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עמוד בית
Wed, 12.06.24

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February 2010
L. Perl, A. Weissler, Y.A. Mekori and A. Mor
Stem cell therapy has developed extensively in recent years, leading to several new clinical fields. The use of mesenchymal stromal cells sparks special interest, as it reveals the importance of the paracrine and immunomodulatory effects of these supporting cells, in disease and in cure. This review discusses our current understanding of the basic clinical principles of stem cell therapy and demonstrates the broad range of this treatment modality by examining two relatively new therapeutic niches – autoimmune and cardiac diseases.
November 2009
Leor Perl, MD, Yoseph A. Mekori, MD and Adam Mor, MD.
February 2009
December 2008
March 2001
Adam Mor, MD and Yoseph A. Mekori, MD
April 2000
Ella Zeltzer MD, Jacques Bernheim MD, Ze’ev Korzets MB BSc,, Doron Zeeli PhD, Mauro Rathaus MD, Yoseph A. Mekori MD and Rami Hershkoviz MD

Background: Cell-mediated immunity is impaired in uremia. Cell-matrix interactions of immune cells such as CD4+T lymphocytes with extracellular matrix are an important requirement for an intact immune response. The adherence of CD4+T cells of healthy subjects (normal T cells) to ECM components is inhibited in the presence of uremic serum. Such decreased adhesive capacity is also found in T cells of dialysis patients. Various chemokines and cytokines affect the attachment of CD4+T cells to ECM.

Objective: To evaluate chemokine (MIP-1β and RANTES) and tumor necrosis factor α-induced adhesion of CD4+T cells to ECM in a uremic milieu.

Methods: We examined adhesion of normal CD4+T cells (resting and activated) to intact ECM in response to soluble or bound chemokines (MIP-1β and RANTES) and to TNF-α following incubation in uremic versus normal serum. Thereafter, we evaluated the adhesion of resting CD4+T cells from dialysis patients in a similar fashion and compared it to that obtained from a healthy control group.

Results: Addition of uremic serum diminished soluble and anchored chemokine-induced attachment of normal resting and activated CD4+T cells to ECM compared to a normal milieu (a peak response of 10–11% vs. 24–29% for soluble chemokines, P<0.001; 12–13% vs. 37–39% for bound chemokines on resting cells, P<0.01; and 18–20% vs. 45–47% for bound chemokines on activated cells, P<0.02). The same pattern of response was noted following stimulation with immobilized TNF-α (7 vs. 12% for resting cells, P<0.05; 17 vs. 51% for activated cells, P<0.01).  Adherence of dialysis patients’ cells to ECM following stimulation with both bound chemokines was reduced compared to control T cells (15–17% vs. 25–32%, P<0.0000). In contrast, adherence following stimulation by TNF-α was of equal magnitude.

Conclusions: Abnormal adhesive capacity of T lymphocytes to ECM in uremia may, in part, be related to a diminished response to MIP-1β, RANTES and TNF-α. However, whereas reduced adhesion to chemokines was present in both normal CD4+T cells in a uremic environment and in dialysis patients’ T cells, TNF-α-induced adhesion was found to be inhibited only in normal cells in a uremic milieu.

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ECM = extracellular matrix

TNF-α = tumor necrosis factor-a

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