scholarly journals Cyclophilins A, B, and C Role in Human T Lymphocytes Upon Inflammatory Conditions

2021 ◽  
Vol 12 ◽  
Author(s):  
Sandra Gegunde ◽  
Amparo Alfonso ◽  
Rebeca Alvariño ◽  
Eva Alonso ◽  
Luis M. Botana
Keyword(s):  
Cell Migration ◽  
T Lymphocytes ◽  
Receptor Expression ◽  
Main Function ◽  
Human T Lymphocytes ◽  
T Cell Migration ◽  
Inflammatory Conditions ◽  
Activated T Lymphocytes ◽  
First Time ◽  
The Relationship

Cyclophilins (Cyps) are a group of peptidyl-prolyl cis/trans isomerases that play crucial roles in regulatory mechanisms of cellular physiology and pathology in several inflammatory conditions. Their receptor, CD147, also participates in the development and progression of the inflammatory response. Nevertheless, the main function of Cyps and their receptor are yet to be deciphered. The release of CypA and the expression of the CD147 receptor in activated T lymphocytes were already described, however, no data are available about other Cyps in these cells. Therefore, in the present work intra and extracellular CypA, B and C levels were measured followed by induced inflammatory conditions. After activation of T lymphocytes by incubation with concanavalin A, both intra and extracellular Cyps levels and the CD147 membrane receptor expression were increased leading to cell migration towards circulating CypA and CypB as chemoattractants. When CypA was modulated by natural and synthetic compounds, the inflammatory cascade was avoided including T cell migration. Our results strengthen the relationship between CypA, B, and C, their receptor, and the inflammatory process in human T lymphocytes, associating CypC with these cells for the first time.

Interaction between prostaglandins and human T lymphocytes: Effect of PGE2 on E-receptor expression

1980 ◽  
Vol 2 (2) ◽  
pp. 165-171 ◽  
Author(s):  
D. Venza-Teti ◽  
A. Misefari ◽  
V. Sofo ◽  
V. Fimiani ◽  
M.F. LaVia
Keyword(s):  
T Lymphocytes ◽  
Receptor Expression ◽  
Human T Lymphocytes

CCR2 knockout exacerbates cerulein-induced chronic pancreatitis with hyperglycemia via decreased GLP-1 receptor expression and insulin secretion

2013 ◽  
Vol 304 (8) ◽  
pp. G700-G707 ◽  
Author(s):  
Yuji Nakamura ◽  
Takanori Kanai ◽  
Keita Saeki ◽  
Miho Takabe ◽  
Junichiro Irie ◽  
...  
Keyword(s):  
Cell Migration ◽  
Insulin Secretion ◽  
Chronic Pancreatitis ◽  
Immune Cells ◽  
Receptor Expression ◽  
Wild Type ◽  
Multiple Series ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
The Relationship

Glucagon-like peptide-1 (GLP-1) promotes insulin release; however, the relationship between the GLP-1 signal and chronic pancreatitis is not well understood. Here we focus on chemokine (C-C motif) ligand 2 (CCL2) and its receptor (CCR2) axis, which regulates various immune cells, including macrophages, to clarify the mechanism of GLP-1-mediated insulin secretion in chronic pancreatitis in mice. One and multiple series of repetitive cerulein administrations were used to induce acute and chronic cerulein pancreatitis, respectively. Acute cerulein-administered CCR2-knockout (KO) mice showed suppressed infiltration of CD11b+Gr-1low macrophages and pancreatic inflammation and significantly upregulated insulin secretion compared with paired wild-type (WT) mice. However, chronic cerulein-administered CCR2-KO mice showed significantly increased infiltration of CD11b+/Gr-1− and CD11b+/Gr-1high cells, but not CD11b+/Gr-1low cells, in pancreas with severe inflammation and significantly decreased insulin secretion compared with their WT counterparts. Furthermore, although serum GLP-1 levels in chronic cerulein-administered WT and CCR2-KO mice were comparably upregulated after cerulein administrations, GLP-1 receptor levels in pancreases of chronic cerulein-administered CCR2-KO mice were significantly lower than in paired WT mice. Nevertheless, a significantly higher hyperglycemia level in chronic cerulein-administered CCR2-KO mice was markedly restored by treatment with a GLP-1 analog to a level comparable to the paired WT mice. Collectively, the CCR2/CCL2 axis-mediated CD11b+-cell migration to the pancreas is critically involved in chronic pancreatitis-mediated hyperglycemia through the modulation of GLP-1 receptor expression and insulin secretion.

scholarly journals Mildly oxidized low-density lipoproteins decrease early production of interleukin 2 and nuclear factor κB binding to DNA in activated T-lymphocytes

1999 ◽  
Vol 337 (2) ◽  
pp. 269-274 ◽  
Author(s):  
Sylvie CASPAR-BAUGUIL ◽  
Jean TKACZUK ◽  
Marie-José HAURE ◽  
Martine DURAND ◽  
Julie ALCOUFFE ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
T Lymphocyte ◽  
Active Form ◽  
Nuclear Factor Κb ◽  
Low Density Lipoproteins ◽  
Receptor Expression ◽  
Low Density ◽  
Nuclear Factor ◽  
Oxidized Low Density Lipoproteins ◽  
Activated T Lymphocytes

Activated T-lymphocytes are found early in atherosclerosis lesions, but little is known about their role. Oxidized low-density lipoproteins (oxLDLs) are considered to be involved in the pathogenesis of the lesions, and we have previously demonstrated that oxLDLs inhibit not only interleukin (IL)-2-receptor expression on the surface of in vitro-activated T-lymphocytes but also their proliferation. We have now investigated the effect of oxLDLs on blast differentiation, on IL-2 synthesis and on the activation of the nuclear factor κB (NF-κB) system in activated lymphocytes. Mildly oxLDLs (50 and 100 µg/ml) decreased the number of lymphoblasts and the level of IL-2 concentration in the culture supernatants after activation of lymphocytes by phytohaemagglutinin and PMA+ionomycin. The inhibition of IL-2 production was observed in the CD3+ T-lymphocyte cytoplasm as early as 4 h after activation by PMA+ionomycin. The study of NF-κB showed that oxLDLs led to a decrease of activation-induced p65/p50 NF-κB heterodimer binding to DNA, whereas the presence of the constitutive nuclear form of p50 dimer was unchanged. This was correlated with an unchanged level of the active form of the cytosolic inhibitor protein IκB-α. Taken together, these observations suggest that the immunosuppressive effect of oxLDLs might operate via a dysregulation of the T-lymphocyte activation mechanisms.

scholarly journals Does CXCR3 chemokine receptor expression by CD8+ T cells affect their moving towards or only their binding to virus-infected monocytes?

F1000Research ◽  
2015 ◽  
Vol 4 ◽  
pp. 922
Author(s):  
Johannes M. Dijkstra
Keyword(s):  
T Cells ◽  
Cell Migration ◽  
T Cell ◽  
Chemokine Receptor ◽  
Receptor Expression ◽  
Binding Effect ◽  
T Cell Migration ◽  
Migration Effect ◽  
Virus Clearance ◽  
Infected Cells

This correspondence concerns a recent publication in Immunity by Hickman et al.1 who analyzed the effect of Cxcr3 knockout on migration of CD8+ T cells towards and within vaccinia virus-infected mouse ears.  They found that Cxcr3 knockout had no effect on CD8+ T cell migration into the infected ears, a relatively mild effect on virus clearance, and an effect on the contact of CD8+ T cells with virus-infected cells.  Curiously, despite having these basically sound and interesting data, Hickman et al. exaggerated the effect on virus clearance (“dramatically impaired virus clearance”) and focused their conclusions on assumed differences in migration towards infected cells (“CXCR3 chemokine receptor enables local CD8+ T cell migration”) rather than on better proven differences in binding to infected cells.  I believe that from the data presented by Hickman et al. on the effect of Cxcr3 knockout a migration effect independent from the binding effect cannot be concluded beyond discussion.  The fact that CXCR3 is a chemokine receptor, and that most researchers consequently expect a chemokine-gradient-dependent migration effect of the Cxcr3 knockout mutation, increases the risk of misleading readers when approached through the Hickman et al. narrative.  The here-initiated discussion of their article may help to avoid such a misleading.

Activators of protein kinase C and 5-azacytidine induce IL-2 receptor expression on human T lymphocytes

1985 ◽  
Vol 27 (3) ◽  
pp. 267-276 ◽  
Author(s):  
Joel M. Depper ◽  
Warren J. Leonard ◽  
Cynthia L. Drogula ◽  
Martin Krönke ◽  
Thomas A. Waldmann ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
T Lymphocytes ◽  
Receptor Expression ◽  
Human T Lymphocytes ◽  
Kinase C

scholarly journals Myxoma virus suppresses proliferation of activated T lymphocytes yet permits oncolytic virus transfer to cancer cells

Blood ◽  
2015 ◽  
Vol 125 (24) ◽  
pp. 3778-3788 ◽  
Author(s):  
Nancy Y. Villa ◽  
Clive H. Wasserfall ◽  
Amy M. Meacham ◽  
Elizabeth Wise ◽  
Winnie Chan ◽  
...  
Keyword(s):  
T Cells ◽  
T Lymphocytes ◽  
Cancer Cells ◽  
Inflammatory Cytokines ◽  
Oncolytic Virus ◽  
Myxoma Virus ◽  
Human T Lymphocytes ◽  
Virus Transfer ◽  
Key Points ◽  
Activated T Lymphocytes

Key Points MYXV binds human T lymphocytes but does not enter and infect T cells until after activation. MYXV-infected T lymphocytes proliferate less and secrete less inflammatory cytokines but deliver oncolytic virus to augment GVM.

Modulation of E-receptor expression on activated T lymphocytes

1986 ◽  
Vol 38 (1) ◽  
pp. 55-67 ◽  
Author(s):  
Se-Kyung Oh ◽  
William L. Farrar ◽  
Francis W. Ruscetti
Keyword(s):  
T Lymphocytes ◽  
Receptor Expression ◽  
Activated T Lymphocytes
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