Calcium ionophore-treated myeloid cells acquire many dendritic cell characteristics independent of prior differentiation state, transformation status, or sensitivity to biologic agents

Citation
Gk. Koski et al., Calcium ionophore-treated myeloid cells acquire many dendritic cell characteristics independent of prior differentiation state, transformation status, or sensitivity to biologic agents, BLOOD, 94(4), 1999, pp. 1359-1371
Citations number
57
Categorie Soggetti
Hematology,"Cardiovascular & Hematology Research
Journal title
BLOOD
ISSN journal
00064971 → ACNP
Volume
94
Issue
4
Year of publication
1999
Pages
1359 - 1371
Database
ISI
SICI code
0006-4971(19990815)94:4<1359:CIMCAM>2.0.ZU;2-M
Abstract
We previously reported that treatment of human peripheral blood monocytes o r dendritic cells (DC) with calcium ionophore (CI) led to the rapid (18 hou r) acquisition of many characteristics of mature DC, including CD83 express ion. We therefore investigated whether less-mature myeloid cells were simil arly susceptible to rapid CI activation. Although the promyelocytic leukemi a line HL-60 was refractory to cytokine differentiation, CI treatment induc ed near-uniform overnight expression of CD83, CD80 (B7.1), and CD86 (87.2), as well as additional characteristics of mature DC. Several cytokines that alone had restricted impact on HL-50 could enhance CI-induced differentiat ion and resultant T-cell sensitizing capacity, In parallel studies, CD34(po s) cells cultured from normal donor bone marrow developed marked DC-like mo rphology after overnight treatment with either rhCD40L or CI, but only CI s imultaneously induced upregulation of CD83, CD80, and CD86, This contrasted to peripheral blood monocytes, in which such upregulation could be induced with either CI or rhCD40L treatment. We conclude that normal and transform ed myeloid cells at many stages of ontogeny possess the capacity to rapidly acquire many properties of mature DC in response to CI treatment. This app arent ability to respond to calcium mobilization, even when putative signal -transducing agents are inoperative, suggests strategies for implementing h ost antileukemic immune responses.