Tritiated thymidine ([3H]-TdR) and immunocytochemical tracing of cellular fate within the asexually dividing cestode Mesocestoides vogae (syn. M. corti)

Parasitology ◽  
2000 ◽  
Vol 121 (1) ◽  
pp. 105-110 ◽  
Author(s):  
A. G. SMITH ◽  
G. McKERR
Keyword(s):  
Tissue Repair ◽  
Liquid Scintillation ◽  
Tritiated Thymidine ◽  
Fold Increase ◽  
Spatial Arrangement ◽  
Entire Body ◽  
Recruitment Pattern ◽  
Cell Recruitment ◽  
Organ Systems ◽  
Mesocestoides Vogae

This report documents the presence of an active thymidine kinase (TK) system within Mesocestoides vogae tetrathyridia as quantified by tritiated thymidine ([3H]-TdR) incorporation using liquid scintillation counting. A 100-fold increase in [3H]-TdR incorporation was observed at 37 °C when compared with its incorporation at 0 °C. Thymidine's competitive analogue, BrdU, competed for sites within newly replicated DNA. Immunohistochemical trials performed here using antibodies against BrdU identified cells that have entered and passed through S-phase. Positively stained nuclei were most numerous at the anterior tip of tetrathyridia especially within the ganglia, lesser numbers of these cells occurred along the growing commissure and amongst surface tegumental cytons suggesting that stem cells do not exist in one region but are found throughout the entire body. As M. vogae has no internal organ systems the major sites for cell proliferation are those exhibiting maximal cell recruitment and undergoing tissue repair. These results show that it is possible to monitor changes in the cell recruitment pattern within this cestode. Thus use of BrdU and immunohistochemistry demonstrates how spatial arrangement and cellular reorganization can be successfully traced within M. vogae.

scholarly journals Enhanced mesenchymal stromal cell recruitment via natural killer cells by incorporation of inflammatory signals in biomaterials

2011 ◽  
Vol 9 (67) ◽  
pp. 261-271 ◽  
Author(s):  
Catarina R. Almeida ◽  
Daniela P. Vasconcelos ◽  
Raquel M. Gonçalves ◽  
Mário A. Barbosa
Keyword(s):  
Inflammatory Response ◽  
Nk Cells ◽  
Natural Killer ◽  
Tissue Repair ◽  
Bone Repair ◽  
Nk Cell ◽  
Fold Increase ◽  
Cell Recruitment ◽  
Inflammatory Signals ◽  
Differentiation Marker

An exacerbated inflammatory response questions biomaterial biocompatibility, but on the other hand, inflammation has a central role in the regulation of tissue regeneration. Therefore, it may be argued that an ‘ideal’ inflammatory response is crucial to achieve efficient tissue repair/regeneration. Natural killer (NK) cells, being one of the first populations arriving at an injury site, can have an important role in regulating bone repair/regeneration, particularly through interactions with mesenchymal stem/stromal cells (MSCs). Here, we studied how biomaterials designed to incorporate inflammatory signals affected NK cell behaviour and NK cell–MSC interactions. Adsorption of the pro-inflammatory molecule fibrinogen (Fg) to chitosan films led to a 1.5-fold increase in adhesion of peripheral blood human NK cells, without an increase in cytokine secretion. Most importantly, it was found that NK cells are capable of stimulating a threefold increase in human bone marrow MSC invasion, a key event taking place in tissue repair, but did not affect the expression of the differentiation marker alkaline phosphatase (ALP). Of significant importance, this NK cell-mediated MSC recruitment was modulated by Fg adsorption. Designing novel biomaterials leading to rational modulation of the inflammatory response is proposed as an alternative to current bone regeneration strategies.

123 A Novel Way of Thinking About Blast Injury Classification

2021 ◽  
Vol 42 (Supplement_1) ◽  
pp. S82-S83
Author(s):  
Zachary J Collier ◽  
Katherine J Choi ◽  
Ian F Hulsebos ◽  
Christopher H Pham ◽  
Haig A Yenikomshian ◽  
...  
Keyword(s):  
Surgical Intervention ◽  
Healthcare Providers ◽  
Fold Increase ◽  
Tissue Loss ◽  
Blast Injuries ◽  
Full Thickness ◽  
Icu Admission ◽  
Burn Center ◽  
Body Regions ◽  
Organ Systems

Abstract Introduction Blast injuries present unique challenges to civilian and military healthcare providers because of the complex and often severe nature of injuries spanning numerous anatomical regions, tissue types, and organ systems. Due to these factors, we devised a novel wound-focused classification system for implementation during triage and management of blast injuries to optimize outcomes and applied this system to patients treated at an ABA-certified burn center over 5 years. Methods A retrospective analysis of patients treated by an ABA-certified burn center for blast-related injuries from September 1, 2014 to October 31, 2019 was performed. Demographics, mechanism and distribution of injuries, interventions, and outcomes were evaluated. Injuries were classified using a wound-focused classification comprised of four zones: 1) areas closest to blast epicenter that had total or near-total tissue loss from the blast; 2) adjacent areas with thermal and chemical burns; 3) distant sites with shrapnel-related wounds; 4) injuries arising from barotrauma. Results We identified 64 patients who were mostly male (84%), averaging 38 ± 14 years old. Injury mechanisms included fireworks (19%), industrial accidents (16%), volatile fuels and drug labs (45%), and others including can, battery, lighter explosions (20%). All mechanisms had equivalent frequency of Zone 2 injuries with an average TBSA of 17 ± 18%. Drug-related blasts caused the highest TBSA (34 ± 23%) and the most full-thickness burns (33% vs average 23%). Fireworks had over five times (17% vs. 3%) more Zone 3 and three times (25% vs 8%) more Zone 4 injuries compared to the other mechanisms. Upper extremities were involved at twice the rate of other body regions (43% vs 19%). Patients presenting to our burn team over 24 hours after initial injury had infections in 50% of cases – a four-fold increase compared to non-delayed presentations (50% vs 13%). Overall, 45% required surgery (32% grafting, 3% flaps) but 100% of the drug-related blasts needed surgical intervention. Some patients (58%) required ICU admission with the highest rate (83%) in the drug-related group. Conclusions Blast injuries most often required admission for management of the Zone 2 component. Each blast mechanism resulted in distinct distributions of injury although fireworks had the greatest number of Zone 1, 3, and 4 injuries. Firework blasts were often less severe and more likely to present delayed with infectious complications. Larger blast mechanisms including drug-related lab explosions as well as industrial blasts had the highest rates of ICU admission, TBSA, full thickness depth, upper extremity involvement, and need for surgical intervention.

Determination of the Activity Profile of Bosutinib, Dasatinib and Nilotinib against 18 Imatinib Resistant Bcr/Abl Mutants

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 3220-3220
Author(s):  
Sara Redaelli ◽  
Rocco Piazza ◽  
Roberta Rostagno ◽  
Marianna Sassone ◽  
Vera Magistroni ◽  
...  
Keyword(s):  
Active Site ◽  
Catalytic Domain ◽  
Tritiated Thymidine ◽  
Point Mutations ◽  
Fold Increase ◽  
Therapy Resistance ◽  
Thymidine Incorporation Assay ◽  
Activity Spectrum ◽  
Incorporation Assay ◽  
Patients Experience

Abstract The treatment of Chronic Myeloid Leukemia (CML) has been radically modified by the discovery of imatinib (IM), a selective inhibitor of the fusion protein Bcr-Abl, the cause of the disease. A variable portion of CML patients experience resistance to IM therapy. Resistance can arise from different mechanisms but in the vast majority of cases is due to point mutations into the protein sequence that alter directly or indirectly the drug-protein binding. Mutation sites can be schematically clustered in four region: the P loop, the IM binding site, the catalytic domain and the activation loop (A loop). At present more than 70 mutations conferring different levels of resistance have been found in CML patients. Recently, several new inhibitors have been developed in order to obtain an increased potency and a broad range of activity against IM resistant mutants. Nilotinib (NIL) is an IM derivative about 30-fold more potent than IM. Dasatinib (DAS) is a dual-specific Src/Abl inhibitor, structurally unrelated to IM and characterized by an activity 100 to 300-fold higher than IM. Bosutinib (BOS) is a dual Src/Abl inhibitor that shows an activity 10 to 30-fold higher than IM. It is known that resistance to second generation TKIs can also arise and the analysis of mutation profiles reveals substantial differences among different TKIs. Presently the choice of a TKI to treat a patient resistant to IM is mostly based on an empirical basis, e.g. the fact that a certain patient has not been previously exposed to that particular TKI. The possibility to directly compare the different activities of TKIs against a given mutation is of remarkable importance in clinical practice. Such a tool could be used similarly to an antibiogram for bacterial diseases, guiding the choice of the most appropriate inhibitor for each patient. In our study, we investigated the activity of BOS, DAS, IM and NIL against a panel of 18 mutated forms of BCR/ABL chosen to cover the most common mutations found in patients. Stable Ba/F3 transfectant cell lines were generated and the TKIs antiproliferative activity was determined by tritiated thymidine incorporation assay. The relative IC50 increase over wild type BCR/ABL (Relative Resistance RR) was calculated. We classified the RR values in three categories: sensitive (RR≤2), resistant (between 2.01 and 10) or highly resistant (>10) as presented in the table. IC50-fold increase (WT=1) Imatinib Bosutinib Dasatinib Nilotinib Parental 10.78 38.31 >50 38.45 WT 1 1 1 1 P-LOOP L248V 3.54 2.97 5.11 2.80 G250E 6.86 4.31 4.45 4.56 Q252H 1.39 0.81 3.05 2.64 Y253F 3.58 0.96 1.58 3.23 E255K 6.02 9.47 5.61 6.69 E255V 16.99 5.53 3.44 10.31 D276G 2.18 0.60 1.44 2.00 C-Helix E279K 3.55 0.95 1.64 2.05 V299L 1.54 26.10 8.65 1.34 Active site T3151 17.50 45.42 75.03 39.41 F317L 2.60 2.42 4.46 2.22 SH2-contact M351T 1.76 0.70 0.88 0.44 Active site F359V 2.86 0.93 1.49 5.16 A-LOOP L384M 1.28 0.47 2.21 2.33 H396P 2.43 0.43 1.07 2.41 H396R 3.91 0.81 1.63 3.10 G398R 0.35 1.16 0.69 0.49 C terminal lobe F486S 8.10 2.31 3.04 1.85 Sensitive ≤2 Resistant 2.01–10 Highly resistant >10 (Updated table available online at http://www.dimep.medicina.unimib.it/en/staff_174.php?docente_id=32) Our study points out at the differences in the activity spectrum of the 4 TKIs against the 18 Bcr/Abl mutations considered. The activity pattern presented in this work will help to reach a rational and tailored therapy offering to physicians a tool to use the new TKIs in the most efficient way for their patients.

scholarly journals Why do Complications Accumulate in Individual Patients?

2002 ◽  
Vol 4 (3) ◽  
pp. 209-214
Author(s):  
Amnon Sonnenberg
Keyword(s):  
Order Differential Equation ◽  
Continuous Model ◽  
Second Step ◽  
Entire Body ◽  
System Failure ◽  
Entire System ◽  
System Behavior ◽  
First Order ◽  
Organ Systems ◽  
Subsequent Failure

It appears as if the failure of one organ system precipitates the subsequent failure of other organ systems. The aim of the present analysis is to model such system behavior and understand why medical complications accumulate in individual patients. The human body is first modeled as being comprised of multiple subsystems, with the health of each subsystem dependent on input regarding its own health status and that of all other subsystems. In a second step, the discrete model is generalized into a continuous model that captures system failure, as well as system repair, by a first order differential equation. Failure is approximated by a logistic decline and repair is approximated by a logistic rise in health. A small drop in health of a single subsystem spreads throughout the entire system and affects its overall health. Unless counteracted by measures of therapy or repair, any time-related loss in health of individual subsystems leads to a decline in health of the entire system. The delay in onset of therapy represents the most crucial factor to influence the overall cumulative decline in health. The model suggests that medical management needs to be expeditious to minimize the cumulative time-dependent toll of illness on the entire body.

scholarly journals ICAMs Redistributed by Chemokines to Cellular Uropods as a Mechanism for Recruitment of T Lymphocytes

1997 ◽  
Vol 137 (2) ◽  
pp. 493-508 ◽  
Author(s):  
Miguel Angel del Pozo ◽  
Carlos Cabañas ◽  
María C. Montoya ◽  
Ann Ager ◽  
Paloma Sánchez-Mateos ◽  
...  
Keyword(s):  
T Cells ◽  
T Lymphocytes ◽  
Fold Increase ◽  
Time Lapse ◽  
Cell Recruitment ◽  
T Cell Migration ◽  
Physiological Relevance ◽  
Amplification System

The recruitment of leukocytes from the bloodstream is a key step in the inflammatory reaction, and chemokines are among the main regulators of this process. During lymphocyte–endothelial interaction, chemokines induce the polarization of T lymphocytes, with the formation of a cytoplasmic projection (uropod) and redistribution of several adhesion molecules (ICAM-1,-3, CD43, CD44) to this structure. Although it has been reported that these cytokines regulate the adhesive state of integrins in leukocytes, their precise mechanisms of chemoattraction remain to be elucidated. We have herein studied the functional role of the lymphocyte uropod. Confocal microscopy studies clearly showed that cell uropods project away from the cell bodies of adhered lymphocytes and that polarized T cells contact other T cells through the uropod structure. Time-lapse videomicroscopy studies revealed that uropod-bearing T cells were able, through this cellular projection, to contact, capture, and transport additional bystander T cells. Quantitative analysis revealed that the induction of uropods results in a 5–10-fold increase in cell recruitment. Uropod-mediated cell recruitment seems to have physiological relevance, since it was promoted by both CD45R0+ peripheral blood memory T cells as well as by in vivo activated lymphocytes. Additional studies showed that the cell recruitment mediated by uropods was abrogated with antibodies to ICAM-1, -3, and LFA-1, whereas mAb to CD43, CD44, CD45, and L-selectin did not have a significant effect, thus indicating that the interaction of LFA-1 with ICAM-1 and -3 appears to be responsible for this process. To determine whether the increment in cell recruitment mediated by uropod may affect the transendothelial migration of T cells, we carried out chemotaxis assays through confluent monolayers of endothelial cells specialized in lymphocyte extravasation. An enhancement of T cell migration was observed under conditions of uropod formation, and this increase was prevented by incubation with either blocking anti– ICAM-3 mAbs or drugs that impair uropod formation. These data indicate that the cell interactions mediated by cell uropods represent a cooperative mechanism in lymphocyte recruitment, which may act as an amplification system in the inflammatory response.

Hepatic stimulator substance: physicochemical characteristics and specificity

1982 ◽  
Vol 242 (3) ◽  
pp. G281-G288 ◽  
Author(s):  
D. R. LaBrecque ◽  
N. R. Bachur
Keyword(s):  
Rat Liver ◽  
Nuclear Dna ◽  
Tritiated Thymidine ◽  
Fold Increase ◽  
Physicochemical Characteristics ◽  
Adult Rats ◽  
Hepatic Stimulator Substance ◽  
Adult Rat ◽  
Heat Stable ◽  
Organ Specific

This laboratory has reported previously that a cytoplasmic extract of weanling or regenerating adult rat liver (but not normal rat liver) will produce a 2.5-fold increase in the incorporation of tritiated thymidine ([3H]dThd) into liver DNA of a 34%-hepatectomized test animal. (J. Physiol. London 248: 273-284, 1975). The present study showed that hepatic stimulator substance (HSS) will stimulate DNA synthesis in normal adult rats and CF1 mice as well. The increased incorporation of [3H]dThd into DNA produced in the normal, nonhepatectomized adult rat was comparable with that induced by a 34% hepatectomy. Autoradiographic studies revealed that the [3H]dThd was incorporated into nuclear DNA and that the stimulation occurred almost exclusively in parenchymal cells. HSS was shown to be heat stable (100 degrees C for 15 min) and was precipitated but not inactivated by alcohol. Ultrafiltration and dialysis studies suggested a molecular weight slightly greater than 10,000. HSS proved to be organ specific, stimulating the liver but not the kidney, bone marrow, or spleen. HSS was found to contain no insulin, glucagon, epidermal growth factor, or peptides of the nonsuppressible insulinlike/multiplication-stimulating activity (somatomedin) group.

Asymmetrical retinoic acid synthesis in the dorsoventral axis of the retina

Development ◽  
1992 ◽  
Vol 115 (2) ◽  
pp. 371-382 ◽  
Author(s):  
P. McCaffery ◽  
M.O. Lee ◽  
M.A. Wagner ◽  
N.E. Sladek ◽  
U.C. Drager
Keyword(s):  
Retinoic Acid ◽  
Spatial Arrangement ◽  
Acid Synthesis ◽  
Early Embryo ◽  
Entire Body ◽  
Dorsoventral Axis ◽  
Adult Retina ◽  
Dorsal Pathway ◽  
Ventral Pathway ◽  
Dorsal Retina

An aldehyde dehydrogenase present at high levels in the dorsal retina of the embryonic and adult mouse was identified as the isoform AHD-2 known to oxidize retinaldehyde to retinoic acid. Comparative estimates of retinoic acid levels with a reporter cell line placed the retinas among the richest tissues in the entire body of the early embryo; levels in ventral retina, however, exceeded dorsal levels. Retinoic acid synthesis from retinaldehyde in the dorsal pathway was less effective than the ventral pathway at low substrate levels and more effective at high levels. The dorsal pathway was preferentially inhibited by disulfiram, while ventral synthesis was preferentially inhibited by p-hydroxymercuribenzoate. When protein fractions separated by isoelectric focusing were analyzed for retinoic acid synthesizing capacity by a zymography-bioassay, most of the synthesis in dorsal retina was found to be mediated by AHD-2, and ventral synthesis was mediated by dehydrogenase activities distinct in charge from AHD-2. Postnatally, levels of highest retinoic acid synthesis shifted from ventral to dorsal retina. In the adult retina, the dorsal pathway persisted, but the preferential ventral pathway was no longer detectable. Our observations raise the possibility that retinoic acid plays a role in the determination and maintenance of the dorsoventral axis of the retina, and that the morphogenetically significant asymmetry here lies in the spatial arrangement of synthetic pathways.

A comparison of results obtained between two methods of detecting the existence of circadian rhythmicity in cell division: an autoradiographical and a biochemical approach

1981 ◽  
Vol 47 (1) ◽  
pp. 249-265
Author(s):  
D. Challoner ◽  
J.D. Simnett ◽  
K. Hellmann
Keyword(s):  
Liquid Scintillation ◽  
Tritiated Thymidine ◽  
Circadian Rhythmicity ◽  
Biochemical Assay ◽  
Synthetic Activity ◽  
Data Sets ◽  
Thymidine Labelling Index ◽  
Assay Procedure ◽  
The Hours ◽  
Biochemical Approach

In the course of a study of circadian rhythmicity in the number of cells in the S-phase of the cell cycle in mouse kidney, a comparison was made between 2 methods of estimation of DNA synthetic activity. One of the methods used was an autoradiographical analysis of the tritiated thymidine labelling index; the other was a biochemical assay of the DNA content of the tissues coupled with liquid scintillation counting, to obtain an estimate of the incorporation of tritiated thymidine, expressed as dpm per microgram of DNA. The correlation between individual estimates of DNA-synthetic activity, using the 2 methods was highly significant, as was the correlation between the 2 data sets with respect to time of zeniths. There was a suggestion that the biochemical assay procedure may be the more sensitive indicator of circadian rhythmicity in relatively homogeneous tissues with low proliferative rates. Estimated over a 3-da period, the time of maximal DNA synthetic activity lay between the hours of 22.00 and 02.00. The nadir of the curve was less well defined and occurred between 02.00 and 14.00 hours. The autoradiographical study took 5 weeks to complete exclusive of histological and autoradiographic preparation. The biochemical assay was completed in 4 days.

scholarly journals Regulation of pyruvate carboxylase in 3T3-L1 cells

1995 ◽  
Vol 306 (1) ◽  
pp. 205-210 ◽  
Author(s):  
J Zhang ◽  
W L Xia ◽  
F Ahmad
Keyword(s):  
Enzyme Activity ◽  
Relative Abundance ◽  
Pyruvate Carboxylase ◽  
Protein Concentration ◽  
Specific Activity ◽  
Cdna Probe ◽  
Fold Increase ◽  
Spatial Arrangement ◽  
Cellular Protein ◽  
Prosthetic Group

When 3T3-L1 fibroblasts differentiate to adipocytes, the specific activity of pyruvate carboxylase (PC) increases about 25-fold in parallel with its intracellular protein concentration. The increase in PC protein concentration is accompanied by a 9-10-fold increase in the relative abundance of 4.2 kb PC mRNA measured by Northern-blot analysis using a cDNA probe encoding a segment of the PC gene of 3T3-L1 adipocytes. The effects of cyclic AMP (cAMP) alone and together with insulin on levels of cellular protein, PC activity, PC protein and on the relative abundance of PC mRNA were examined in mature 3T3-L1 adipocytes. Adipocytes exposed to cAMP for 24 h exhibited a 25% decrease in cellular protein and marked decreases in enzyme activity (88%) and PC mRNA abundance (98%) compared with untreated adipocyte controls. After 48 h of exposure to cAMP, PC activity and PC mRNA diminished to levels approaching their detection limits. When exposed to medium containing cAMP plus insulin, adipocyte enzyme activity and PC mRNA declined more slowly during the first 24 h exposure (about 20% decrease) but after 48 h fell to values comparable with those of adipocytes exposed to cAMP alone. Despite these decreases in enzyme activity, the PC protein content of adipocytes treated with cAMP alone or cAMP plus insulin are nearly identical with that of control adipocytes. The inactivation of PC in cAMP-treated adipocytes does not involve loss of the prosthetic group from the holoenzyme. Cross-linking experiments suggest that the spatial arrangement of protomers in inactive PC may differ from that in the active tetrameric enzyme. Data presented suggest that, in addition to inducing inactivation, cAMP may also regulate adipocyte PC by decreasing transcription of the PC gene and/or enhancing the rate of degradation of PC mRNA.

Multipotent Adult Progenitor Cells (MAPC) Are Immunoprivileged and Demonstrate Immunosuppressive Properties on Activated T Cell Population.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 5227-5227
Author(s):  
Magdalena Kovacsovics-Bankowski ◽  
Philip R. Streeter ◽  
Erin Hewett ◽  
Wouter J. Van’t Hof ◽  
Robert J. Deans ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Progenitor Cells ◽  
Mhc Class Ii ◽  
Tissue Repair ◽  
Dependent Manner ◽  
Rat Strains ◽  
Multipotent Adult Progenitor Cells ◽  
Hematopoietic Lineage ◽  
Organ Systems

Abstract Multipotent Adult Progenitor cells (MAPC) are rare progenitor cells present within the bone marrow that have the capacity to differentiate into mesodermal, endodermal and ectodermal lineage cells. The capacity to differentiate into these diverse cell types distinguishes MAPC from Mesenchymal Stem Cells (MSC), and suggests that MAPC may provide biological solutions for tissue repair or regeneration in multiple organ systems (Jiang Y et al. Nature.2002; 418:41–9). We have developed the technology for the large-scale expansion of MAPC with stable phenotype and biological properties. Cell surface marker analysis of MAPC revealed that these cells express low levels of MHC class I, CD44, CD90 and CD49c and are negative for MHC class II, CD45 and CD106 suggesting that MAPC do not express markers associated with the hematopoietic lineage. However, to optimize in vivo utilization, the identification of MAPC immunological properties is necessary. The objectives of the current studies were 1) to determine the immunogenicity of MAPC and 2) to assess the immunomodulatory properties of MAPC. First, MAPC from two different rat strains did not stimulate allogeneic T cells proliferation, while splenocytes of the same rat strains elicited strong proliferative responses in a mixed lymphocytic culture. Second, the immunosuppressive properties of MAPC were investigated using alloactivated T cells. Addition of MAPC at the initiation of a mixed lymphocyte reactions (MLR) suppressed T cell proliferation in a dose dependent manner. The inhibition was detectable at as low as 3,000 MAPC/well. Lymphocyte proliferation in MAPC-containing cultures was inhibited by up to 80% when compared to cultures without MAPC. The ability to inhibit T cell alloresponses was independent of the MHC, allowing the use of “third party” MAPC as inhibitory cells. MAPC also inhibited proliferative responses to the T cell mitogen Concanavalin A (50%), although inhibition required higher MAPC:responder cell ratios. Taken together, these data suggest that MAPC are progenitor cells that do not express markers of the hematopoietic lineage; they are non-immunogenic, suggesting that universal MAPC donors may be used for tissue repair or regeneration; and MAPC exhibit potent immunosuppressive properties, a result which suggests that these calls may be useful in the management and/or prevention of GVHD.

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