scholarly journals Establishment of a new Zinnia experimental system including separation of the distinct cell population with flow cytometry and its culture

2004 ◽  
Vol 21 (2) ◽  
pp. 103-108 ◽  
Author(s):  
Yasuko ITO ◽  
Reiko INO ◽  
Shigeo YOSHIDA ◽  
Hiroo FUKUDA
Keyword(s):  
Flow Cytometry ◽  
Cell Population ◽  
Experimental System ◽  
Distinct Cell

scholarly journals NK cell markers predict the efficacy of IV immunoglobulins in CIDP

2020 ◽  
Vol 7 (6) ◽  
pp. e884
Author(s):  
Anne K. Mausberg ◽  
Maximilian K. Heininger ◽  
Gerd Meyer Zu Horste ◽  
Steffen Cordes ◽  
Michael Fleischer ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Nk Cells ◽  
Cell Population ◽  
Nk Cell ◽  
Chronic Inflammatory Demyelinating Polyneuropathy ◽  
Ivig Treatment ◽  
Clinical Aspects ◽  
Prospective Longitudinal Study ◽  
Cell Markers ◽  
Prospective Longitudinal

ObjectiveTo assess whether IV immunoglobulins (IVIgs) as a first-line treatment for chronic inflammatory demyelinating polyneuropathy (CIDP) have a regulative effect on natural killer (NK) cells that is related to clinical responsiveness to IVIg.MethodsIn a prospective longitudinal study, we collected blood samples of 29 patients with CIDP before and after initiation of IVIg treatment for up to 6 months. We used semiquantitative PCR and flow cytometry in the peripheral blood to analyze the effects of IVIg on the NK cells. The results were correlated with clinical aspects encompassing responsiveness.ResultsWe found a reduction in the expression of several typical NK cell genes 1 day after IVIg administration. Flow cytometry furthermore revealed a reduced cytotoxic CD56dim NK cell population, whereas regulatory CD56bright NK cells remained mostly unaffected or were even increased after IVIg treatment. Surprisingly, the observed effects on NK cells almost exclusively occurred in IVIg-responsive patients with CIDP.ConclusionsThe correlation between the altered NK cell population and treatment efficiency suggests a crucial role for NK cells in the still speculative mode of action of IVIg treatment. Analyzing NK cell subsets after 24 hours of treatment initiation appeared as a predictive marker for IVIg responsiveness. Further studies are warranted investigating the potential of NK cell status as a routine parameter in patients with CIDP before IVIg therapy.Classification of evidenceThis study provides Class I evidence that NK cell markers predict clinical response to IVIg in patients with CIDP.

scholarly journals flowDensity: reproducing manual gating of flow cytometry data by automated density-based cell population identification

2014 ◽  
Vol 31 (4) ◽  
pp. 606-607 ◽  
Author(s):  
Mehrnoush Malek ◽  
Mohammad Jafar Taghiyar ◽  
Lauren Chong ◽  
Greg Finak ◽  
Raphael Gottardo ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Cell Population ◽  
Flow Cytometry Data

FISH Redoux — A Novel Way to Emulate CLL Leukemic Cells From Buffy Coat Samples

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 3606-3606
Author(s):  
Stephanie A. Smoley ◽  
Patricia T. Greipp ◽  
Neil E. Kay ◽  
Tait D. Shanafelt ◽  
Jeanette E. Eckel-Passow ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
B Cells ◽  
B Cell ◽  
Cell Population ◽  
Cell Sorting ◽  
Mayo Clinic ◽  
Buffy Coat ◽  
Fish Analysis ◽  
Cell Type ◽  
The Mean

Abstract Abstract 3606 Background: Cytogenetic abnormalities are important prognostic indicators in CLL. At Mayo Clinic, CLL FISH analyses are derived from buffy coat samples not purified for lymphocytes. Scoring is therefore performed on consecutive qualifying nuclei regardless of cell size, shape or morphology. This scoring may not reflect the percent of abnormal nuclei of the affected cell type, but rather the entire population of cells present in the sample. We sought to determine whether the percent abnormal nuclei in only the affected cell type (e.g. lymphocytes) of patients with CLL differed from that of the general cell population. Scoring only B-lymphocytes could increase the sensitivity of the test in patients with low B-cell counts, either early in their disease or after treatment. Cell sorting techniques could be used to reach this goal but can be expensive, labor intensive and add to completion time. We propose a “Poor Man's Cell Sorting” technique based on cell morphology when stained with 4',6-diamidino-2-phenylindole (DAPI). In CLL samples, both round and so called “lobed” cells are seen by DAPI staining but we hypothesize that the CLL B-cells typically present as perfectly round in shape (Fig. 1). Thus our hypothesis: if only the round cells are scored for a genetic defect, would this more accurately represent the malignant leukemic B-cell population and allow for enhanced disease status by FISH? Methods: After IRB approval, we identified 87 CLL patients (75% male; 25% female, mean age 62.4 y, range 43–89 y) in the Mayo Clinic CLL Database, who were seen at Mayo Clinic between March, 2002 - July, 2010. We selected patients known to have low level FISH abnormalities and who therefore should have a significant population of both lymphocytes and neutrophils. Selection criteria included <20×106 B-cells per microliter (by flow cytometry) of peripheral blood and ≤40% of interphase nuclei expressing a specific FISH abnormality. Although most of the 87 patients exhibited more than one FISH abnormality, we focused on only one FISH defect per patient for this study. The original specimen (slide or fixed cell pellet) was rescored for % abnormal nuclei among 100 consecutive round and 100 consecutive lobed (or multilobular) nuclei, using DAPI to identify nuclear architecture. These scores were compared to each other and to the original clinical FISH analysis (scored for 200 consecutive nuclei and not selected for nuclear morphology). Results: Among 87 cases, FISH signals were scored for 6q-(1), 11q-(9), +12(15), 13q-(58), 17p-(2) and 2 IGH rearrangements. In 86/87 cases, the abnormal lobed nuclei did not have FISH defects. One patient exhibited 35% +12 by clinical assay, 52% +12 in the round nuclei, and 11% by lobed nuclei. For all cases, the mean percentage of abnormal nuclei was greater in the round cells (46%) vs original scoring (23.6%). In 79/87 patients (91%), the % of abnormal nuclei was greater in the round cells vs original FISH (mean increase 24.3%; range 1.5–57%). One patient's score was the same in round cells vs original, and 7 patients exhibited fewer abnormal nuclei in the round cells vs original. For these 7 cases, the mean % abnormal nuclei was 5.6% for round nuclei vs 8.4% for original score (score differences ranged from 1 – 5.5%). Overall, by univariate regression analysis, round cells (p=0.0043) have a better correlation with % B-cells, ascertained by flow cytometry, than either the current clinical approach (p=0.0462) or the lobed-cell approach (p=0.4058). Discussion: In virtually all cases (99%), the abnormal FISH patterns were confined to the round nuclei, and the lobed nuclei were virtually always normal by FISH. For patients with <20×106 lymphocytes, selecting for round nuclei uniformly resulted in identification of a higher percentage of abnormal cells. Further studies, including comparison of our round nucleus approach to CLL FISH analysis to actual sorted B-lymphocyte cell selection and the association of this leukemic restricted estimation of abnormal FISH levels to clinical outcome are necessary. Given our findings, we believe that estimating FISH defects restricted to the leukemic B-cell population will become an important adjunct to cytogenetic analysis for patients with low lymphocyte counts, including those in clinical remission and those with minimal residual disease. Disclosures: No relevant conflicts of interest to declare.

Usefulness of Unicel DxH 800 Cell Population Data in the Detection of Plasmacell Leukemia: 2 Cases Report

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 4915-4915
Author(s):  
Donatella Raspadori ◽  
Santina Sirianni ◽  
Alessandro Gozzetti ◽  
Francesco Lauria ◽  
Claudio Fogli ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Flow Cytometry ◽  
Cell Population ◽  
Blood Smear ◽  
Normal Values ◽  
Population Data ◽  
Morphological Features ◽  
Short Report ◽  
Lymphocyte Population ◽  
Literature Report

Abstract Abstract 4915 Introduction and methods. Lymphoproliferative disorders (LD) are characterized and described by lymphocyte population with heterogeneous morphological features both in optical microscopy revision and in flow cytometry. Several literature report the clinical usefulness of Cell Population Data (CPD) provided by Beckman Coulter hematology analyzers. Abnormal values of CPD correlate with morphological abnormalities of leukocytes. In this work we present a case report of a plasmacell leukemia analyzed with UniCel DxH800 device. DxH800 performs leukocytes differential with the Flow Cytometric Digital Morphology (FCDM) technology, based on the measurements of Volume (V), Conductivity (C) and 5-angle Scatter light laser (MALS, UMALS, LMALS, LALS, AL2) on cells in their native state. Mean and standard deviation of FCDM measurements are collected in 56 CPD. Normal CPD values were computed from a 42 normal samples. Results. A 47-years old woman, referring continuous asthenia, was addressed to our lab with clinical suspect of LD with leukocytosis (WBC=17190/μl, LY#=3800). DxH800 analysis confirmed WBC count adding some important comments. WBC histogram showed a big peak in lymphocyte population. Differential values reported neutrophilia and lymphocytosis while scatterplot showed a lymphocyte cluster very close to the neutrophil one. CPD suggested a heterogeneous neutrophil population with low volume and low scatters (MALS, UMALS, LMALS, LALS, AL2 in arbitrary units) respectively of 106, 90, 112, 62, 75 vs normal values of 144, 137, 143, 158, 159. Examination of blood smear showed a lot of lymphocyte with nuclear immaturity and plasmoblast features. Immunophenotype revealed that 63% of the WBC were CD138+/CD38+, CD56+ CD200-, CD27- CD20-. Bone marrow biopsy confirmed the plasmacell leukemia diagnosis. A 65-years old man was admitted to our department for a light lymphocytosis associated with a IgGk monoclonal component. Immunophenotipic analysis showed a NK proliferation (CD3 50%, CD4 38%, CD8 34%, CD2 92%, CD7 92%, CD16 45%, CD56 48%, CD57 54%). DxH800 analysis reported LY#=3.6/μl and MO#=1,6/μl. LY CPD indicate cells with light signals of degranulation (MALS=56, UMALS=60, LMALS=63 vs normal values of 66, 60 and 63 ) together with abnormal monocyte CPD such as MV=157, MC=136, MALS=79, UMALS=80, LALS=75 vs normal values of 164, 129, 85, 80 and 75 respectively. All this data induced us to look for a mononuclear population different both from lymphocytes and monocytes in the peripheral blood smear. Bone marrow microscopy analysis showed morphologically abnormal cells that were classified as plasmacells after immunophenotyping (CD138+/CD38+, CD56+, CD45-, CD117+, CD20-, CD27-, CD200+. Further immunophenotypic analysis showed in PB 14% of plasmacells CD138+/CD38+/CD45-. Conclusion. We presented 2 cases report of a plasmacell leukemia whose diagnosis were supported by the useful information of the CPD provided by DxH 800. CPD abnormal values for lymphocytes and monocytes were known to correlate with morphological abnormalites of the cells. For this reason we were triggered to deeply investigate the blood smear of the two patient and we performed the immunophenotyping. This short report confirm the usefulness of CPD provided by UniCel DxH800 as the first check point for the diagnostic route. Moreover we confirm that morphological features in the PB smear discovered during the diagnosis, supported by flow-cytometry data, were properly correlated with CPD values. Disclosures: Fogli: Instrumentation Laboratory: Employment. Di Gaetano:Instrumentation Laboratory: Employment.

Circulating Megakaryocyte-Derived Cells Detected by Flow Cytometry As Marker of Aggressive Neoplasms of Megakaryocytic Lineage in Acute Megakaryoblastic Leukemia and Allied Malignancies Presenting As Primary Myelofibrosis

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 1461-1461
Author(s):  
Serena Marotta ◽  
Giovanna Giagnuolo ◽  
Giulia Scalia ◽  
Maddalena Raia ◽  
Santina Basile ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Flow Cytometry ◽  
Differential Diagnosis ◽  
Cell Population ◽  
Peripheral Blood ◽  
Primary Myelofibrosis ◽  
Giant Platelets ◽  
Megakaryoblastic Leukemia ◽  
History Of ◽  
Blast Cells

Abstract Abstract 1461 The differential diagnosis of myelofibrotic disorders encompasses chronic primary myelofibrosis (PMF), myelodysplastic syndromes with fibrosis (MDS-F), acute panmyelosis with myelofibrosis (APMF) and acute megakaryoblastic leukemia (AMKL). Most of these conditions are recognized as distinct entities by the WHO 2008 revised classification of myeloid neoplasms; however, the WHO admits that often a definitive diagnosis is problematic, mostly because of specimens with insufficient cellularity (e.g., “dry tap”). Nevertheless, the correct identification of the most aggressive fibrotic disorders (APMF and AMKL) remains crucial, given their poor prognosis and subsequent need of intensive treatment (including transplantation). Even the most recent molecular studies did not result in any contribution in the differential diagnosis. Here we report our experience on a cohort of about 300 patients who were admitted in our bone marrow failure unit because of cytopenia in the last 7 years. All these patients were evaluated by standard peripheral blood and bone marrow cytology, karyotype analysis and bone marrow thephine biopsy, aiming to a definitive hematological diagnosis. Flow cytometry analysis was performed at initial presentation and then serially during the follow up on both peripheral blood and bone marrow aspirate. All patients were classified according to the WHO 2008 revised classification of myeloid neoplasms, and received the best standard treatment based on the specific disease, age and comorbidities. This report focuses on 8 patients who shared a unique flow cytometry finding of an aberrant megakaryocyte-derived cell population, which seems associated with a distinct disease evolution. Two of these patients received the diagnosis of AMKL according to bone marrow aspirate and trephine biopsy; the karyotype was complex in one case (monosomal karyotype, including a 5q-), whereas no Jak-2 mutation or any other genetic lesions could be demonstrated. Their blast cells were CD34+, CD38+, CD45+, CD117+, CD33+, CD13+; in addition, in the peripheral blood, we detected the presence of an aberrant cell population which was CD45-, CD42b+ (CD34+ in one case and CD34- in the other one). In the blood smear, we observed megakaryocyte fragments which likely correspond to this aberrant cell population, as identified by flow cytometry. Other three patients presented with a severe pancytopenia: all of them had a dry tap, and their trephine biopsies documented a massive fibrosis. They had no previous hematological disorder (one suffered from Behcet syndrome), normal karyotype and absence of any typical genetic lesion (i.e., wild-type Jak-2). All of them did not show splenomegaly, increased LDH or leukoerythroblastosis; their peripheral blood smear showed abnormal giant platelets, often resembling megakaryocyte fragments. Flow cytometry documented in the peripheral blood the presence of a distinct population of CD45-, CD42b+, CD61+ cells, which was also CD34+ in one case. These 3 patients were initially classified as PMF, even if APMF could not be ruled out; however, within 6 months they all progressed to AMKL. At this stage, typical CD34+, CD45+ blast cells were accompanied by a progressive increase of CD45+, CD42b+, CD61+ cells. This aberrant megakaryocyte-derived cell population (which could not be demonstrated in patients with thrombocytopenia) was also identified in 3 additional patients, who have a previous history of hematologic disorders: two had a history of pure red cell aplasia (successfully treated by immunosuppressive therapy), and one a 5q- melodysplastic syndrome (responding to lenalidomide, even with transient cytogenetic remission). In all of them we observed the appearance of CD45-, CD42b+ cells in the peripheral blood, which appeared as giant platelets/megakaryocyte fragments in the blood film; this finding within a few weeks was followed by progression to AMKL (5q- was detected in 2 of 3 cases). In conclusion, we demonstrate that aberrant circulating megakaryocyte-derived cells detected by flow cytometry may be useful in the differential diagnosis of myelofibrotic disorders. These giant platelets or megakaryocyte fragments, regardless the initial diagnosis, were associated with early evolution into AMKL, likely representing a surrogate marker for aggressive neoplasms of the megakaryocytic lineage. Disclosures: Risitano: Alexion: Membership on an entity's Board of Directors or advisory committees, Research Funding.

Pluripotent Fibrosis Initiating Mesenchymal Stromal Cell Linked To Cytopenias In LGL Leukemia Through Genetic Reprogramming

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 1218-1218
Author(s):  
Pearlie K. Epling-Burnette ◽  
Adam W. Mailloux ◽  
Ling Zhang ◽  
Lynn C. Moscinski ◽  
Sheng Wei ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Flow Cytometry ◽  
Microarray Analysis ◽  
Cell Population ◽  
Collagen Type ◽  
Type I ◽  
Bone Marrow Fibrosis ◽  
Control Mscs ◽  
Marrow Fibrosis ◽  
Lgl Leukemia

Abstract Background Large Granular Lymphocyte (LGL) leukemia is associated with chronic lymphoproliferation in association with unexplained cytopenias. Discovery of somatic mutations in STAT3 provides new insights into the molecular basis of LGL leukemia, but the precise mechanism leading to cytopenias remains unresolved. To gain insight into this mechanism, bone marrow fibrosis (Fig. 1A) was found to occur in 88% of cases and is significantly associated with splenomegaly, the presence of cytopenias, and co- existence of autoimmune diseases. In this study, we are reporting the identification of the fibrosis initiating cell population. Methods Primary mesenchymal stromal cultures (MSCs) from LGL leukemia BM were isolated and grown under reduced oxygen conditions using undifferentiated and differentiation-specific culture conditions (Fig. 1B). These cultured cells were confirmed to deposit greater amounts of fibrillar Type I, III and V collagen matrix consistent with the heavy reticulin and trichrome positive stains observed in bone marrow biopsies (Fig. 1C). This collagen-producing cell population failed to support normal hematopoietic progenitor proliferation and colony formation in co-culture assays. Microarray analysis of the collagen-producing mesenchymal cell population was conducted and pathway analysis was performed using the GeneGo analysis platform from MetaCore™. Each list of genes was individually grouped and evaluated for membership on the set of GeneGo® pathway maps under the functional ontology enrichment tool. Calculation of p-values using hypergeometric distribution was used to determine pathway statistical significance. Flow cytometry was conducted to further evaluate the mesenchymal lineage. Results Supervised hierarchical clustering was performed to determine the overall similarity of LGL MSCs to publicly available, platform-compatible, microarrays from cells of mesenchymal lineage. Clustering showed that both patient and control MSCs display expression patterns distinct from committed mesenchymal lineages including osteoblasts, chondrocytes, and adipocytes. Mesenchymal-derived fibroblast differentiation can be distinguished by down-regulated CD29, CD44, CD105, CD106, CD117, bone morphogenetic protein receptor, and Sca-1 expression, and by up-regulated collagen type I, collagen type III, tenacin C, fibronectin, matrix metalloproteinase 1, fibroblast-specific protein 1, and vimentin. By microarray analysis and flow cytometry, we find no evidence that the cells are differentiated cells aside from collagen over expression. In order to define their pluripotent potential, sub-confluent cultures were grown in three types of differentiating media. Primary MSCs from both LGL leukemia patients and healthy controls were similar in their capacity to undergo trilineage differentiation into osteoblasts (stained with Alizarin Red S), adipocytes (Oil red O), and chondrocytes (Alican blue) (Fig. 1D). Next, pathway analyses revealed significant re-programming of the pluripotent MSCs. ECM production pathways were increased while proliferation pathways were down-regulated. Proliferation of MSCs is governed by production of autocrine growth factors. Both leukemia inhibitor factor (LIF) and basic fibroblast growth factor (FGFb) were significantly reduced compared to control MSCs (p<0.001) and the proliferative capacity of the LGL MSCs was severely diminished. Exogenous FGFb, but not LIF, restored LGLL MSC proliferation comparable to normal MSCs (Fig. 1E), normalized their spindle-shaped morphology, and maintained MSC plasticity. Interestingly, treatment with exogenous FGFb normalized collagen deposition (Fig. 1F) and restored hematopoietic supporting function. Conclusion STAT-activated LGL leukemia cells, like myeloproliferative neoplasms, share a propensity for the development of bone marrow fibrosis. These results indicate that MSCs from LGL leukemia are pluripotent, but are re-programmed to deposit excessive amounts of collagen. Restoration of FGFb maintains the pluripotency of these MSCs while reversing the fibrosis phenotype. Our data suggests that FGFb-cultured MSCs may be used to reverse cytopenias in LGL leukemia. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Sodium azide enhancement of interleukin-2 production

Blood ◽  
1983 ◽  
Vol 61 (4) ◽  
pp. 815-818 ◽  
Author(s):  
SP Feldman ◽  
R Mertelsmann ◽  
S Venuta ◽  
M Andreeff ◽  
K Welte ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Flow Cytometry ◽  
Cell Population ◽  
Sodium Azide ◽  
Human Lymphocytes ◽  
Interleukin 2 ◽  
Final Concentration ◽  
Cell Cycle Analysis ◽  
Normal Human ◽  
Responsive Cell

Abstract The production of large quantities of Interleukin-2 (IL-2) from normal human lymphocytes has been limited by the short production and release period, as well as its absorption by the responsive cell population. We report the utilization of sodium azide (NaN3, 0.01% final concentration) to allow continued production of IL-2 as long as 72–96 hr and thereby increase the yield significantly. Cell cycle analysis performed by flow cytometry indicates that NaN3 blocks cells at the G0- G1 transition and the G1-S transition, depending on the time of addition of NaN3 to the cultures.

19 ROLE OF IL-33 IN PURINE METABOLISM AND ILC2 ACTIVATION DURING COLITIS-ASSOCIATED CANCER

2020 ◽  
Vol 26 (Supplement_1) ◽  
pp. S34-S34
Author(s):  
Carlo De Salvo ◽  
Kristine-Ann Buela ◽  
Hannah Havran ◽  
Theresa Pizarro
Keyword(s):  
Flow Cytometry ◽  
Cell Population ◽  
Intestinal Inflammation ◽  
Inflammatory Diseases ◽  
Purine Metabolism ◽  
Lymphoid Cells ◽  
Mesenteric Lymph Nodes ◽  
Increased Risk ◽  
A Cell ◽  
Deficient Mice

Abstract UC patients have an increased risk of developing colorectal cancer, however, the immune cells and cytokines that mediate the transition from intestinal inflammation to cancer are poorly understood. Mucosal IL-33 is increased in UC patients, in addition, IL-33 and its receptor, ST2, are expressed in polyps in AOM/DSS models of colitis-associated cancer (CAC). Therefore, several studies have implicated IL-33, which is also an important activator of Innate Lymphoid Cells type 2 (ILC2s), in the formation of tumors. Moreover, it has been shown that ecto-5’-nucleotidase (CD73), critical ectoenzyme in purine metabolism which hydrolyzes extracellular AMP to adenosine, is upregulated in cancerous tissues, and an incompetent purine metabolic pathway has been associated with inflammation and inappropriate resolution in numerous inflammatory diseases, including IBD. In order to induce colitis-associated polyposis, we performed AOM/DSS protocol on 10-wk-old C57BL/6, IL-33KO and CD73KO mice as follow: the carcinogen Azoxymethane (AOM) was injected intraperitoneally (i.p.) on day 0. After two weeks, 3% dextran sodium sulfate (DSS) was administered in drinking water for a week, followed by two weeks of recovery with normal water. DSS administration and recovery was repeated one more time before euthanizing mice for tissue collection and analysis. Flow cytometry analysis showed that all ILC2s, and more specifically CD73 expressing ILC2s were significantly decreased in mesenteric lymph nodes (MLNs) of AOM/DSS treated mice lacking IL-33, compared to WT, on the other hand, CD73 deficient mice displayed a strongly reduced number of polyps compared to WT and flow cytometry revealed an ST2 expressing ILC2 cell population that was markedly reduced in CD73 deficient mice in comparison to WT. We next injected AOM/DSS treated C57BL/6 mice with either inhibitor of CD73 or sodium polyoxotungstate 1 (POM-1) CD39 inhibitor, therefore targeting the key enzymes in the purine metabolism pathway. We injected the mice i.p. with 10 mg per Kg body weight per day of either compounds or PBS, every day during the 2 weeks of DSS, to mimic a possible therapeutic treatment to prevent purine metabolism-depentent CAC. Histologic investigation of colon tissues isolated from mice treated with CD39 or CD73 inhibitors showed a significant decrease in inflammation and polyp numbers compared to vehicle-treated mice. The data so far collected suggest that a cell population of CD73 expressing ILC2s is involved in polyp formation in AOM/DSS-treated mice and that ILC2s expansion and activity depends on IL-33/ST2 and purine metabolism synergy. Therefore the possibility exists that blockade of IL-33/ST2 axis and purine metabolism might be effective in reducing ILC2s expansion and thus be beneficial in preventing or reducing early events promoting CAC.

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