Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P06126 (CD1a)
 2,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was purposed to investigate the possibility of differentiating the acute promyelocytic leukemia (APL) cells into dendritic cells (DCs) induced by all-trans retinoic acid (ATRA) combined with classic cytokines so as to provide a new approach for development of APL-DC vaccine. The bone marrow mononuclear cells from a new diagnosed patient with APL and HL-60 cells were separately cultured in complete culture medium. The cells were treated by ATRA, GM-CSF, IL-4 and TNFalpha in experimental groups and no ATRA was added in control and blank control groups. The cell morphology was observed by light microscopy, the phenotypes of DCs were detected by flow cytometry, the level of IL-12 was measured by using ELISA, the mixed lymphocyte reaction (MLR) and effect of cytotoxic T-lymphocyte (CTL) were assayed by MTT method. The results indicated that in experiment groups, the cells had dendritic appearance and cytogenetic characteristics of APL; expression of CD1a, CD83, CD80, CD86, HLA-DR and CD1d as well as level of IL-12 obviously increased; the MLR and CTL effects were significant, but increase of CD1a expression in HL60-DCs did not show statistical difference from control and blank control groups. It is concluded that ATRA can successfully induce APL cells to differentiate into functionally mature DSs which obviously mediate MLR and CTL effects. The APL-DCs derived by ATRA can notably express CD1d that may activate CD1d-restricted NKT cells and promote proliferation of NRT cells. The exact mechanism of which should be further studied.
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PMID:[Induction of dendritic cells derived from acute promyelocytic leukemia cells by all trans retinoic acid]. 1892 13

Immune thrombocytopenia (ITP) is an autoimmune disease in which dendritic cells (DCs) play a crucial role in the breakdown of self-tolerance. Studies have identified the function of mesenchymal stem cells (MSCs) in promoting the development of regulatory DCs (regDCs). Our previous work revealed that MSCs in ITP exerted senescence, apoptosis, and impaired immunosuppressive effects on T and B cells. However, it is unclear whether the effects of MSCs on regDC induction are altered in ITP. Our data demonstrated that MSCs in ITP were impaired in inhibiting CD1a+ DC and CD14+ DC differentiation from CD34+ hematopoietic progenitor cells (CD34+ HPCs). DCs differentiated with MSCs in ITP exhibited an increased expression of costimulatory molecules CD80/CD86 and secretion of proinflammatory interleukin-12 (IL-12). Accordingly, the tolerogenic characteristics were deficient in DCs induced by MSCs in ITP. DCs differentiated with MSCs in ITP exhibited an impaired ability to inhibit CD3+ T cell proliferation, to suppress T helper (Th)1 cell differentiation, and to induce anergic and regulatory T cells (Tregs). The expression of Notch signaling components was measured in MSCs in ITP. Reduced expression of the ligand Jagged-1, the receptor Notch-1 intracellular domain (NICD-1), and the target gene Hes-1 was identified in MSCs in ITP. The addition of biologically active Jagged-1 to CD34+ HPCs was observed to promote regDC differentiation. When cultured on Jagged-1-coated plates, MSCs in ITP showed an enhancement of the Notch-1 pathway activation, Jagged-1 expression, and the function in inducing regDCs. Pretreatment with all-trans retinoic acid (ATRA) was found to partially restore the capacity of MSCs in both ITP patients and healthy controls in inducing CD34+-derived regDCs. Our data elucidated that MSCs in ITP were impaired in inducing CD34+-regDCs, associated with the Notch-1/Jagged-1 signaling pathway. ATRA could partially correct the impairment of MSCs, suggesting that ATRA could serve as a potential therapeutic alternative for ITP.
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PMID:Impaired Function of Bone Marrow Mesenchymal Stem Cells from Immune Thrombocytopenia Patients in Inducing Regulatory Dendritic Cell Differentiation Through the Notch-1/Jagged-1 Signaling Pathway. 2894 11