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Abnormal cytokine production by bone marrow stromal cells of multiple myeloma patients in response to RPMI8226 myeloma cells

100%
Zdzisinska B., Bojarska-Junak A., Dmoszynska A., Kandefer-Szerszen M.
Archivum Immunologiae et Therapiae Experimentalis
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2008
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vol. 56
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issue 3
207-221
EN
Introduction Recent studies indicate that bone marrow stromal cells (BMSCs) derived from patients with multiple myeloma (MM) differ from those of healthy donors in their expression of extracellular matrix compounds and in cytokine production. It is not known whether these abnormalities are primary or are acquired by BMSCs on contact with MM cells. Materials and Methods: Interleukin (IL)-6, IL-11, IL-10, and tumor necrosis factor (TNF)-alpha production by CD166+ mesenchymal BMSCs and the CD38+/CD138+ RPMI8226 myeloma cell line cultivated in vitro in monocultures or co-cultivated under cell-to-cell contact or non-contact conditions in the presence of a tissue culture insert were measured. Intracellular cytokines were measured by flow cytometry analysis as the percentage of cytokine-producing cells or by mean fluorescence intensity as the level of cytokine expression in cells. Additionally, ELISA was used to measure IL-6, soluble IL-6 receptor (sIL-6R), IL-11, IL-10, TNF- alpha, B-cell-activating factor of the TNF family (BAFF), hepatocyte growth factor (HGF), and osteopontin (OPN) production in the supernatants of the cultures and co-cultures. Results A higher ability of the BMSCs of MM patients than in controls was detected to produce IL-6, IL-10, TNF- alpha, OPN, and especially HGF and BAFF in response to the RPMI8226 cells. Moreover, the BMSCs of the MM patients significantly enhanced the production of sIL-6R by the RPMI8226 cells. Discussion Cytokines over-expressed by BMSCs of MM patients can function as growth factors for myeloma cells (IL-6, IL-10, HGF), migration stimulatory factors for tumor plasma cells (TNF-alpha, HGF), adhesion stimulatory factors (HGF, BAFF and OPN), stimulators of osteoclastogenesis (IL-6, TNF-alpha), and angiogenic factors (TNF-alpha). The results of this experiment strongly suggest that the BMSCs from MM patients differed in spontaneous and myeloma cell-induced production of cytokines, especially of HGF and BAFF, and these abnormalities were both primary and acquired by the BMSCs on contact with the MM cells. This in turn suggests the presence of an undefined, autocrine stimulation pathway resulting in a prolonged production of cytokines even in long-term cultures in vitro and in vivo. These abnormalities might provide optimal conditions for the proliferation and differentiation of residual tumor cells or their precursors in the affected bone marrow.
2
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Bone marrow stromal cells in traumatic brain injury (TBI) therapy: true perspective or false hope?

100%
Opydo-Chanek M.
Acta Neurobiologiae Experimentalis
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2007
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vol. 67
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issue 2
187-195
EN
Recent studies regard bone marrow stromal cells as a potential andidate for cellular therapy of traumatic brain injury and thus as an attractive alternative for embryonic and fetal stem cells. Numerous experiments indicate that bone marrow stromal cells play an important role in the repair of injured brain tissue and also support healing processes. Findings of in vitro and in vivo studies show that these cells have an ability to differentiate into cells of multiple tissues, including neurons and glial cells and to secrete an array of growth factors and cytokines, which have an influence on repair of damaged tissue. In addition, treatment of traumatic brain injury with bone marrow stromal cells promotes functional recovery of injured animals. Taking this into consideration, there is hope for using bone marrow stromal cells in brain injury therapy, which is very difficult because of specific events that occur in the pathological conditions. However, mechanisms responsible for the observed therapeutic potential of bone marrow stromal cells still remain unclear. The review presents achievements in studies on bone marrow stromal cells as a source of therapeutic benefits in treatment of traumatic brain injury and addresses the question of their possible future use in clinical trials.
3

Mechanisms of tumor escape: role of tumor microenvironment in inducing apoptosis of cytolytic effector cells

88%
Poggi A., Zocchi M. R.
Archivum Immunologiae et Therapiae Experimentalis
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2006
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vol. 54
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issue 5
323-333
EN
Spontaneous tumors grow and kill the host unless therapy reduces their mass to a level where the immune system, it is thought, can control their growth and diffusion. Indeed, in many instances tumors can reappear, become resistant to therapy, and escape the host immune response. Many mechanisms of tumor escape operating in the tumor microenvironment have been proposed: 1) low or absent expression of molecules on tumor cells involved in tumor target cell recognition; 2) absence of co-stimulation leading to tolerization of T cells; 3) soluble factors secreted by tumor cells inhibiting T cell response; and 4) regulatory T cells, myeloid suppressor cells, and stromal cells may impair immune-cell responses to tumors. Furthermore, tumors can release soluble molecules such as HLA-I (sHLA-I). This, in turn, reduces T cell-mediated immune response and induces apoptosis of cytolytic effector cells such as natural killer and CD8+ T lymphocytes through the engagement of HLA-I receptors such as CD8 and/or activating isoforms of the inhibitory receptor superfamily. The release of soluble ligand for activating receptors, e.g. UL16 binding proteins and/or MHC class I-related proteins A and B, the natural ligands of NKG2D, may impair activation, effector cell-mediated recognition, and cytolysis of tumor cells. Furthermore, the elimination of anti-tumor effector cells may be achieved by induction of apoptosis consequent to triggering elicited via activating molecules, such as receptors responsible for natural cytotoxicity, upon their binding with ligands expressed on tumor cells.
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