| 1. |
- Cervenak, L, et al.
(author)
-
Abolished angiogenicity and tumorigenicity of Burkitt lymphoma by interleukin-10
- 2000
-
In: Blood. - 0006-4971. ; 96:7, s. 73-2568
-
Journal article (peer-reviewed)abstract
- Because of its immunosuppressive properties, interleukin-10 (IL-10) is thought to play an important role in a number of human disease states, including inflammation, autoimmunity, and transplant rejection. In this study, we demonstrate that introduction of human or viral IL-10 genes into Burkitt's lymphoma cells markedly reduced their ability to grow as subcutaneous (sc) tumors in SCID mice. In vivo assays for angiogenesis revealed an inhibition of the angiogenic capacity of the IL-10-transfected lines. Recombinant human IL-10 abolished and viral IL-10 reduced vascular endothelial growth factor (VEGF)-165-induced neovascularization. Furthermore, IL-10 blocked the VEGF- and fibroblast growth factor (FGF)-2-induced proliferation of microvascular endothelial cells in vitro. The current observations suggest a direct role for IL-10 in the prevention of angiogenesis in human lymphoid malignancies.
|
|
| 2. |
|
|
| 3. |
|
|
| 4. |
|
|
| 5. |
- Kambayashi, T, et al.
(author)
-
Cutting edge: Regulation of CD8(+) T cell proliferation by 2B4/CD48 interactions
- 2001
-
In: Journal of immunology (Baltimore, Md. : 1950). - : The American Association of Immunologists. - 0022-1767 .- 1550-6606. ; 167:12, s. 6706-6710
-
Journal article (peer-reviewed)abstract
- The biological function of 2B4, a CD48-binding molecule expressed on T cells with an activation/memory phenotype, is not clear. In this report, we demonstrate that proliferation of CD8+ T cells is regulated by 2B4. Proliferative responses of CD8+ T cells were significantly reduced by anti-2B4 Ab. The effects were not potentiated by anti-CD48 Ab, suggesting that the observed responses were driven by 2B4/CD48 interactions. Surprisingly, the 2B4/CD48-dependent proliferative responses were also observed in the absence of APCs. This suggests that 2B4/CD48 interactions can occur directly between T cells. Furthermore, when activated 2B4+CD8+ T cells were mixed with 2B4−CD8+ TCR-transgenic T cells and specific peptide-loaded APC, the proliferation of the latter T cells was inhibited by anti-2B4 Ab. Taken together, this suggests that 2B4 on activated/memory T cells serves as a ligand for CD48, and by its ability to interact with CD48 provides costimulatory-like function for neighboring T cells.
|
|
| 6. |
- Kambayashi, T, et al.
(author)
-
Emergence of CD8+ T cells expressing NK cell receptors in influenza A virus-infected mice
- 2000
-
In: Journal of immunology (Baltimore, Md. : 1950). - : The American Association of Immunologists. - 0022-1767 .- 1550-6606. ; 165:9, s. 4964-4969
-
Journal article (peer-reviewed)abstract
- Both innate and adaptive immune responses play an important role in the recovery of the host from viral infections. In the present report, a subset of cells coexpressing CD8 and NKR-P1C (NK1.1) was found in the lungs of mice infected with influenza A virus. These cells were detected at low numbers in the lungs of uninfected mice, but represented up to 10% of the total CD8+ T cell population at day 10 postinfection. Almost all of the CD8+NK1.1+ cells were CD8αβ+CD3+TCRαβ+ and a proportion of these cells also expressed the NK cell-associated Ly49 receptors. Interestingly, up to 30% of these cells were virus-specific T cells as determined by MHC class I tetramer staining and by intracellular staining of IFN-γ after viral peptide stimulation. Moreover, these cells were distinct from conventional NKT cells as they were also found at increased numbers in influenza-infected CD1−/− mice. These results demonstrate that a significant proportion of CD8+ T cells acquire NK1.1 and other NK cell-associated molecules, and suggests that these receptors may possibly regulate CD8+ T cell effector functions during viral infection.
|
|
| 7. |
|
|
| 8. |
|
|
| 9. |
- Kambayashi, T, et al.
(author)
-
Memory CD8+ T cells provide an early source of IFN-gamma
- 2003
-
In: Journal of immunology (Baltimore, Md. : 1950). - : The American Association of Immunologists. - 0022-1767 .- 1550-6606. ; 170:5, s. 2399-2408
-
Journal article (peer-reviewed)abstract
- During the non-Ag-specific early phase of infection, IFN-γ is believed to be primarily provided by NK and NKT cells in response to pathogen-derived inflammatory mediators. To test whether other cell types were involved in early IFN-γ release, IFN-γ-producing cells were visualized in spleens and lymph nodes of LPS-injected mice. In addition to NK and NKT cells, IFN-γ was also detected in a significant fraction of CD8+ T cells. CD8+ T cells represented the second major population of IFN-γ-producing cells in the spleen (∼30%) and the majority of IFN-γ+ cells in the lymph nodes (∼70%). LPS-induced IFN-γ production by CD8+ T cells was MHC class I independent and was restricted to CD44high (memory phenotype) cells. Experiments performed with C3H/HeJ (LPS-nonresponder) mice suggested that CD8+ T cells responded to LPS indirectly through macrophage/dendritic cell-derived IFN-α/β, IL-12, and IL-18. IFN-γ was also detected in memory CD8+ T cells from mice injected with type I IFN or with poly(I:C), a synthetic dsRNA that mimics early activation by RNA viruses. Taken together, these results suggest that in response to bacterial and viral products, memory T cells may contribute to innate immunity by providing an early non-Ag-specific source of IFN-γ.
|
|
| 10. |
|
|
