T Cell Proliferation

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Keiya Ozawa - One of the best experts on this subject based on the ideXlab platform.

  • niTric oxide plays a criTical role in suppression of T Cell proliferaTion by mesenchymal sTem Cells
    Blood, 2007
    Co-Authors: Kazuya Sato, Katsutoshi Ozaki, Iekuni Oh, Akiko Meguro, Keiko Hatanaka, Tadashi Nagai, Kazuo Muroi, Keiya Ozawa
    Abstract:

    The molecular mechanisms by which mesenchymal sTem Cells (MSCs) suppress T-Cell proliferaTion are poorly undersTood, and wheTher a soluble facTor plays a major role remains conTroversial. Here we demonsTraTe ThaT The T-Cell–recepTor complex is noT a TargeT for The suppression, suggesTing ThaT downsTream signals mediaTe The suppression. We found ThaT STaT5 phosphorylaTion in T Cells is suppressed in The presence of MSCs and ThaT niTric oxide (NO) is involved in The suppression of STaT5 phosphorylaTion and T-Cell proliferaTion. The inducTion of inducible NO synThase (NOS) was readily deTecTed in MSCs buT noT T Cells, and a specific inhibiTor of NOS reversed The suppression of STaT5 phosphorylaTion and T-Cell proliferaTion. This producTion of NO in The presence of MSCs was mediaTed by CD4 or CD8 T Cells buT noT by CD19 B Cells. FurThermore, inhibiTors of prosTaglandin synThase or NOS resTored The proliferaTion of T Cells, whereas an inhibiTor of indoleamine 2,3-dioxygenase and a Transforming growTh facTor–β–neuTralizing anTibody had no effecT. Finally, MSCs from inducible NOS−/− mice had a reduced abiliTy To suppress T-Cell proliferaTion. Taken TogeTher, These resulTs suggesT ThaT NO produced by MSCs is one of The major mediaTors of T-Cell suppression by MSCs.

Kazuya Sato - One of the best experts on this subject based on the ideXlab platform.

  • niTric oxide plays a criTical role in suppression of T Cell proliferaTion by mesenchymal sTem Cells
    Blood, 2007
    Co-Authors: Kazuya Sato, Katsutoshi Ozaki, Iekuni Oh, Akiko Meguro, Keiko Hatanaka, Tadashi Nagai, Kazuo Muroi, Keiya Ozawa
    Abstract:

    The molecular mechanisms by which mesenchymal sTem Cells (MSCs) suppress T-Cell proliferaTion are poorly undersTood, and wheTher a soluble facTor plays a major role remains conTroversial. Here we demonsTraTe ThaT The T-Cell–recepTor complex is noT a TargeT for The suppression, suggesTing ThaT downsTream signals mediaTe The suppression. We found ThaT STaT5 phosphorylaTion in T Cells is suppressed in The presence of MSCs and ThaT niTric oxide (NO) is involved in The suppression of STaT5 phosphorylaTion and T-Cell proliferaTion. The inducTion of inducible NO synThase (NOS) was readily deTecTed in MSCs buT noT T Cells, and a specific inhibiTor of NOS reversed The suppression of STaT5 phosphorylaTion and T-Cell proliferaTion. This producTion of NO in The presence of MSCs was mediaTed by CD4 or CD8 T Cells buT noT by CD19 B Cells. FurThermore, inhibiTors of prosTaglandin synThase or NOS resTored The proliferaTion of T Cells, whereas an inhibiTor of indoleamine 2,3-dioxygenase and a Transforming growTh facTor–β–neuTralizing anTibody had no effecT. Finally, MSCs from inducible NOS−/− mice had a reduced abiliTy To suppress T-Cell proliferaTion. Taken TogeTher, These resulTs suggesT ThaT NO produced by MSCs is one of The major mediaTors of T-Cell suppression by MSCs.

Olivier Hermine - One of the best experts on this subject based on the ideXlab platform.

  • Immunosuppressive role of semaphorin-3A on T Cell proliferaTion is mediaTed by inhibiTion of acTin cyToskeleTon reorganizaTion
    European Journal of Immunology, 2006
    Co-Authors: Yves Lepelletier, Ari Barzilai, Ivan Cruz Moura, Réda Hadj-slimane, Cédric Baude, Amedee Renand, S Fiorentino, Anat Shirvan, Olivier Hermine
    Abstract:

    Timely negaTive regulaTion of The immune sysTem is criTical To allow iT To perform iTs duTy while mainTaining iT under TighT conTrol To avoid overacTivaTion. We previously reporTed ThaT The neuronal recepTor neuropilin-1 (NP-1) is expressed in human lymph nodes. However, The role of NP-1 inTeracTion wiTh iTs physiological ligand semaphorin-3A (Sema-3A) on immune Cells remains elusive. Here we show ThaT Sema-3A is expressed by acTivaTed DC and T Cells, and ThaT iTs secreTion in DC/T Cell coculTures is delayed. Sema-3A/NP-1 inTeracTion down-modulaTed T Cell acTivaTion since addiTion of Sema-3A in DC/T Cell coculTures dramaTically inhibiTed allogeneic T Cell proliferaTion. More imporTanTly, neuTralizaTion by blocking anTibodies or by anTagonisT pepTide of endogenous Sema-3A produced by DC/T Cell coculTures resulTed in a 130% increase in T Cell proliferaTion. Sema-3A acTed direcTly on T Cells, since iT could block anTi-CD3/CD28-sTimulaTed proliferaTion of T Cells. Finally, immunomodulaTory funcTions of Sema-3A relied on The blockage of acTin cyToskeleTon reorganizaTion, affecTing TCR polarizaTion and inTerfering wiTh early TCR signal TransducTion evenTs such as ZAP-70 or focal adhesion kinase phosphorylaTion. Therefore, we propose ThaT Sema-3A secreTion and The resulTing NP-1/Sema-3A inTeracTion are involved in a laTe negaTive feedback loop conTrolling DC-induced T Cell proliferaTion.

Mary Mclaughlin - One of the best experts on this subject based on the ideXlab platform.

Katsutoshi Ozaki - One of the best experts on this subject based on the ideXlab platform.

  • niTric oxide plays a criTical role in suppression of T Cell proliferaTion by mesenchymal sTem Cells
    Blood, 2007
    Co-Authors: Kazuya Sato, Katsutoshi Ozaki, Iekuni Oh, Akiko Meguro, Keiko Hatanaka, Tadashi Nagai, Kazuo Muroi, Keiya Ozawa
    Abstract:

    The molecular mechanisms by which mesenchymal sTem Cells (MSCs) suppress T-Cell proliferaTion are poorly undersTood, and wheTher a soluble facTor plays a major role remains conTroversial. Here we demonsTraTe ThaT The T-Cell–recepTor complex is noT a TargeT for The suppression, suggesTing ThaT downsTream signals mediaTe The suppression. We found ThaT STaT5 phosphorylaTion in T Cells is suppressed in The presence of MSCs and ThaT niTric oxide (NO) is involved in The suppression of STaT5 phosphorylaTion and T-Cell proliferaTion. The inducTion of inducible NO synThase (NOS) was readily deTecTed in MSCs buT noT T Cells, and a specific inhibiTor of NOS reversed The suppression of STaT5 phosphorylaTion and T-Cell proliferaTion. This producTion of NO in The presence of MSCs was mediaTed by CD4 or CD8 T Cells buT noT by CD19 B Cells. FurThermore, inhibiTors of prosTaglandin synThase or NOS resTored The proliferaTion of T Cells, whereas an inhibiTor of indoleamine 2,3-dioxygenase and a Transforming growTh facTor–β–neuTralizing anTibody had no effecT. Finally, MSCs from inducible NOS−/− mice had a reduced abiliTy To suppress T-Cell proliferaTion. Taken TogeTher, These resulTs suggesT ThaT NO produced by MSCs is one of The major mediaTors of T-Cell suppression by MSCs.