Qian-Lin Hao
Children's Hospital Los Angeles
Network
Latest external collaboration on country level. Dive into details by clicking on the dots.
Publication
Featured researches published by Qian-Lin Hao.
Journal of Immunology | 2009
Yasmin Khan Parrish; Ineavely Baez; Terry-Ann Milford; Abigail Benitez; Nicholas R. Galloway; Jaqueline Willeman Rogerio; Eva Sahakian; Mercy Kagoda; Grace Huang; Qian-Lin Hao; Yazmar Sevilla; Lora Barsky; Ewa Zielinska; Mary Price; Nathan R. Wall; Sinisa Dovat; Kimberly J. Payne
IL-7 is critical for B cell production in adult mice; however, its role in human B lymphopoiesis is controversial. One challenge was the inability to differentiate human cord blood (CB) or adult bone marrow (BM) hematopoietic stem cells (HSCs) without murine stroma. Here, we examine the role of IL-7 in human B cell development using a novel, human-only model based on coculturing human HSCs on primary human BM stroma. In this model, IL-7 increases human B cell production by >60-fold from both CB and adult BM HSCs. IL-7-induced increases are dose-dependent and specific to CD19+ cells. STAT5 phosphorylation and expression of the Ki-67 proliferation Ag indicate that IL-7 acts directly on CD19+ cells to increase proliferation at the CD34+ and CD34− pro-B cell stages. Without IL-7, HSCs in CB, but not BM, give rise to a small but consistent population of CD19lo B lineage cells that express EBF (early B cell factor) and PAX-5 and respond to subsequent IL-7 stimulation. Flt3 ligand, but not thymic stromal-derived lymhopoietin (TSLP), was required for the IL-7-independent production of human B lineage cells. As compared with CB, adult BM shows a reduction of in vitro generative capacity that is progressively more profound in developmentally sequential populations, resulting in an ∼50-fold reduction in IL-7-dependent B lineage generative capacity. These data provide evidence that IL-7 is essential for human B cell production from adult BM and that IL-7-induced expansion of the pro-B compartment is increasingly critical for human B cell production during the progression of ontogeny.
Journal of Immunology | 2000
Qian-Lin Hao; Denise Petersen; Lora Barsky; David C. Bockstoce
The effect of IL-3 on the B lymphoid potential of human hemopoietic stem cells is controversial. Murine studies suggest that B cell differentiation from uncommitted progenitors is completely prevented after short-term exposure to IL-3. We studied B lymphopoiesis after IL-3 stimulation of uncommitted human CD34+CD38− cells, using the stromal cell line S17 to assay the B lymphoid potential of stimulated cells. In contrast to the murine studies, production of CD19+ B cells from human CD34+CD38− cells was significantly increased by a 3-day exposure to IL-3 (p < 0.001). IL-3, however, did not increase B lymphopoiesis from more mature progenitors (CD34+CD38+ cells) or from committed CD34−CD19+ B cells. B cell production was increased whether CD34+CD38− cells were stimulated with IL-3 during cocultivation on S17 stroma, on fibronectin, or in suspension. IL-3Rα expression was studied in CD34+ populations by RT-PCR and FACS. High IL-3Rα protein expression was largely restricted to myeloid progenitors. CD34+CD38− cells had low to undetectable levels of IL-3Rα by FACS. IL-3-responsive B lymphopoiesis was specifically found in CD34+ cells with low or undetectable IL-3Rα protein expression. IL-3 acted directly on progenitor cells; single cell analysis showed that short-term exposure of CD34+CD38− cells to IL-3 increased the subsequent cloning efficiency of B lymphoid and B lymphomyeloid progenitors. We conclude that short-term exposure to IL-3 significantly increases human B cell production by inducing proliferation and/or maintaining the survival of primitive human progenitors with B lymphoid potential.
Blood | 2008
Hisham Abdel-Azim; Yuhua Zhu; Roger P. Hollis; Xingchao Wang; Shundi Ge; Qian-Lin Hao; Goar Smbatyan; Donald B. Kohn; Michael Rosol; Crooks Gm
Self-renewal capacity is rapidly lost during differentiation of hematopoietic stem cells to lineage-committed progenitors. We demonstrate here that regulated intracellular signaling through the cytokine receptor Mpl induces profound expansion of not only multipotent (ie, lymphomyeloid) but also lymphoid-committed human hematopoietic progenitors. A fusion protein containing the intracellular signaling domain of Mpl and a dimerization domain was constitutively expressed in populations enriched in human lymphomyeloid progenitor/stem cells (CD34(+)CD38(-)Lin(-)CD7(-)) and multilymphoid progenitors (CD34(+)CD38(-)Lin(-)CD7(+)). Intracellular dimerization of Mpl in target cells was induced by in vitro or in vivo administration of a diffusible synthetic ligand. In vitro, Mpl dimerization produced divisions of clonogenic, multilineage CD34(+) cells able to engraft immunodeficient mice. When dimerization was induced in vivo after transplantation of either lymphomyeloid or multilymphoid progenitors, donor-derived hematopoiesis was sustained for at least 12 weeks and primitive CD34(+)Lin(-) progenitors were expanded more than 1000-fold. Lineage potential of progenitors was not altered and differentiation was not prevented by synthetically induced Mpl signaling. These data demonstrate that dimerization of a single cytokine receptor can deliver a profound expansion signal in both uncommitted and lymphoid-committed human hematopoietic progenitors.
Blood | 1996
Qian-Lin Hao; Ft Thiemann; D Petersen; Smogorzewska Em; Crooks Gm
Blood | 2001
Qian-Lin Hao; Judy Zhu; Mary Price; Kimberly J. Payne; Lora Barsky
Blood | 1998
Qian-Lin Hao; Smogorzewska Em; Lora Barsky; Crooks Gm
Blood | 2007
Qian-Lin Hao; Ann George; Judy Zhu; Lora Barsky; Ewa Zielinska; Xingchao Wang; Price M; Ge S; Crooks Gm
Human Gene Therapy | 1995
Qian-Lin Hao; Punam Malik; Roberto Salazar; Hui Tang; Erlinda M. Gordon; Donald B. Kohn
Clinical Immunology | 2007
Mercy Kagoda; Yasmin Khan Parrish; Jaqueline Willeman Rogerio; Ineavely Baez; Qian-Lin Hao; Lora Barsky; Ewa Zielinska; Monika Smogorzewska; Kimberly J. Payne
Clinical Immunology | 2006
Yasmin K. Parrish; Jaqueline Rogerio; Eva Sahakian; Grace Huang; Qian-Lin Hao; Lora Barsky; Ewa Zielinska; Price M; Kimberly J. Payne