scholarly journals In vitro hematopoiesis produces a distinct class of immature dendritic cells from spleen progenitors with limited T cell stimulation capacity

2004 ◽  
Vol 16 (4) ◽  
pp. 567-577 ◽  
Author(s):  
B. Quah
Keyword(s):  
Dendritic Cells ◽  
T Cell ◽  
Cell Stimulation ◽  
Distinct Class ◽  
Immature Dendritic Cells ◽  
T Cell Stimulation

scholarly journals Rho-mDia1 pathway is required for adhesion, migration, and T-cell stimulation in dendritic cells

Blood ◽  
2010 ◽  
Vol 116 (26) ◽  
pp. 5875-5884 ◽  
Author(s):  
Hideaki Tanizaki ◽  
Gyohei Egawa ◽  
Kayo Inaba ◽  
Tetsuya Honda ◽  
Saeko Nakajima ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Dendritic Cells ◽  
T Cell ◽  
Immune Responses ◽  
Lymph Nodes ◽  
Actin Polymerization ◽  
Cell Stimulation ◽  
T Cell Stimulation ◽  
Acquired Immune Responses

Abstract Dendritic cells (DCs) are essential for the initiation of acquired immune responses through antigen acquisition, migration, maturation, and T-cell stimulation. One of the critical mechanisms in this response is the process actin nucleation and polymerization, which is mediated by several groups of proteins, including mammalian Diaphanous-related formins (mDia). However, the role of mDia in DCs remains unknown. Herein, we examined the role of mDia1 (one of the isoforms of mDia) in DCs. Although the proliferation and maturation of bone marrow-derived DCs were comparable between control C57BL/6 and mDia1-deficient (mDia1−/−) mice, adhesion and spreading to cellular matrix were impaired in mDia1−/− bone marrow–derived DCs. In addition, fluorescein isothiocyanate-induced cutaneous DC migration to draining lymph nodes in vivo and invasive migration and directional migration to CCL21 in vitro were suppressed in mDia1−/− DCs. Moreover, sustained T-cell interaction and T-cell stimulation in lymph nodes were impaired by mDia1 deficiency. Consistent with this, the DC-dependent delayed hypersensitivity response was attenuated by mDia1-deficient DCs. These results suggest that actin polymerization, which is mediated by mDia1, is essential for several aspects of DC-initiated acquired immune responses.

scholarly journals Human Invariant NKT Cell Subsets Differentially Promote Differentiation, Antibody Production, and T Cell Stimulation by B Cells In Vitro

2013 ◽  
Vol 191 (4) ◽  
pp. 1666-1676 ◽  
Author(s):  
Shijuan Grace Zeng ◽  
Yasmeen G. Ghnewa ◽  
Vincent P. O’Reilly ◽  
Victoria G. Lyons ◽  
Ann Atzberger ◽  
...  
Keyword(s):  
T Cell ◽  
B Cells ◽  
Antibody Production ◽  
Nkt Cell ◽  
Cell Stimulation ◽  
T Cell Stimulation ◽  
Invariant Nkt Cell

scholarly journals The Extracellular Domain of CD83 Inhibits Dendritic Cell–mediated T Cell Stimulation and Binds to a Ligand on Dendritic Cells

2001 ◽  
Vol 194 (12) ◽  
pp. 1813-1821 ◽  
Author(s):  
Matthias Lechmann ◽  
Daniëlle J.E.B. Krooshoop ◽  
Diana Dudziak ◽  
Elisabeth Kremmer ◽  
Christine Kuhnt ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
T Cell ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Functional Aspects ◽  
T Cell Stimulation ◽  
Ig Superfamily ◽  
Ig Domain ◽  
Dc Maturation

CD83 is an immunoglobulin (Ig) superfamily member that is upregulated during the maturation of dendritic cells (DCs). It has been widely used as a marker for mature DCs, but its function is still unknown. To approach its potential functional role, we have expressed the extracellular Ig domain of human CD83 (hCD83ext) as a soluble protein. Using this tool we could show that immature as well as mature DCs bind to CD83. Since CD83 binds a ligand also expressed on immature DCs, which do not express CD83, indicates that binding is not a homophilic interaction. In addition we demonstrate that hCD83ext interferes with DC maturation downmodulating the expression of CD80 and CD83, while no phenotypical effects were observed on T cells. Finally, we show that hCD83ext inhibits DC-dependent allogeneic and peptide-specific T cell proliferation in a concentration dependent manner in vitro. This is the first report regarding functional aspects of CD83 and the binding of CD83 to DCs.

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