CD69 and Regulatiof the Immune Function

Marzio, R.; Mauël, Jacques; Betz-Corradin, Sally

doi:10.3109/08923979909007126

Cited by 191 publications

(159 citation statements)

References 55 publications

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“…In contrast, on BLC-stimulated CTL, the expression of CD69 and CD25 had subsided, and CD62L expression, highly expressed in CD8 ϩ T cells at the beginning of coculture, had largely been lost. The findings in BLC-stimulated CD8 ϩ T cells are in accordance with numerous in vitro and in vivo reports showing the loss of early activation markers 2-3 days after activation of T cells by BLC or other professional APC (21)(22)(23). A direct correlation between the number of cell divisions and loss of CD25 and CD69 also has recently been reported (27).…”

Section: Discussionsupporting

confidence: 76%

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Human Vascular Endothelial Cells Stimulate Memory But Not Naive CD8+ T Cells to Differentiate into CTL Retaining an Early Activation Phenotype

Dengler

Pober

2000

The Journal of Immunology

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Endothelial cell (EC)-selective alloreactive CTL may mediate alloimmune vascular injury. In the present study, EC-selective CTL were generated in cocultures of purified human CD8+ T cells with allogeneic EC and were compared with conventional CTL against corresponding B lymphoblastoid cells (BLC). EC caused activation and expansion of memory but not naive CD8+ T cells, which differentiated into EC-selective CTL that retained high surface expression of CD69, CD25, and CD62L and displayed low intracellular perforin content. In contrast, BLC-stimulated CTL could be generated from naive or memory CD8+ T cells and showed a more mature phenotype (low CD69, CD25, and CD62L with higher levels of perforin). The expansion of alloreactive T cells by EC stimulation was 5- to 20-fold less effective than in corresponding BLC-stimulated cultures, accounting for a reduction in the assayable cytotoxicity of individual microcultures. In these IL-2-supplemented cocultures, no effect on CTL generation or phenotype was observed by mAb blocking of costimulation provided by LFA-3, ICAM-1, or CD40, by addition of comitogenic anti-CD28 mAb, or by preactivation of EC with CD40 ligand. Cyclosporine inhibited CTL expansion and cytotoxicity similarly in both EC- and BLC-stimulated cultures but did not affect the phenotype of those CTL that did emerge. This study extends the characterization of endothelium as an immunoregulatory cell type distinct from conventional APC and may explain why graft rejection within the arterial intima, an anatomic compartment in which EC may be the primary type of APC, is separable from rejection in the graft parenchyma.

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Section: Discussionsupporting

confidence: 76%

“…CD69 and CD25 are generally considered early activation markers (21)(22)(23), and L-selectin is usually lost rapidly during the course of T cell activation (24 -26). Also, the expression level of perforin per cell in EC-selective CTL was markedly lower than in corresponding conventional CTL.…”

Section: Discussionmentioning

confidence: 99%

Human Vascular Endothelial Cells Stimulate Memory But Not Naive CD8+ T Cells to Differentiate into CTL Retaining an Early Activation Phenotype

Dengler

Pober

2000

The Journal of Immunology

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“…NOD T cells expressing high levels of CD40 are capable of inducing clinical diabetes [21], while CD86 upregulation on islet infiltrating NOD B cells is associated with development of insulitis [22]. CD69 is an early activation marker, but its sustained upregulation has been associated with a number of inflammatory and autoimmune diseases [23]. The anomalous levels of CD69 and L-selectin were observed on NOD peritoneal B cells from 3 weeks of age.…”

Section: Discussionmentioning

confidence: 99%

“…Antigen presentation assay NOD and BALB/c mice were immunised subcutaneously on the hind flank with 50 μg insulin peptide (Insulin B [9][10][11][12][13][14][15][16][17][18][19][20][21][22][23]; Anaspec, San Jose, CA, USA). After 10 days, spleens were collected from these animals and splenic CD4 + T cells purified using CD4 MicroBeads (Miltenyi Biotec, Bergisch Gladbach, Germany).…”

Section: Methodsmentioning

confidence: 99%

Enhanced trafficking to the pancreatic lymph nodes and auto-antigen presentation capacity distinguishes peritoneal B lymphocytes in non-obese diabetic mice

et al. 2009

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Aims/hypothesis NOD.Igµ null mice lacking mature B cells are highly resistant to diabetes and display poor CD4 T cell responses to autoantigens. Nevertheless, the degree to which different B cell subsets contribute to diabetes in NOD mice remains unresolved. Due to their role in the recognition of microbial and autoantigens, peritoneal B cell characteristics were examined in NOD mice to see if they differ developmentally, phenotypically or functionally in aspects relevant to diabetogenesis. Methods The population dynamics, activation state, migratory behaviour and antigen presentation function were investigated in NOD peritoneal B cells. Results NOD peritoneal B cells were found to express abnormally high levels of co-stimulatory molecules (CD40, CD86 and CD69). In contrast, the expression of L-selectin and integrin α4β1 was markedly reduced in NOD mice compared with BALB/c and C57BL/6 mice. The number of B cells in the peritoneum was lower in NOD than in control mice throughout development; migration of B cells from the peritoneum to the pancreatic lymph nodes in NOD mice was enhanced tenfold. NOD B cells showed no chemotactic response to sphingosine-1-phosphate, which normally acts to retain B cells in the peritoneum. Peritoneal B cells of NOD mice also presented insulin autoantigen to CD4 T cells, inducing T cell proliferation. Conclusions/interpretation NOD peritoneal B cells are hyperactivated, migrate to the pancreatic lymph nodes and are capable of driving insulin-specific CD4 T cell activation. These characteristics could make them important for inducing or amplifying T cell responses against islet-antigens.

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“…To distinguish between these possibilities, we analyzed CD69 induction in anti-CD3-activated CD4 ϩ and CD8 ϩ T cells. The CD69 molecule is a type II C-type lectin receptor expressed on a small proportion of mature T cells (13)(14)(15). CD69 expression is associated with activation and is a good indicator of sensitivity of T cells (16).…”

Section: Gilt-deficient T Cells Display Higher Levels Of Cd69 On Actimentioning

confidence: 99%

Inhibitory Role of IFN-γ-Inducible Lysosomal Thiol Reductase in T Cell Activation

Barjaktarević

Rahman

Radoja

et al. 2006

The Journal of Immunology

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IFN-γ-inducible lysosomal thiol reductase (GILT) is a unique thiol reductase with optimal enzymatic activity at low pH. GILT plays a crucial role in unfolding the antigenic proteins in preparation for their proteolytic cleavage and presentation of resulting peptides by MHC class II. In this study, we demonstrate that GILT is expressed in T lymphocytes and that it has an APC-nonrelated role in the regulation of T cell activation. Surprisingly, comparison of wild-type and GILT-deficient T cell activation in vitro revealed stronger responsiveness in the absence of GILT. The effect of GILT in reducing the proliferative and cytotoxic responses was endogenous to T cells and resulted from decreased sensitivity at the individual cell level. Therefore, a molecule with primarily lysosomal localization suppresses T cell activation, a process characterized by signal transmission from plasma membrane to cytoplasm and nucleus.

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CD69 and Regulatiof the Immune Function

Cited by 191 publications

References 55 publications

Human Vascular Endothelial Cells Stimulate Memory But Not Naive CD8+ T Cells to Differentiate into CTL Retaining an Early Activation Phenotype

Human Vascular Endothelial Cells Stimulate Memory But Not Naive CD8+ T Cells to Differentiate into CTL Retaining an Early Activation Phenotype

Enhanced trafficking to the pancreatic lymph nodes and auto-antigen presentation capacity distinguishes peritoneal B lymphocytes in non-obese diabetic mice

Inhibitory Role of IFN-γ-Inducible Lysosomal Thiol Reductase in T Cell Activation

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