Transcriptional profiling of human lymphoblastoid TK6 cells comparing mock irradiaed cells resuspended in fresh untreated RPMI 1640 medium with cells resuspended in medium activated by exposure to 2.5 Gy HZE (1 GeV/amu iron ions accelerated at the NASA Space Research Laboratory (NSRL) of Brookhaven National Laboratory). Two-condition experiment mock irradiated vs. cells exposed to activated medium. 3 biological replicates were independently grown and harvested during three different runs at the NSRL. One replicate per array.

Transcriptional profiling of human lymphoblastoid TK6 cells comparing mock irradiated cells with cells exposed 24 hours previously to 1.67 Gy HZE (1 GeV/amu iron ions accelerated at the NASA Space Research Laboratory (NSRL) of Brookhaven National Laboratory) or 2.5 Gy 137Cs gamma rays. TK6 cells were mock irradiated or exposed to HZE or gamma-rays and RNA was harvested 24 hours later. 3 biological replicates were independently grown and harvested during three different runs at the NSRL. One replicate per array.

Transcriptional profiling of human lymphoblastoid TK6 cells comparing mock irradiated cells with cells exposed 24 hours previously to 1.67 Gy HZE (1 GeV/amu iron ions accelerated at the NASA Space Research Laboratory (NSRL) of Brookhaven National Laboratory) or 2.5 Gy 137Cs gamma rays. TK6 cells were mock irradiated or exposed to HZE or gamma-rays and RNA was harvested 24 hours later. 3 biological replicates were independently grown and harvested during three different runs at the NSRL. One replicate per array.

Transcriptional profiling of human lymphoblastoid TK6 cells comparing mock irradiated cells with cells exposed 24 hours previously to 1.67 Gy HZE (1 GeV/amu iron ions accelerated at the NASA Space Research Laboratory (NSRL) of Brookhaven National Laboratory) or 2.5 Gy 137Cs gamma rays. TK6 cells were mock irradiated or exposed to HZE or gamma-rays and RNA was harvested 24 hours later. 3 biological replicates were independently grown and harvested during three different runs at the NSRL. One replicate per array.

Irradiated cell lines exposed to 1-10 Gy 2 Lymphoblastoid cell lines (GM15510 and GM15036) irradiated 1 2.5 5 7.5 10 Gy RNA is isolated and labeled using a T7 amplification Arcturus kit for hybridization on triplicate arrays.

We investigated differentially regulated genes in human Jurkat T lymphocytic cells in 20s and 5min microgravity and in hypergravity and compared expression profiles to identify potential gravity-regulated genes and adaptation processes. This dataset is part of a series of three and the other two datasets are deposited in GLDS-172 and GLDS-189.

Regulatory T cells prevent autoimmunity by suppressing the reactivity of potentially aggressive self-reactive T cells. Contact-dependent CD4+ CD25+ 'professional' suppressor cells and other cytokine-producing CD4+ and CD8+ T-cell subsets mediate this protective function. Evidence will be reviewed that T cells primed with transforming growth factor (TGF)-β expand rapidly following restimulation. Certain CD4+ T cells become contact-dependent suppressor cells and other CD4+ and CD8+ cells become cytokine-producing regulatory cells. This effect is dependent upon a sufficient amount of IL-2 in the microenvironment to overcome the suppressive effects of TGF-β. The adoptive transfer of these suppressor cells generated ex vivo can protect mice from developing chronic graft-versus-host disease with a lupus-like syndrome and alter the course of established disease. These data suggest that autologous T cells primed and expanded with TGF-β have the potential to be used as a therapy for patients with systemic lupus erythematosus and other chronic inflammatory diseases. This novel adoptive immunotherapy also has the potential to prevent the rejection of allogeneic transplants.

Here in this study we systematically examined the patterns of DNA methylation and hydroxy-methylation with its functional implications in gene regulation for the cultured TK6 lymphoblastoid cells upon exposure to micro-gravity conditions. The results reported here indicate that simulated microgravity alters methylation patterns in a limited way and subsequently the expression of genes involved in stress response like ATF3 FBXO17 MAP3K13 and VCL in TK6 cells. Overall design: Examination of 2 different DNA modifications with 2 replicates each for 1 cell type.

CD4+ memory T cells (Tm) from rheumatoid arthritis peripheral blood (RAPB) or peripheral blood from normal donors produced IL-2, whereas fewer cells secreted IFN-γ or IL-4 after a brief stimulation. RAPB Tm contained significantly more IFN-γ producers than normal cells. Many rheumatoid arthritis (RA) synovial Tm produced IFN-γ alone (40%) and fewer cells produced IL-2 or IL-4. An in vitro model was employed to generate polarized T-helper (Th) effectors. Normal and RAPB Tm differentiated into both IFN-γ- and IL-4-producing effectors. RA synovial fluid (RASF) Tm demonstrated defective responsiveness, exhibiting diminished differentiation of IL-4 effectors, whereas RA synovial tissue (RAST) Tm exhibited defective generation of IFN-γ and IL-4 producers.

Accumulating data support the concept that ionizing radiation therapy (RT) has the potential to convert the tumor into an in situ individualized vaccine; however this potential is rarely realized by RT alone. Transforming growth factor xce xb2 (TGF xce xb2) is an immunosuppressive cytokine that is activated by RT and inhibits the antigen-presenting function of dendritic cells and the differentiation of effector CD8+ T cells. Here we tested the hypothesis that TGF xce xb2 hinders the ability of RT to promote anti-tumor immunity. Development of tumor-specific immunity was examined in a pre-clinical model of metastatic breast cancer. Mice bearing established 4T1 mouse mammary carcinoma treated with pan-isoform specific TGF xce xb2 neutralizing antibody 1D11 showed significantly improved control of the irradiated tumor and non-irradiated metastases but no effect in the absence of RT. Notably whole tumor transcriptional analysis demonstrated the selective upregulation of genes associated with immune-mediated rejection only in tumors of mice treated with RT+TGF xce xb2 blockade. Mice treated with RT+TGF xce xb2 blockade exhibited cross-priming of CD8+ T cells producing IFN xce xb3 in response to three tumor-specific antigens in tumor-draining lymph nodes which was not evident for single modality treatment. Analysis of the immune infiltrate in mouse tumors showed a significant increase in CD4+ and CD8+ T cells only in mice treated with the combination of RT+TGF xce xb2 blockade. Depletion of CD4+ or CD8+ T cells abrogated the therapeutic benefit of RT+TGF xce xb2 blockade. These data identify TGF xce xb2 as a master inhibitor of the ability of RT to generate an in situ tumor vaccine which supports testing inhibition of TGF xce xb2 during radiotherapy to promote therapeutically effective anti-tumor immunity. We used genome-wide microarray to depict main biological processes responsibles for the therapeutic benefit of the combination ofTGF-beta blockade and local radiotherapy. To gain a more comprehensice protrait of the effects of RT and TGFbeta blockade on gene expressionin tumors we collected 4T1 tumors 4 days after completion of RT. Three tumors from each group were then subjected to RNA extraction and hybridization on affymetrix array.