Selective addition of CXCR3+CCR4-CD4+ Th1 cells enhances generation of cytotoxic T cells by dendritic cells in vitro

Yoon, Sung Hee; Yun, Sangchul; Park, Jung Yong; Won, Hee Yeun; Kim, Min Jung; Sohn, Hyun Jung; Cho, Hyun Il; Kim, Tai Gyu

doi:10.3858/emm.2009.41.3.019

Cited by 23 publications

(20 citation statements)

References 33 publications

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“…'s study. [26] These results explained phenotypic or cytokine changes in TH1 cells in other tumors, which were observed in measurement of TH1 in tumor tissues, in blood circulation and during recovery after immunotherapy. Numerous studies even using genetic methods of cytokines secreted by TH1 and TH2 and Western blot method have shown the dominance of TH2's clones in gastric cancers,[10] which are consistent with the method of the present study regarding the phenotype of measured chemokine receptors.…”

Section: Discussionmentioning

confidence: 60%

CCR3, CCR4, CCR5, and CXCR3 expression in peripheral blood CD4+ lymphocytes in gastric cancer patients

et al. 2013

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Background:CD4+(TH1, and TH2) cell groups in the point of view of chemokine receptor expression were considered in blood of stomach cancer patients.Materials and Methods:The percentage of blood CD4+ T cells expressing chemokine receptors (before and after gastrectomy) was determined by flow cytometry (Becton Dickinson, USA) using the following chemokine receptor antibodies: anti-CCR5, anti-CXCR3, anti-CCR3 and anti-CCR4.Results:The means of CD4+ CCR5+ expressing cells was 1.23% ± 0.90, 0.83% ± 0.34 and 1.34% ± 0.74 in control, pre- and post-operation groups, respectively. CD4+ CXCR3+ expressing cells were 19.09% ± 8.4, 16.95% ± 5.71 and 25.08% ± 9.31, respectively. Similar pattern was seen for CD4+ CCR3+ and CD4+ CCR4+ expressing cells. Pearson correlation analysis shows no relationship between CCR3 and CCR4 expressions on TCD4 cells (r = 0.211, P = 0.126). The complex expression TH1 (CD4+ CXCR3+ CCR5+) receptors determined 1.14% ± 0.54 for control group, 0.86% ± 0.49 for pre-T and 1.57% ± 0.67 for post-T group. Moreover, the TH2 (CD4+ CCR3+ CCR4+) expression was 1.60% ± 1.05 for control group, 1.57% ± 0.83 for pre-T and 1.27% ± 0.66 for post-treatment group. Pearson correlation analysis shows that only the CCR3 and CCR5 expression was statistically correlated (r = 0.321, P = 0.018).Conclusion:Due to low expression of CCR5 in TH1 and CCR3 in TH2 cells, it seems that utility of these is extremely limited for clinical evaluation, but not scientific purpose. Moreover, considering the CXCR3 for TH1 cells and CCR4 expression for TH2 cells, due to considerable expression, may be practical.

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Section: Discussionmentioning

confidence: 60%

CCR3, CCR4, CCR5, and CXCR3 expression in peripheral blood CD4+ lymphocytes in gastric cancer patients

et al. 2013

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“…It remains to be investigated if CXCR3 is required for CTL entry into all virus-infected tissues (e.g., brain). The CXCR3-inflammatory loop potentially may not only increase recruitment of CTLs into peripheral tissues, but also may enhance the generation of CTLs [50] and promote increased effector responses through STAT1 signaling [51]. …”

Section: Cxcr3-dependent Amplification Of Immune Responsesmentioning

confidence: 99%

CXCR3 in T cell function

Groom¹,

Luster²

2011

Experimental Cell Research

753

648

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CXCR3 is a chemokine receptor that is highly expressed on effector T cells and plays an important role in T cell trafficking and function. CXCR3 is rapidly induced on naïve cells following activation and preferentially remains highly expressed on Th1-type CD4+ T cells and effector CD8+ T cells. CXCR3 is activated by three interferon-inducible ligands CXCL9 (MIG), CXCL10 (IP-10) and CXCL11 (I-TAC). Early studies demonstrated a role for CXCR3 in the trafficking of Th1 and CD8 T cells to peripheral sites of Th1-type inflammation and the establishment on Th1 amplification loop mediated by IFNγ and the IFNγ-inducible CXCR3 ligands. More recent studies have also suggested that CXCR3 plays a role in the migration of T cells in the microenvironment of the peripheral tissue and lymphoid compartment, facilitating the interaction of T cells with antigen presenting cells leading to the generation of effector and memory cells.

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“…A standard 4-h Cr release assay was performed with minor modifications [14]. In brief, K562, U937, CEM, or P815 target cells were labeled with 51 Cr (Perkin Elmer, Boston, MA, USA) at 50 Ci/5 ϫ 10 5 cells and cocultured at 5 ϫ 10 3 cells /well with serially diluted NK cell cultures for 4 h. For redirected ADCC, P815 cells were preincubated with anti-human 2B4 mAb before the coculture.…”

Section: Cr Release Assaysmentioning

confidence: 99%

FK506 causes cellular and functional defects in human natural killer cells

Kim

Kim²,

Kang

et al. 2010

Journal of Leukocyte Biology

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The role of NK cells in allogeneic HCT has been increasingly appreciated, particularly in the GVL effect. Although FK506 has been used widely to prevent GVHD, its action was considered to be primarily through activated T cells. In this study, we provide direct evidence for the first time that human NK cells are immediate targets of FK506. Our in vivo data from patients undergoing peripheral blood stem cell transplantation or BMT showed a reduced number of NK cells with down-regulated CD25 expression in their peripheral blood compartment. Likewise, FK506 caused profound inhibition of NK cell proliferation in vitro and suppressed NK cytotoxicity and cytokine secretion in response to IL-2. These defects were accompanied by impaired cell clustering and selective down-regulation of adhesion molecules, ICAM-1, CD2, CD49d, and CD58. Furthermore, FK506 specifically inhibited expression of NKG2D, CD48, and DNAM1 receptors without affecting that of 2B4, NKp30, NKp44, and NKp46. As a result, natural cytotoxicity against K562 tumor targets was impaired, while leaving redirected ADCC via 2B4 intact. Finally, FK506-treated NK cells showed impaired IL-2R signaling and inhibition of STAT3. Collectively, these signaling impairments and selective down-regulation of NK receptors by FK506 may underlie the proliferative and functional defects of NK cells. Thus, our data provide a new insight into the mechanism of immunosuppression by FK506, which should be considered to interpret the outcome of graft transplantation.

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Selective addition of CXCR3+CCR4-CD4+ Th1 cells enhances generation of cytotoxic T cells by dendritic cells in vitro

Abstract: Abstract

Cited by 23 publications

References 33 publications

CCR3, CCR4, CCR5, and CXCR3 expression in peripheral blood CD4+ lymphocytes in gastric cancer patients

CCR3, CCR4, CCR5, and CXCR3 expression in peripheral blood CD4+ lymphocytes in gastric cancer patients

CXCR3 in T cell function

FK506 causes cellular and functional defects in human natural killer cells

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