Surface Expression of IgE Receptors, IgE Occupancy and Histamine Releasability of Mast Cells: Influence of Genetic and T Cell Factors

1995 ◽  
Vol 107 (1-3) ◽  
pp. 132-134 ◽  
Author(s):  
Xiao-Jun Chen ◽  
Lennart Enerbäck
Keyword(s):  
T Cell ◽  
Mast Cells ◽  
Surface Expression ◽  
Ige Receptors ◽  
Histamine Releasability

scholarly journals T cell receptor-independent CD2 signal transduction in FcR+ cells.

1991 ◽  
Vol 173 (4) ◽  
pp. 859-868 ◽  
Author(s):  
A R Arulanandam ◽  
S Koyasu ◽  
E L Reinherz
Keyword(s):  
Signal Transduction ◽  
T Cell ◽  
Mast Cells ◽  
Nk Cells ◽  
Signal Transduction Pathway ◽  
Cell Receptor ◽  
Surface Expression ◽  
Fc Receptor ◽  
Free Calcium ◽  
Murine Mast Cell

CD2 subserves both adhesion and signal transduction functions in T cells, thymocytes, and natural killer (NK) cells. In mature T lymphocytes, CD2-mediated signaling function apparently requires surface expression of T cell receptors (TCRs). In contrast, in CD2+ CD3- NK cells and thymocytes, signal transduction through CD2 is TCR independent. To resolve this paradox and characterize TCR-independent triggering mechanisms, we transfected a human CD2 cDNA into a murine mast cell line, C1.MC/57 (Fc epsilon RI+, Fc gamma RII+, Fc gamma RIII+), which is known to produce interleukin 6 (IL-6) as well as release histamine in response to crosslinking of Fc epsilon RI. In the CD2 transfectant, a combination of anti-T11(2) + anti-T11(3) monoclonal antibodies (mAbs) induced a rise in intracellular free calcium [( Ca2+]i), IL-6 production, and histamine release. As expected, no activation was mediated by the same mAbs in C1.MC/57. F(ab)'s fragments of the activatory combination of anti-T11(2) + anti-T11(3) mAbs induced IL-6 in the CD2-transfected mast cells, demonstrating an Fc gamma receptor ectodomain-independent triggering mechanism. In addition, either intact anti-T11(2) or anti-T11(3) IgG alone, which failed to induce [Ca2+]i mobilization in the transfectant, was able to induce IL-6 production. A mAb directed against both Fc gamma RII (previously denoted as Fc gamma RIIb) and Fc gamma RIII (previously denoted as Fc gamma RIIa) inhibits this induction. These results indicate that: (a) Ca2+ mobilization is not essential for IL-6 production; and (b) crosslinking of CD2 and Fc gamma receptors via intact anti-CD2 IgG stimulates IL-6 production. Thus, CD2-mediated IL-6 production occurs by both Fc receptor ectodomain-independent as well as Fc receptor ectodomain-dependent mechanisms in these nonlymphoid cells. Northern blot analysis demonstrates that although the mast cells do not express CD3 zeta or CD3 eta mRNA, they express Fc epsilon RI gamma mRNA. The latter is a known component of Fc gamma RIII as well as Fc epsilon RI, has significant homology to CD3 zeta/eta, and is thought to have a signal transduction function. In these mast cells, CD2 signaling machinery does not require CD3 zeta/eta and may be linked to the Fc epsilon RI gamma subunit. We predict that this subunit or a related structure may confer a TCR-independent signal transduction pathway upon CD2 in CD3- NK cells, thymocytes, and certain B lymphocytes.

scholarly journals Dynamic Imaging of IEL-IEC Co-Cultures Allows for Quantification of CD103-Dependent T Cell Migration

2021 ◽  
Vol 22 (10) ◽  
pp. 5148
Author(s):  
Karin Enderle ◽  
Martin Dinkel ◽  
Eva-Maria Spath ◽  
Benjamin Schmid ◽  
Sebastian Zundler ◽  
...  
Keyword(s):  
T Cell ◽  
Cross Talk ◽  
Intestinal Inflammation ◽  
Ex Vivo ◽  
New Technology ◽  
Surface Expression ◽  
Intraepithelial Lymphocytes ◽  
Dynamic Imaging ◽  
The Body ◽  
Therapeutic Interventions

Intraepithelial lymphocytes (IEL) are widely distributed within the small intestinal epithelial cell (IEC) layer and represent one of the largest T cell pools of the body. While implicated in the pathogenesis of intestinal inflammation, detailed insight especially into the cellular cross-talk between IELs and IECs is largely missing in part due to lacking methodologies to monitor this interaction. To overcome this shortcoming, we employed and validated a murine IEL-IEC (organoids) ex vivo co-culture model system. Using livecell imaging we established a protocol to visualize and quantify the spatio-temporal migratory behavior of IELs within organoids over time. Applying this methodology, we found that IELs lacking CD103 (i.e., integrin alpha E, ITGAE) surface expression usually functioning as a retention receptor for IELs through binding to E-cadherin (CD324) expressing IECs displayed aberrant mobility and migration patterns. Specifically, CD103 deficiency affected the ability of IELs to migrate and reduced their speed during crawling within organoids. In summary, we report a new technology to monitor and quantitatively assess especially migratory characteristics of IELs communicating with IEC ex vivo. This approach is hence readily applicable to study the effects of targeted therapeutic interventions on IEL-IEC cross-talk.

Mast cells and T-cell expansion

Blood ◽  
2008 ◽  
Vol 111 (5) ◽  
pp. 2497-2498
Author(s):  
Susumu Nakae ◽  
Keisuke Oboki ◽  
Hirohisa Saito
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
T Cell ◽  
Mast Cells ◽  
Cell Expansion ◽  
Memory T Cells ◽  
T Cell Expansion

IgE/antigen-FcϵRI crosslinking promotes antigen internalization and apoptosis in mouse mast cells. Dendritic cells uptake the apoptotic mast cells carrying internalized antigens, and thus can efficiently present the antigens to memory T cells.

scholarly journals Ubiquitin ligase MARCH 8 cooperates with CD83 to control surface MHC II expression in thymic epithelium and CD4 T cell selection

2016 ◽  
Vol 213 (9) ◽  
pp. 1695-1703 ◽  
Author(s):  
Haiyin Liu ◽  
Reema Jain ◽  
Jing Guan ◽  
Vivian Vuong ◽  
Satoshi Ishido ◽  
...  
Keyword(s):  
T Cell ◽  
Ubiquitin Ligase ◽  
Cell Types ◽  
Surface Expression ◽  
Cd4 T Cell ◽  
Control Surface ◽  
Thymic Epithelial Cells ◽  
Cell Selection ◽  
Mhc Ii ◽  
T Cell Selection

Major histocompatibility complex class II (MHC II) expression is tightly regulated, being subjected to cell type–specific mechanisms that closely control its levels at the cell surface. Ubiquitination by the E3 ubiquitin ligase MARCH 1 regulates MHC II expression in dendritic cells and B cells. In this study, we demonstrate that the related ligase MARCH 8 is responsible for regulating surface MHC II in thymic epithelial cells (TECs). March8−/− mice have elevated MHC II at the surface of cortical TECs and autoimmune regulator (AIRE)− medullary TECs (mTECs), but not AIRE+ mTECs. Despite this, thymic and splenic CD4+ T cell numbers and repertoires remained unaltered in March8−/− mice. Notably, the ubiquitination of MHC II by MARCH 8 is controlled by CD83. Mice expressing a mutated form of CD83 (Cd83anu/anu mice) have impaired CD4+ T cell selection, but deleting March8 in Cd83anu/anu mice restored CD4+ T cell selection to normal levels. Therefore, orchestrated regulation of MHC II surface expression in TECs by MARCH 8 and CD83 plays a major role in CD4+ T cell selection. Our results also highlight the specialized use of ubiquitinating machinery in distinct antigen-presenting cell types, with important functional consequences and implications for therapeutic manipulation.

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