The Role of Monocytes and Responder Cells in Suppression of Antigen-Specific T Cell Proliferation in Chronic Renal Failure

1984 ◽  
Vol 73 (2) ◽  
pp. 97-103 ◽  
Author(s):  
Yael G. Alevy ◽  
Kathleen R. Mueller ◽  
Joseph R. Anderson ◽  
Patricia S. Hutcheson ◽  
Raymond G. Slavin
Keyword(s):  
Cell Proliferation ◽  
Renal Failure ◽  
Chronic Renal Failure ◽  
T Cell ◽  
T Cell Proliferation

scholarly journals Suppression of T-cell proliferation by Mycobacterium leprae and its products: the role of lipopolysaccharide.

1990 ◽  
Vol 87 (3) ◽  
pp. 973-977 ◽  
Author(s):  
A. Molloy ◽  
G. Gaudernack ◽  
W. R. Levis ◽  
Z. A. Cohn ◽  
G. Kaplan
Keyword(s):  
Cell Proliferation ◽  
T Cell ◽  
Mycobacterium Leprae ◽  
T Cell Proliferation

scholarly journals Delta-Like-1 Changes the Immunomodulatory Property of OP9 Cells

2016 ◽  
Vol 2016 ◽  
pp. 1-11
Author(s):  
Lei Zhang ◽  
Rui-Jie Dang ◽  
Yan-Mei Yang ◽  
Dian-Chao Cui ◽  
Ping Li ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
T Cell ◽  
B Cell ◽  
Stromal Cells ◽  
B Lymphocyte ◽  
B Cell Development ◽  
T Cell Proliferation ◽  
No Production ◽  
Immunomodulatory Property

As stromal cells and recently confirmed mesenchymal stem cells, OP9 cells support hematopoiesis stem cell (HSC) differentiation into the B lymphocyte lineage, yet Delta-like-1 (DL1) overexpressing OP9 (OP9DL1) cells promote the development of early T lymphocytes from HSC. However, the immunomodulatory capacity of OP9 or OP9DL1 on mature B and T cell proliferation has not been elucidated. Here, we show that OP9 and OP9DL1 have similar proliferation capacities and immunophenotypes except DL1 expression. Compared with OP9, OP9DL1 displayed more osteogenesis and less adipogenesis when cultured in the respective induction media. Both OP9 and OP9DL1 inhibited mature B and T cell proliferation. Furthermore, OP9 showed stronger inhibition on B cell proliferation and OP9DL1 exhibited stronger inhibition on T cell proliferation. With stimulation, both OP9 and OP9DL1 showed increased nitrate oxide (NO) production. The NO levels of OP9 were higher than that of OP9DL1 when stimulated with TNFα/IFNγor LPS/IL4. Taken together, our study reveals a previously unrecognized role of OP9 and OP9DL1 in mature B and T cell proliferation. DL1 overexpression alone changed the properties of OP9 cells in addition to their role in early B cell development.

scholarly journals Immunosuppressive role of semaphorin-3A on T cell proliferation is mediated by inhibition of actin cytoskeleton reorganization

2006 ◽  
Vol 36 (7) ◽  
pp. 1782-1793 ◽  
Author(s):  
Yves Lepelletier ◽  
Ivan Cruz Moura ◽  
Réda Hadj-Slimane ◽  
Amédée Renand ◽  
Susana Fiorentino ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
T Cell ◽  
Actin Cytoskeleton ◽  
T Cell Proliferation ◽  
Semaphorin 3A ◽  
Cytoskeleton Reorganization

CD11b+gr-1+ myeloid Derived Suppressor Cells (MDSC) In Normal Bone Marrow Suppress T Cell Proliferation and Enhance T-Regulatory Function Via a IL10-, IL4- and IDO-Independent Mechanism

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 4801-4801 ◽  
Author(s):  
Parvin Forghani ◽  
Wayne Harris ◽  
jian-Ming Li ◽  
M.R. Khorramizadeh ◽  
Edmund Waller
Keyword(s):  
Cell Proliferation ◽  
T Cells ◽  
T Cell ◽  
T Cell Activation ◽  
Cell Activation ◽  
Regulatory Function ◽  
T Cell Proliferation ◽  
Suppressive Activity ◽  
Ifn Γ

Abstract Abstract 4801 MDSC have been described as an important negative regulators of autologous anti-cancer immune responses. Considering the important role of MDSC in immune regulation in allogenic stem cell and organ transplantation, we undertook an investigation of the mechanism(s) by which MDSC inhibit T–cell activation and proliferation, and tested the hypothesis that local cytokine secretion or IDO activity is required for suppression of T-cell proliferation. Two separate populations CD11bhiGr-1hi and CD11bhi Gr-1int were isolated by high-speed FACS from lineage- BM antigen presenting cells (C57 & BALB/c mice). Both MDSC subsets had potent capacity for in–vitro suppression of CD4+ and CD8+ T cells proliferation in response to anti-CD3/anti-CD28 beads and Con A. A ratio of 0.5/1 MDSC: T-cells were sufficient to inhibit >66% control levels of T-cell proliferation. MDSC isolated from transgenic mice that had been “knocked-out” for IFN-γ and IDO had equivalent suppressive activity as MDSC from wild-type donors. Addition of saturating concentrations of anti IL-10 and IL-4 MAb, or in combination with anti- IFN-γ MAb did not abrogate MDSC-suppressive activity. Ex-vivo culture of MDSC with mitogen-activated T-cells generated two—fold more Fox-p3 T-reg compared with cultures of T cell plus mitogen. Data will be presented regarding the novel role of MDSC involving in the homeostasis regulation of normal T-cell activation and proliferation in non-tumor-bearing mice. Disclosures: No relevant conflicts of interest to declare.

Pak2 Regulates MDSC Development and Function

Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 705-705
Author(s):  
Yi Zeng ◽  
Seongmin Hahn ◽  
Jessica Stokes ◽  
Emely Hoffman ◽  
Jonathan Chernoff ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
T Cell ◽  
Progenitor Cells ◽  
Lineage Commitment ◽  
T Cell Proliferation ◽  
Myeloid Lineage ◽  
Suppressive Function ◽  
Gm Csf ◽  
Group I

Abstract Myeloid derived suppressor cells (MDSCs) are a heterogeneous cell population at various stages of differentiation that can increase under various pathologic conditions such as cancer, infection or inflammation, displaying suppressive function. It is well recognized that MDSCs contribute to tumor evasion by suppressing cell-mediated immunity. Based on the differential expression of Ly6C and/or Ly6G in mice, MDSCs are characterized as granulocytic (CD11b+Ly6G+Ly6Clow) or monocytic MDSCs (CD11b+Ly6Glow/−Ly6Chi). These subsets induce T-cell hyporesponsiveness and can have various functions and distribution depending on their environment. Although much research has focused on the tumorigenic effects of MDSCs, studies on the regulation of their development during hematopoiesis remain limited. p21-activated kinases (Paks) are serine/threonine kinases that regulate diverse cellular activities including cytoskeletal remodeling, cell motility, proliferation, apoptosis and mitosis. Despite active research on pharmacological inhibition of group I Paks in treating solid tumors, few studies have examined the role of Paks in modulating normal hematopoiesis. Knowledge of the role of Pak2 in regulating long-term hematopoiesis and lineage commitment remains limited. Utilizing a conditional Pak2-KO murine model, we have previously demonstrated that Pak2 disruption in hematopoietic stem/progenitor cells (HSPCs) induces myeloid lineage skewing and CD11b+Gr1+ cell expansion in mice. Compared to mice reconstituted with wild type (WT) bone marrow (BM), mice transplanted with Pak2-KO BM displayed a significantly higher percentage of granulocyte-monocyte progenitors (GMPs) in the BM and higher numbers of CD11b+Gr1+ cells in the spleen. In this study, we demonstrated that CD11b+Gr1high cells isolated from the spleens of mice with Pak2-KO BM displayed significantly greater suppressive function on T cell proliferation in vitro, consistent with MDSC phenotype. There was a near 2-fold increase in the numbers of both granulocytic and monocytic splenic MDSCs in mice reconstituted with Pak2-KO BM. At HSPC level, Pak2-KO BM yielded greater than 3-fold more colonies in response to GM-CSF but not G-CSF or M-CSF when compared to WT cells, indicating selective hypersensitivity to GM-CSF. In parallel experiments, Pak2-KO and WT BM C-kit+ cells that were enriched for hematopoietic progenitor cells (HPCs) were cultured in liquid culture in the presence of GM-CSF. Pak2-KO BM C-kit+ cells yielded greater than 2-fold higher numbers of CD11b+Gr1+ MDSCs that displayed potent suppression on CD8+ T cell proliferation. These data demonstrate that Pak2 disruption increases HPC sensitivity to GM-CSF signaling and drives lineage commitment toward granulocyte-monocyte lineage thus promoting MDSC development. In addition, we have also found that Pak2 deficient MDSCs are more proliferative and more resistant to apoptosis when compared to WT CD11b+Gr1+cells, thus contributing to expansion of this population in vivo. Loss of Pak2 decreases MDSC sensitivity to apoptosis through differential regulation of multiple pro- and anti-apoptotic gene expression. Furthermore, Pak2 disruption down regulates the expression of IRF8, a well-described myeloid transcription factor. Together, our data indicate that loss of Pak2 promotes HPC myeloid lineage commitment and CD11b+Gr1+ MDSC proliferation while suppressing apoptotic cell death in these cells. Further studies are ongoing to determine the interaction between Pak2 and IRF8. Disclosures No relevant conflicts of interest to declare.

Role of C3b receptors in the enhancement of interleukin-2-dependent T-cell proliferation

1984 ◽  
Vol 21 (12) ◽  
pp. 1215-1221 ◽  
Author(s):  
Anna Erdei ◽  
E. Spaeth ◽  
J. Alsenz ◽  
E. Rüde ◽  
T. Schulz ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
T Cell ◽  
Interleukin 2 ◽  
T Cell Proliferation

Role of Early-Activation Antigens in T-cell Proliferation

1987 ◽  
Vol 494 (1 Third Colloqu) ◽  
pp. 287-290 ◽  
Author(s):  
TOSHIMITSU UEDE ◽  
HIROO YUASA ◽  
HIRONOBU KOHDA ◽  
KOKICHI KIKUCHI ◽  
HISAO OSAWA ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
T Cell ◽  
T Cell Proliferation ◽  
Early Activation ◽  
Activation Antigens
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