Accessory cell function of human endothelial cells: presentation of antigen to T cells

1984 ◽  
pp. 385-392
Author(s):  
Henry Hirschberg
Keyword(s):  
T Cells ◽  
Endothelial Cells ◽  
Cell Function ◽  
Accessory Cell ◽  
Human Endothelial Cells

scholarly journals The B7/BB1 antigen is expressed by Reed-Sternberg cells of Hodgkin's disease and contributes to the stimulating capacity of Hodgkin's disease-derived cell lines

Blood ◽  
1993 ◽  
Vol 82 (9) ◽  
pp. 2845-2852 ◽  
Author(s):  
J Delabie ◽  
JL Ceuppens ◽  
P Vandenberghe ◽  
M de Boer ◽  
L Coorevits ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Hodgkin's Disease ◽  
Cell Function ◽  
Cell Lymphoma ◽  
Hodgkin’S Disease ◽  
B Cell Lymphoma ◽  
Accessory Cell ◽  
Hodgkin's Lymphomas ◽  
Antigen Presenting

The B7/BB1 molecule has recently been found to be expressed on professional antigen-presenting cells and to be the natural ligand for CD28 and CTLA-4 on T cells. On binding of B7/BB1, CD28 transduces a signal that synergizes with triggering of the T-cell antigen receptor, resulting in enhanced cytokine secretion. In view of the data supporting an antigen-presenting function of Reed-Sternberg cells, we evaluated the expression of B7/BB1 in lymph nodes affected by Hodgkin's disease. B7/BB1 was found to be strongly expressed by the Reed- Sternberg cells in all 47 cases of Hodgkin's disease studied. Moreover, Reed-Sternberg cells were frequently surrounded by CD28-expressing T cells. Evidence for a functional role of B7/BB1 on Reed-Sternberg cells was obtained by our findings that T-cell proliferation and interleukin- 2 (IL-2) production in the primary allogenic mixed lymphocyte reaction (MLR), using the B7/BB1-expressing Hodgkin's disease-derived cell lines L428 and KM-H2 as stimulators, could be partially blocked by adding anti-B7 monoclonal antibody. B7/BB1 expression was also evaluated in a group of non-Hodgkin's lymphomas (n = 46). Whereas B7/BB1 was not expressed by the neoplastic cells of most non-Hodgkin's lymphomas, including T-cell-rich B-cell lymphoma (n = 11), it was present on the neoplastic cells of anaplastic large-cell lymphoma (Ki-1 lymphoma) (n = 5) and follicular lymphoma (n = 4). Our data provide further evidence for an accessory cell function of Reed-Sternberg cells. The accessory cell function of Reed-Sternberg cells might lead to pronounced T-cell activation in vivo, which might contribute to the Hodgkin's syndrome. In addition, our study indicates that B7/BB1 may be a useful marker for differentiating Hodgkin's disease from morphologically similar conditions such as T-cell-rich B-cell lymphoma.

Accessory cell function of airway epithelial cells

2004 ◽  
Vol 287 (2) ◽  
pp. L318-L331 ◽  
Author(s):  
Erwin Oei ◽  
Thomas Kalb ◽  
Prarthana Beuria ◽  
Matthieu Allez ◽  
Atsushi Nakazawa ◽  
...  
Keyword(s):  
T Cells ◽  
Epithelial Cells ◽  
Cell Function ◽  
Airway Epithelial Cells ◽  
Accessory Cell ◽  
Airway Epithelial ◽  
Macrophage Colony Stimulating Factor ◽  
Ifn Γ ◽  
Macrophage Colony ◽  
Stimulating Factor

Oei, Erwin, Thomas Kalb, Prarthana Beuria, Matthieu Allez, Atsushi Nakazawa, Miyuki Azuma, Michael Timony, Zanetta Stuart, Houchu Chen, and Kirk Sperber. Accessory cell function of airway epithelial cells.We previously demonstrated that airway epithelial cells (AECs) have many features of accessory cells, including expression of class II molecules CD80 and CD86 and functional Fcγ receptors. We have extended these studies to show that freshly isolated AECs have mRNA for cathepsins S, V, and H [proteases important in antigen (Ag) presentation], invariant chain, human leukocyte antigen (HLA)-DM-α and HLA-DM-β, and CLIP, an invariant chain breakdown product. A physiologically relevant Ag, ragweed, was colocalized with HLA-DR in AECs, and its uptake was increased by granulocyte-macrophage colony-stimulating factor and IFN-γ treatments, which had no effect on CD80 and CD86 expression. We demonstrate the presence of other costimulatory molecules, including B7h and B7-H1, on AECs and the increased expression of B7-H1 on AECs after treatment with granulocyte-macrophage colony-stimulating factor and IFN-γ. Finally, we compared T cell proliferation after allostimulation with AECs and dendritic cells (DCs). The precursor frequency of peripheral blood T cells responding to AECs was 0.264% compared with 0.55% for DCs. DCs stimulated CD45RO+, CD45RA+, CCR7+and CCR7−CD4+, and CD8+T cells, whereas AECs stimulated only CD45RO+, CD45RA−, CCR7−, CD4+, and CD8+T cells. There was no difference in cytokine production, type of memory T cells stimulated (effector vs. long-term memory), or apoptosis by T cells cocultured with AECs and DCs. The localization of AECs exposed to the external environment may make them important in the regulation of local immune responses.

scholarly journals Early development of the T cell repertoire. In vivo treatment of neonatal mice with anti-Ia antibodies interferes with differentiation of I-restricted T cells but not K/D-restricted T cells.

1983 ◽  
Vol 157 (6) ◽  
pp. 1932-1946 ◽  
Author(s):  
A M Kruisbeek ◽  
M J Fultz ◽  
S O Sharrow ◽  
A Singer ◽  
J J Mond
Keyword(s):  
T Cells ◽  
Cell Function ◽  
Cytotoxic T Lymphocyte ◽  
Suppressor Cells ◽  
Accessory Cell ◽  
Cell Repertoire ◽  
Positive Elements ◽  
In Vivo Treatment ◽  
Ctl Responses

Monoclonal antibodies to I-Ak were injected into neonatal H-2k mice for a period of 3 wk. The spleens of such mice are devoid of Ia-positive cells. Allo- and trinitrophenyl (TNP)-self-specific cytotoxic T lymphocyte (CTL) responses in such anti-I-A-treated mice were almost completely abrogated at the end of the 2-3 wk in vivo treatment period. Development of suppressor cells, carry-over of blocking antibodies, lack of responder accessory cells, or defective CTL function were not responsible for the observed defect. As concanavalin A supernatant could restore the defect, it is more likely that the defect is due to the absence of competent Ia-specific T helper cells. In addition, anti-I-A-treated mice exhibit reduced I-A antigen expression in the thymus and defective Ia-bearing accessory cell function in the spleen. It is postulated that, for development of Ia-specific T cells to occur, precursor T cells need to interact with Ia-encoded products in the thymus, and anti-Ia treatment interferes with this process. Finally, the mechanism of this interference was shown to be due to actual removal or functional inactivation of those I-A-positive elements responsible for the education of I-A-recognizing T cells, since in (H-2b X H-2k)F1 mice, treatment with anti-I-Ak antibodies results in abrogation of CTL responses to TNP in association with both parental haplotypes, while in the thymus of these mice expression of both I-Ak and I-Ab was reduced.

scholarly journals Native X-DING-CD4 protein secreted by HIV-1 resistant CD4+T cells blocks activity of IL-8 promoter in human endothelial cells infected with enteric bacteria

2011 ◽  
Vol 18 (4) ◽  
pp. 571-579 ◽  
Author(s):  
Anna Ivanova ◽  
Rasheda Y Shilpi ◽  
Rakhee Sachdeva ◽  
Guanhua Li ◽  
Malgorzata Simm
Keyword(s):  
T Cells ◽  
Endothelial Cells ◽  
Cd4 T Cells ◽  
Enteric Bacteria ◽  
Human Endothelial Cells ◽  
Hiv 1

Characterization of adherent T cells to human endothelial cells in patients with HTLV-I-associated myelopathy

1994 ◽  
Vol 122 (2) ◽  
pp. 204-209 ◽  
Author(s):  
Katsuhiro Ichinose ◽  
Tatsufumi Nakamura ◽  
Yoshihiro Nishiura ◽  
Kunihiko Nagasato ◽  
Kiyosumi Ohishi ◽  
...  
Keyword(s):  
T Cells ◽  
Endothelial Cells ◽  
Human Endothelial Cells

scholarly journals The CXCL2/IL8/CXCR2 Pathway Is Relevant for Brain Tumor Malignancy and Endothelial Cell Function

2021 ◽  
Vol 22 (5) ◽  
pp. 2634
Author(s):  
Ruth Urbantat ◽  
Anne Blank ◽  
Irina Kremenetskaia ◽  
Peter Vajkoczy ◽  
Güliz Acker ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Function ◽  
The Cancer Genome Atlas ◽  
Human Endothelial Cells ◽  
In Vitro Proliferation ◽  
Endothelial Cell Function ◽  
Human Gbm ◽  
And Migration ◽  
The Impact

We aimed to evaluate the angiogenic capacity of CXCL2 and IL8 effecting human endothelial cells to clarify their potential role in glioblastoma (GBM) angiogenesis. Human GBM samples and controls were stained for proangiogenic factors. Survival curves and molecule correlations were obtained from the TCGA (The Cancer Genome Atlas) database. Moreover, proliferative, migratory and angiogenic activity of peripheral (HUVEC) and brain specific (HBMEC) primary human endothelial cells were investigated including blockage of CXCR2 signaling with SB225502. Gene expression analyses of angiogenic molecules from endothelial cells were performed. Overexpression of VEGF and CXCL2 was observed in GBM patients and associated with a survival disadvantage. Molecules of the VEGF pathway correlated but no relation for CXCR1/2 and CXCL2/IL8 was found. Interestingly, receptors of endothelial cells were not induced by addition of proangiogenic factors in vitro. Proliferation and migration of HUVEC were increased by VEGF, CXCL2 as well as IL8. Their sprouting was enhanced through VEGF and CXCL2, while IL8 showed no effect. In contrast, brain endothelial cells reacted to all proangiogenic molecules. Additionally, treatment with a CXCR2 antagonist led to reduced chemokinesis and sprouting of endothelial cells. We demonstrate the impact of CXCR2 signaling on endothelial cells supporting an impact of this pathway in angiogenesis of glioblastoma.

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