更新于：2024-11-01

CD45RB抗原

更新于：2024-11-01

基本信息

别名-

简介-

关联

项与 CD45RB抗原相关的药物

CD45RB mAb

靶点

CD45RB抗原

作用机制

CD45RB抗原拮抗剂

在研机构-

原研机构

Research Corporation Technologies, Inc.

在研适应症-

非在研适应症

器官移植排斥 [+1]

最高研发阶段无进展

首次获批国家/地区-

首次获批日期1800-01-20

100 项与 CD45RB抗原相关的临床结果

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100 项与 CD45RB抗原相关的转化医学

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0 项与 CD45RB抗原相关的专利（医药）

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项与 CD45RB抗原相关的文献（医药）

2019-03-01·The FASEB Journal2区 · 生物学

CD8⁺, but not CD4⁺effector/memory T cells, express the CD44^highCD45RB^highphenotype with aging, which displays reduced expression levels of P2X₇receptor and ATP‐induced cellular responses

2区 · 生物学

Article

作者: Bobé, Pierre ; Mellouk, Amine

Previously we reported that the sensitivity of CD4⁺ T cells to ATP does not depend on P2X₇ receptor (P2X₇R) expression levels but on their activation and differentiation stages. Therefore, here we have investigated a potential relationship between the sensitivity of CD8⁺ T cells to ATP and their stages of differentiation. Thus, the CD8⁺ subpopulation exhibits a drastically reduced sensitivity to ATP with aging, which parallels the strong increase of an effector/memory CD8⁺ subset expressing high levels of CD44 cell adhesion molecule and CD45RB transmembrane phosphatase (CD44^hiCD45RB^hi). Using l-selectin/CD62L, CC-chemokine receptor 7, and CD127/IL-7 receptor-α markers, we showed that effector/memory CD8⁺ T cells belong to a central or effector memory subset. In contrast, the CD44^hiCD45RB^hi effector/memory subset is absent or poorly expressed in the CD4⁺ T subpopulation regardless of age. While ATP treatment can trigger channel and pore formation, CD62L shedding, phosphatidylserine exposure, and cell death in the CD44^loCD45RB^hi-naive CD8⁺ subset, it is unable to induce these cellular activities in the CD44^hiCD45RB^hi effector/memory CD8⁺ subset. Importantly, both CD44^loCD45RB^hi-naive and CD44^hiCD45RB^hi effector/memory subsets express similar low levels of P2X₇R, demonstrating that the sensitivity of CD8⁺ T cells to ATP depends on the stage of differentiation instead of P2X₇R expression levels.-Mellouk, A., Bobé, P. CD8⁺, but not CD4⁺ effector/memory T cells, express the CD44^highCD45RB^high phenotype with aging, which displays reduced expression levels of P2X₇ receptor and ATP-induced cellular responses.

2017-02-01·Immunology & Cell Biology3区 · 医学

Anti‐CD45RB and donor‐specific spleen cells transfusion inhibition allograft skin rejection mediated by memory T cells

3区 · 医学

Article

作者: Jian, You‐Qiang ; Li, Fu‐Rong ; Deng, Shao‐Ping ; Deng, Chun‐Yan ; Qi, Hui ; Ye, Jian

Donor‐reactive memory T (Tm)cells mediate accelerated rejection, which is known as a barrier to the survival of transplanted organs. Selective interference with the anti‐CD45RB monoclonal antibody (α‐CD45RB) reliably induces donor‐specific tolerance. In this study, pre‐sensitization to female C57BL/6 mice with the skin of female BLAB/c mice generated a large number of Tm cells and resulted in rapid rejection of the secondly transplanted allografts. α‐CD45RB did induce the tolerance to skin allograft primarily transplanted but failed to induce tolerance in the pre‐sensitized mice. Donor‐specific spleen cell transfusion (DST) alone also failed to induce the tolerance in the pre‐sensitized recipients. Interestingly, combination of α‐CD45RB with DST inhibited the rejection induced by memory T cells in the pre‐sensitized mice. CD25+ T‐cell depletion in α‐CD45RB combined with DST therapy recipients could prevent skin allograft tolerance from establishing. In addition, adoptive transfer of donor‐primed memory T cells into the tolerant recipients markedly broke the established tolerance. Our findings indicate that α‐CD45RB and DST can synergistically inhibit the accelerated rejection mediated by memory T cells and induce long‐term skin allograft acceptance in mice.

2015-02-01·Gut1区 · 医学

Protective effects of Fc-fused PD-L1 on two different animal models of colitis

1区 · 医学

Article

作者: Hong, Chun-Pyo ; Kim, Jung-Hwan ; Lee, Ji Yeung ; Kim, Sae Won ; Park, Yunji ; Yang, Bo-Gie ; Lee, Seung-Woo ; Sung, Young-Chul ; Kim, Kwang Soon ; Park, Seong Jeong ; Song, Mi-Young ; Jang, Myoung Ho

OBJECTIVEProgrammed death-ligand 1 (PD-L1) has been shown to negatively regulate immune responses via its interaction with PD-1 receptor. In this study, we investigated the effects of PD-L1-Fc treatment on intestinal inflammation using two murine models of inflammatory colitis induced by dextran sulfate sodium (DSS) and T-cell transfer.DESIGNThe anti-colitis effect of adenovirus expressing Fc-conjugated PD-L1 (Ad/PD-L1-Fc) and recombinant PD-L1-Fc protein was evaluated in DSS-treated wild-type and Rag-1 knockout (KO) mice. We examined differentiation of T-helper cells, frequency of innate immune cells, and cytokine production by dendritic cells (DCs) in the colon from DSS-treated mice after PD-L1-Fc administration. In Rag-1 KO mice reconstituted with CD4 CD45RB(high) T cells, we assessed the treatment effect of PD-L1-Fc protein on the development of colitis.RESULTSAdministration of Ad/PD-L1-Fc significantly ameliorated DSS-induced colitis, which was accompanied by diminished frequency of interleukin (IL)-17A-producing CD4 T cells and increased interferon-γ-producing CD4 T cells in the colon of DSS-fed mice. The anti-colitic effect of PD-L1-Fc treatment was also observed in DSS-treated Rag-1 KO mice, indicating lymphoid cell independency. PD-L1-Fc modulated cytokine production by colonic DCs and the effect was dependent on PD-1 expression. Furthermore, PD-L1-Fc protein could significantly reduce the severity of colitis in CD4 CD45RB(high) T-cell-transferred Rag-1 KO mice.CONCLUSIONSBased on the protective effect of PD-L1-Fc against DSS-induced and T-cell-induced colitis, our results suggest that PD-1-mediated inhibitory signals have a crucial role in limiting the development of colonic inflammation. This implicates that PD-L1-Fc may provide a novel therapeutic approach to treat inflammatory bowel disease.