scholarly journals DNA-like class R inhibitory oligonucleotides (INH-ODNs) preferentially block autoantigen-induced B-cell and dendritic cell activation in vitro and autoantibody production in lupus-prone MRL-Faslpr/lpr mice in vivo

2009 ◽  
Vol 11 (3) ◽  
pp. R79 ◽  
Author(s):  
Petar Lenert ◽  
Kei Yasuda ◽  
Liliana Busconi ◽  
Patrice Nelson ◽  
Courtney Fleenor ◽  
...  
Keyword(s):  
Dendritic Cell ◽  
B Cell ◽  
Cell Activation ◽  
Dendritic Cell Activation ◽  
Autoantibody Production

scholarly journals CXCL8 Associated Dendritic Cell Activation Marker Expression and Recruitment as Indicators of Favorable Outcomes in Colorectal Cancer

2021 ◽  
Vol 12 ◽  
Author(s):  
Enhao Li ◽  
Xiaobao Yang ◽  
Yuzhang Du ◽  
Guanzheng Wang ◽  
David W. Chan ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Dendritic Cell ◽  
Cell Activation ◽  
Suppressor Cells ◽  
The Cancer Genome Atlas ◽  
Dendritic Cell Activation ◽  
Antitumor Effects ◽  
Activation Markers

Accumulating evidence suggests that tumor-infiltrating immune cells (TICs) in the tumor microenvironment (TME) serve as promising therapeutic targets. CXCL8 (IL-8) may also be a potential therapeutic target in cancer. CXCL8 is a potent chemotactic factor for neutrophils, myeloid-derived suppressor cells (MDSCs) and monocytes, which are considered immunosuppressive components in cancer-bearing hosts. Here, we identified the TME-related gene CXCL8 in a high-ImmuneScore population that contributed to better survival in colorectal cancer (CRC) patients from The Cancer Genome Atlas (TCGA) database. An integrated gene profile and functional analysis of TIC proportions revealed that the dendritic cell (DC) activation markers CD80, CD83, and CD86 were positively correlated with CXCL8 expression, suggesting that CXCL8 may be functional as antitumor immune response status in the TME. The gene signature was further validated in independent GSE14333 and GSE38832 cohorts from the Gene Expression Omnibus (GEO). To test the differential contributions of immune and tumor components to progression, three CRC cell lines, CT26, MC38 and HCT116, were used. In vitro results suggested no significant growth or survival changes following treatment with an inhibitor of the CXCL8 receptor (CXCR1/2) such as reparixin or danirixin. In vivo treatment with danirixin (antagonists of CXCR2) promoted tumor progression in animal models established with CT26 cells. CXCR2 antagonism may function via an immune component, with CXCR2 antagonist treatment in mice resulting in reduced activated DCs and correlating with decreased Interferon gamma (IFN-γ) or Granzyme B expressed CD8+ T cells. Furthermore, CXCL8 induced DC migration in transwell migration assays. Taken together, our data suggested that targeting the CXCL8-CXCR2 axis might impede DC activation or recruitment, and this axis could be considered a favorable factor rather than a target for critical antitumor effects on CRC.

scholarly journals sp2-Iminosugar glycolipids as inhibitors of lipopolysaccharide-mediated human dendritic cell activation in vitro and of acute inflammation in mice in vivo

2019 ◽  
Vol 169 ◽  
pp. 111-120 ◽  
Author(s):  
Evelyne Schaeffer ◽  
Elena M. Sánchez-Fernández ◽  
Rita Gonçalves-Pereira ◽  
Vincent Flacher ◽  
Delphine Lamon ◽  
...  
Keyword(s):  
Dendritic Cell ◽  
Cell Activation ◽  
Acute Inflammation ◽  
Human Dendritic Cell ◽  
Dendritic Cell Activation

CNI-1493 mediated suppression of dendritic cell activation in vitro and in vivo

Immunobiology ◽  
2004 ◽  
Vol 209 (1-2) ◽  
pp. 89-97 ◽  
Author(s):  
Elisabeth Zinser ◽  
Nadine Turza ◽  
Alexander Steinkasserer
Keyword(s):  
Dendritic Cell ◽  
Cell Activation ◽  
Dendritic Cell Activation

scholarly journals APRIL-Deficient Mice Have Normal Immune System Development

2004 ◽  
Vol 24 (3) ◽  
pp. 997-1006 ◽  
Author(s):  
Eugene Varfolomeev ◽  
Frank Kischkel ◽  
Flavius Martin ◽  
Dhaya Seshasayee ◽  
Hua Wang ◽  
...  
Keyword(s):  
B Cell ◽  
Cell Activation ◽  
System Development ◽  
Physiological Role ◽  
B Cell Activation ◽  
Tnf Superfamily ◽  
Immune System Development ◽  
Humoral Responses

ABSTRACT APRIL (a proliferation-inducing ligand) is a member of the tumor necrosis factor (TNF) superfamily. APRIL mRNA shows high levels of expression in tumors of different origin and a low level of expression in normal cells. APRIL shares two TNF receptor family members, TACI and BCMA, with another TNF homolog, BLyS/BAFF. BLyS is involved in regulation of B-cell activation and survival and also binds to a third receptor, BR3/BAFF-R, which is not shared with APRIL. Recombinant APRIL and BLyS induce accumulation of B cells in mice, while BLyS deficiency results in severe B-cell dysfunction. To investigate the physiological role of APRIL, we generated mice that are deficient in its encoding gene. APRIL−/− mice were viable and fertile and lacked any gross abnormality. Detailed histological analysis did not reveal any defects in major tissues and organs, including the primary and secondary immune organs. T- and B-cell development and in vitro function were normal as well, as were T-cell-dependent and -independent in vivo humoral responses to antigenic challenge. These data indicate that APRIL is dispensable in the mouse for proper development. Thus, BLyS may be capable of fulfilling APRIL's main functions.

Enhanced B Cell Activation in the Absence of CD81

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 2578-2578
Author(s):  
Mrinmoy Sanyal ◽  
Rosemary Fernandez ◽  
Shoshana Levy
Keyword(s):  
B Cells ◽  
B Cell ◽  
Cell Activation ◽  
Cell Receptor ◽  
Free Calcium ◽  
B Cell Activation ◽  
Membrane Reorganization ◽  
A Cell

Abstract CD81 is a component of the CD19/CD21 coreceptor complex in B cells. This tetraspanin molecule was previously shown to enable membrane reorganization in B cells responding to complement-bound antigens. Here we stimulated B cells via their B cell receptor (BCR) and demonstrate that Cd81−/− B cells fluxed higher intracellular free calcium ion along with increased phosphorylation of PLCγ2 and Syk. The stimulated Cd81−/− B cells also proliferated faster and secreted higher amounts of antibodies. Moreover, activation of the TLR4 pathway in Cd81−/− B cells induced increased proliferation and antibody secretion. Furthermore, Cd81−/− mice mounted a significantly higher immune response to T-cell independent antigens than their wildtype counterparts. Finally, analysis of Cd81−/− B cells that were generated by bone marrow transplantation into Rag1−/− mice confirmed a cell intrinsic hyperactive phenotype. Taken together, these results indicate that CD81 plays a negative role in B cell activation in vitro and in vivo.

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