novel mechanisms on the barrier functions of vascular endothelium to regulate blood vessel-related inflammatory diseases are concisely reviewed. Though targeting the PD-1/PD-L1 axis has received immense recognition—the Nobel Prize in clinical oncology was awarded in the year 2018 for this discovery—the use of therapeutic modulating strategies for the PD-L1/PD-1 pathway in chronic inflammatory blood vessel diseases is still limited to experimental models. However, studies using clinical specimens that support the role of PD-1 and PD-L1 in patients with underlying atherosclerosis are also detailed. Of note, delicate balances in the expression levels of PD-L1 that are needed to preserve T cell immunity and to curtail acute as well as chronic infections in underlying blood vessel diseases are discussed. A significant link exists between altered lipid and glucose metabolism in different cells and the expression of PD-1/PD-L1 molecules, and its possible implications on vascular inflammation are justified. This review summarizes the most recent insights concerning the role of the PD-L1/PD-1 axis in vascular inflammation and, in addition, provides an overview exploring the novel therapeutic approaches and challenges of manipulating these immune checkpoint proteins, PD-1 and PD-L1, for suppressing blood vessel inflammation.

scholarly journals 084 UVB induces prolonged T cell activation in lupus-prone mice via type I IFN inhibition of T regulatory cells

2019 ◽  
Vol 139 (5) ◽  
pp. S14
Author(s):  
S. Wolf ◽  
S.N. Estadt ◽  
J. Theros ◽  
T. Moore ◽  
J. Ellis ◽  
...  
Keyword(s):  
T Cell ◽  
T Cell Activation ◽  
Cell Activation ◽  
T Regulatory Cells ◽  
Type I ◽  
Type I Ifn ◽  
Regulatory Cells

scholarly journals Proteoglycan Aggrecan Conducting T Cell Activation and Apoptosis in a Murine Model of Rheumatoid Arthritis

2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
A. Hanyecz ◽  
K. Olasz ◽  
O. Tarjanyi ◽  
P. Nemeth ◽  
K. Mikecz ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
T Cells ◽  
T Cell ◽  
T Cell Activation ◽  
Cell Activation ◽  
Systemic Autoimmune Disease ◽  
T Cell Epitopes ◽  
T Cell Apoptosis ◽  
Autoreactive T Cell

Rheumatoid arthritis (RA) is a systemic autoimmune disease and its targeting of the joints indicates the presence of a candidate autoantigen(s) in synovial joints. Patients with RA show immune responses in their peripheral blood to proteoglycan (PG) aggrecan. One of the most relevant animal models of RA appears to be proteoglycan-induced arthritis (PGIA), and CD4+T cells seem to play a crucial role in the initiation of the disease. In this review, the role of various T cell epitopes of aggrecan in the induction of autoreactive T cell activation and arthritis is discussed. We pay special attention to two critically important arthritogenic epitopes, 5/4E8 and P135H, found in the G1 and G3 domains of PG aggrecan, respectively, in the induction of autoimmune arthritis. Finally, results obtained with the recently developed PG-specific TCR transgenic mice system showed that altered T cell apoptosis, the balance of activation, and apoptosis of autoreactive T cells are critical factors in the development of autoimmunity.

scholarly journals HIV Envelope Suppresses CD4+T Cell Activation Independent of T Regulatory Cells

2008 ◽  
Vol 180 (8) ◽  
pp. 5593-5600 ◽  
Author(s):  
Haitao Hu ◽  
Kathy Fernando ◽  
Houping Ni ◽  
Drew Weissman
Keyword(s):  
T Cell ◽  
T Cell Activation ◽  
Cell Activation ◽  
T Regulatory Cells ◽  
Cd4 T Cell ◽  
Regulatory Cells ◽  
Hiv Envelope
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