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501.
Archna Ravi Lavinia Palamiuc Ryan M. Loughran Joanna Triscott Gurpreet K. Arora Avi Kumar Vivian Tieu Chantal Pauli Matthias Reist Rachel J. Lew Shauna L. Houlihan Christof Fellmann Christian Metallo Mark A. Rubin Brooke M. Emerling 《Developmental cell》2021,56(11):1661-1676.e10
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502.
Elizabeth A. Thompson Katherine Cascino Alvaro A. Ordonez Weiqiang Zhou Ajay Vaghasia Anne Hamacher-Brady Nathan R. Brady Im-Hong Sun Rulin Wang Avi Z. Rosenberg Michael Delannoy Richard Rothman Katherine Fenstermacher Lauren Sauer Kathyrn Shaw-Saliba Evan M. Bloch Andrew D. Redd Aaron A.R. Tobian Jonathan D. Powell 《Cell reports》2021,34(11):108863
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503.
C6 rat glioma cells incubated in serum-free medium with D-[14C]glucosamine secrete, on stimulation with nerve growth factor (NGF) or monosialogangliosides (MSGs), several glycoproteins (Gps), the most prominent of which are a 270-, 220-, and 69-kDa Gp. Several growth factors, hormones, phorbol ester, and disialo- and trisialogangliosides did not stimulate secretion. Western blot analysis of the conditioned medium from C6 cells stimulated with NGF or MSG identified one distinct band of approximately 220 kDa for fibronectin and J1/tenascin, which comigrated. Antiserum to NGF prevented NGF-stimulated release and also blocked MSG-evoked release. The 220-kDa band was labeled after pulse labeling with [35S]methionine in the presence of NGF, and by a 15-min chase period radioactively labeled J1/tenascin could be immunoprecipitated. Tunicamycin drastically inhibited almost completely release of the 220-kDa Gp labeled by D-[14C]glucosamine or [35S]methionine. These results extend the range of neurotrophic properties attributed to NGF to cells of glial origin and suggest that NGF regulates secretion of extracellular matrix proteins. MSG stimulation of fibronectin and J1/tenascin secretion may be mediated by NGF or an NGF-like molecule also secreted by the C6 glioma cells. 相似文献
504.
A. Eisenthal Yechiel Goldman Yehuda Skornick Anna Gelfand Diana Buyaner Issac Kaver Alon Yellin Henry Yehoshua Beatriz Lifschitz-Mercer Amnon Gonnene M. Shinitzky 《Cancer immunology, immunotherapy : CII》1998,46(6):304-310
Hydrostatic pressure (P) combined with membrane protein crosslinking (CL) by adenosine dialdehyde (AdA) can render tumor
cells immunogenic. We have recently shown that PCL treatment of murine tumor cells augmented the presentation of MHC-restricted
tumor-associated antigens and enhanced cell-mediated immunity. In cancer patients inoculated with autologous PCL-modified
tumor cells, a significant delayed-type hypersensitivity response was elicited. Since the balance between cell-mediated immunity
and humoral immunity is reciprocally controlled by immunoregulatory cytokines, we have examined the proliferative response
and cytokine secretion pattern in cultures of human peripheral blood mononuclear cells (PBMC) stimulated by autologous PCL-modified
and unmodified tumor cells. These tumor cells were obtained from freshly resected tumor tissue of 16 patients with colon (8),
lung (4) and renal (4) carcinomas. The results demonstrated that PCL-modified tumor cells promoted an increase in PBMC proliferation
in 5 out of 8 (63%), 1 out of 4 (25%) and 4 out of 4 (100%) colon, lung and renal cell carcinomas. Fourteen of the above cultures
were also analyzed for the secretion of interleukin-10 and interferon-γ. Overall, a substantial decrease in IL-10 secretion
was detected in 9 out of 14 (64%) cultures while a reciprocal increase in interferon-γ secretion was noted in 8 out of 14
(57%) cultures. Our results confirmed that PCL-modified human tumor cells of different etiologies can modulate the pattern
of cytokines released from stimulated autologous lymphocytes. Such a procedure could prove valuable in the production of autologous
tumor vaccines.
Received: 8 January 1998 / Accepted: 9 April 1998 相似文献
505.