Adenosine Deaminase Activity In Lymphocytes Research Articles

Curcumin pre-treatment modulate the activities of adenine nucleotide and nucleoside degradation enzymes in lymphocyte of rats infected with Trypanosoma evansi

This study aimed to evaluate nucleoside triphosphate diphosphohydrolase (NTPDase) and adenosine deaminase (ADA) activities in lymphocytes from rats supplemented or not with curcumin 30 days prior to experimental infection with Trypanosoma evansi. Thirty-two adult male Wistar rats were divided in four groups. The pre-infection group 20 (PreI20) received orally 20 mg/kg of curcumin and pre-infection group 60 (PreI60) received orally 60 mg/kg of curcumin for 30 days prior inoculation with T. evansi. The infected e non-infected control groups received only oral vehicle for 30 days. Trypanosoma evansi infected groups were inoculated intraperitoneally with 0.2 ml of blood with 1 × 106 parasites. After inoculation the treatment of the groups continued until the day of euthanasia (15 days). The results showed that curcumin pre-treatment, with both doses, reduced (P < .05) NTPDase and increased (P < .05) ADA activity in lymphocytes of treated groups when compared to untreated and infected animals (control). The results of this study support the evidence that the regulation of ATP and adenosine levels by NTPDase and ADA activities appear to be important to modulate the immune response in T. evansi infection, once the treatment with curcumin maintained the NTPDase activity reduced and enhanced ADA activity in lymphocytes. It is possible to conclude that the use of curcumin prior to infection with T. evansi induces immunomodulatory effects, favoring the response against the parasite.

Effect of gallic acid on purinergic signaling in lymphocytes, platelets, and serum of diabetic rats

Diabetes Mellitus (DM) is associated with an increased susceptibility to various infections, which might be attributed to changes in immune response owing to chronic hyperglycemia. Nucleoside triphosphate diphosphohydrolase (NTPDase), 5′-nucleotidase, and adenosine deaminase (ADA) are important enzymes involved in the generation of anti-aggregant and anti-inflammatory microenvironments. The aim of this study was to evaluate the effect of gallic acid (GA) on the hematological parameters and ectonucleotidase activities in platelets, lymphocytes, and serum of diabetic rats. Experimental rats were categorized into 4 groups: (i) control -saline, (ii) control - GA, (iii) diabetic -saline, and (iv) diabetic - GA. One week after induction of DM using streptozotocin (65 mg/kg), GA (30 mg/kg) or saline was orally administered to the rats for 21 days. Our results demonstrated that the concentration of mean corpuscular hemoglobin was decreased, whereas that of red cell distribution was increased in the diabetic group, however, GA could revert these alterations. Moreover, in diabetic rats, GA reverted the increase in ATP and ADP hydrolysis and ADA activity in lymphocytes, and it prevented the increase in NTPDase and ADA activities in platelets. A decrease in ATP hydrolysis and an increase in ADP and AMP hydrolysis were observed in the serum of diabetic rats; however, GA treatment could solely revert changes in ATP hydrolysis. Our study suggests that GA exhibits beneficial effects on immuno- and thrombo-regulatory responses in DM and that these effects may be related to the modulation of purinergic signaling.

Swimming training prevents alterations in ecto-NTPDase and adenosine deaminase activities in lymphocytes from Nω-nitro-L-arginine methyl ester hydrochloride induced hypertension rats.

Hypertension is accompanied by inflammatory process and purinergic system has been recognized as having an important role in modulating immune functions. Physical training is being considered one of the major lifestyle changes that contributes to the cardiovascular health as well as has an important role in regulating purinergic system. Thus, the aim of this study was to investigate the effect of chronic swimming training on lymphocytic purinergic system enzymes activities related to inflammatory process, as well as in lipid profile and classic inflammatory markers in rats that developed hypertension in response to the oral administration of N-nitro-L-arginine methyl ester hydrochloride (L-NAME). After 6 weeks of training, lymphocytes and serum were separated to be analysed. L-NAME-treated group displayed an increase in SBP as well as in ecto-NTPDase and adenosine deaminase (ADA) activities (P < 0.05). Six weeks of swimming training were able to prevent these alterations and keep the blood pressure and enzymes activities in the same levels of control group. Exercise per se was associated with a decrease in the expression of ecto-NTPDase1 in lymphocytes (-23.4%). Exercise was also efficient in preventing the rise in classic inflammatory markers observed in L-NAME group. These findings highlight the link between purinergic signalling and inflammatory process and suggest a novel mechanism in which moderate aerobic exercise possesses the potential to attenuate inflammation caused by hypertension.

Adenosine deaminase activity in serum, erythrocytes and lymphocytes of rats infected with Leptospira icterohaemorrhagiae

Leptospirosis is a systemic disease of humans and domestic animals, mainly dogs, cattle and swine. The course of human leptospirosis varies from mild to severe fatal forms and the most severe form of human leptospirosis is principally caused by Leptospira interrogans serovar icterohaemorrhagiae (L. icterohaemorrhagiae). The enzyme adenosine deaminase (ADA) plays an important role in the production and differentiation of blood cells. The aim of this study was to evaluate the activity of ADA in serum, erythrocytes and lymphocytes of rats infected with L. icterohaemorrhagiae, as compared with non-infected rats. Twenty-four adult rats, divided into two uniform groups (A and B) were used for the enzymatic assays. The animals in Group B were inoculated intraperitoneally with 2×108leptospires/rat, and the rodents in Group A (control) were not-inoculated. Blood collection was performed on days 5 and 15 post-infection (PI) and the blood used to assess the ADA activity. The infection by L.icterohaemorrhagiae altered erythrocyte count, hemoglobin concentration and hematocrit, causing a decrease in all these parameters on day 15 PI. Lymphocytes decreased significantly on day 15 PI, and ADA activity in serum was inhibited in infected rats on days 5 and 15 PI and its activity in erythrocytes were increased on day 5 PI. On day 5 PI, we found an increase in ADA activity in erythrocytes of infected rats. No correlation was observed between hematocrit and erythrocyte ADA activity on days 5 and 15 PI. The ADA activity was inhibited in rats infected on day 15 PI. A positive correlation (r2=60) was also observed between the number of lymphocytes and ADA activity in lymphocytes on day 15 PI (P<0.05). In conclusion, our results showed that the ADA activity is altered in serum, lymphocytes and erythrocytes in experimental infection by L.icterohaemorrhagiae in rats, concomitantly with hematological parameters.

Activity of the enzyme adenosine deaminase in serum, erythrocytes and lymphocytes of rats infected withTrypanosoma evansi

In Trypanosoma evansi infections changes in the haemogram are commonly observed, and the enzyme adenosine deaminase (ADA) plays an important role in the production and differentiation of blood cells. Thus, the aim of this study was to evaluate the activity of ADA in serum, erythrocytes and lymphocytes of rats infected with T. evansi compared to non-infected rats. Thirty adult rats were used, divided into 3 uniform groups. The animals in groups A and B were infected intraperitoneally with 2 x 10⁶ trypomastigotes/rat. Rodents from group C (control group), were not-infected. Blood collection was performed on days 4 and 20 post-infection (p.i.) in order to obtain acute and chronic infection stages of disease. The blood was used to assess the activity of ADA. In the blood, reduced haematocrit and increased lymphocytes were correlated with ADA activity in erythrocytes and lymphocytes. We observed reduction of ADA activity in serum and erythrocytes in rats infected with T. evansi compared to non-infected rats (P < 0.05). ADA activity in lymphocytes was decreased after 4 days, when the parasitaemia was high and increased after 20 days, when the number of circulating parasites was low. In conclusion, our results showed that the ADA activity was altered in serum, lymphocytes and erythrocytes of rats, concomitantly with haematological parameters, in experimental infection by T. evansi.

Long-Term Safety and Efficacy of Stem Cell Gene Therapy for ADA-SCID.

Severe combined immunodeficiency (SCID) due to adenosine deaminase (ADA) deficiency is a fatal congenital disorder of the immune system associated with systemic toxicity due to accumulation of purine metabolites. We previously showed that retroviral-mediated ADA gene transfer into autologous hematopoietic stem/progenitor cells (HSC) allowed restoration of immune and metabolic functions. We have now enrolled eight ADA-SCID children (age: 7–67 months) in our phase I/II gene therapy trial in which HSC are combined with low intensity conditioning with busulfan (total dose 4 mg/Kg i.v.). Previous treatment included haploidentical bone marrow transplant (n=3) or long-term (>1 year) enzyme replacement therapy (PEG-ADA) (n=4) associated with insufficient immune reconstitution or severe autoimmunity. In the latter case, PEG-ADA was discontinued to favour the growth advantage for gene corrected cells. The patients received a median dose of 8.8x106/Kg bone marrow CD34+ cells (range 0.9–10.8), containing on average 26.2±9.6% transduced CFU-C. Five patients experienced ANC <0.5x109/L, which was extended beyond day +30 in two patients. With a median follow up of 3.1 years (range 0.4–5.9), no adverse events related to gene transfer have been observed. Long-term engraftment of transduced HSC was demonstrated by stable multilineage marking, persisting more than 5 years from gene therapy. The average proportion of transduced cells in the peripheral blood at one year post-gene therapy (n=6) was 5% for granulocytes, 95% for T cells, 56% for B cells and 62% for NK cells. Comparison of the insertion sites retrieved ex vivo from patients with those identified in pre-transplant transduced CD34+ cells showed no skewing in the profile of genome distributions or in the gene families hit by the vector, and no clonal expansion. In the six children with a follow-up >1 year after gene therapy, we observed a progressive increase in lymphocyte counts which was sustained over time (median at 1.5 years 1.6x109/L), polyclonal thymopoiesis and normalization of T-cell functions in vitro. Serum Ig levels improved and evidence of antigen-specific antibodies was obtained, leading to IVIG discontinuation in five patients. All the children are currently healthy and thriving, and none of them showed severe infections. Sustained ADA activity in lymphocytes and RBC resulted in a dramatic reduction of RBC purine toxic metabolites (dAXP<30 nmoles/ml in 5 patients) and amelioration of children's growth and development. In summary, these data confirm that gene therapy is safe and efficacious in correcting both the immune and metabolic defect in ADA-SCID, with proven clinical benefit.

Lymphocyte adenosine deaminase activity in children with idiopathic nephrotic syndrome

Adenosine deaminase (ADA) activity, as a marker of cell-mediated immunity, was evaluated in the serum (S-ADA) and lymphocytes (L-ADA) of 47 children with idiopathic nephrotic syndrome, and 23 healthy controls. The mean S-ADA and L-ADA levels were significantly raised in active nephrotic syndrome (ANS) and in its sub-groups in comparison with controls. The ADA activity was significantly more elevated in relapsers than for the first attack of nephrotic patients, and the frequent relapsers had the highest enzymatic levels both in serum as well as lymphocytes. A significant positive correlation was found between serum and lymphocyte ADA levels (r =0.736, p <0.01). In remission, the S-ADA showed a significant fall in comparison with their corresponding ANS value (p <0.001) and reached the level of controls. The mean L-ADA also showed reduction but the difference was statistically insignificant and the value was significantly raised, when compared with controls. The enzyme activity in serum and lymphocytes normalized in the long-term remission group. Thus, ADA activity was abnormal in ANS cases, and L-ADA demonstrated change both in active as well as remission stage of the disease.

Adenosine deaminase activities in sera, lymphocytes and granulocytes in patients with cutaneous leishmaniasis.

Adenosine deaminase (ADA) activities in sera, lymphocytes and granulocytes in patients with cutaneous leishmaniasis were investigated and compared with control groups. Fifty patients and 50 healthy individuals were studied. The clinical diagnosis was parasitologically confirmed by culture and Giemsa stain. ADA activities were measured by colorimetric method. Serum ADA activities 37.80 +/- 11.90, 18.28 +/- 6.08 IU/L (p < 0.0001), lymphocyte specific ADA activities 14.90 +/- 7.42, 8.38 +/- 7.42 U/mg protein (p = 0.04), granulocyte specific ADA activities 1.15 +/- 0.73, 1.09 +/- 0.67 U/mg protein (p > 0.05) were found in patients and control groups, respectively. ADA activity increases in some infectious diseases were cell mediated immune mechanisms are dominant. In cutaneous leishmaniasis, lymphokine-mediated macrophage activity is the main effector mechanism. Increase in serum and lymphocyte ADA activities in patients with cutaneous leishmaniasis may be dependent on and reflects the increase in phagocytic activity of macrophages and maturation of T-lymphocytes.

Treatment of severe combined immunodeficiency disease (SCID) due to adenosine deaminase deficiency with CD34+ selected autologous peripheral blood cells transduced with a human ADA gene. Amendment to clinical research project, Project 90-C-195, January 10, 1992.

Significant increases in lymphocyte adenosine deaminase activity, T cell numbers and immune function have been achieved in the two children with SCID thus far treated with autologous T cells genetically-corrected by retroviral-mediated insertion of a normal ADA gene. Although the data obtained to date demonstrate that the use of ADA gene corrected peripheral T cells appears to be an effective treatment for ADA(-)SCID, it is theoretically preferable to try to develop a treatment for these children that will result in stem cell gene correction. The genetic correction of T cell progenitors with long-term immune reconstituting ability would be more desirable because repeated infusions of genetically altered cells should not be necessary and the generation of a more complete repertoire of T cell specificities might also be possible. Furthermore, the present treatment protocol involves indefinite continuation of enzyme replacement treatment with PEG-ADA. The demonstration of ADA gene expression in the progeny of transduced stem cells may simplify the decision concerning cessation of this very costly enzyme treatment (approximately $250,000/yr./patient). Recent evidence suggests that a small fraction of bone marrow or peripheral blood mononuclear cells bearing the CD34 antigen contains hematopoietic stem cells with both lymphoid and myeloid reconstituting ability. We propose in this amendment to supplement the infusion of human ADA gene-transduced autologous T cells in children with ADA(-)SCID with autologous peripheral blood CD34+ cells transduced with a second, readily distinguishable ADA vector.(ABSTRACT TRUNCATED AT 250 WORDS)

Lymphocyte adenosine deaminase activity (L-ADA) in leprosy, during and after treatment of reactions.

Twenty-five patients with type 1 (lepra) and type 2 (E.N.L.) leprosy reactions were studied for lymphocyte adenosine deaminase activity (L-ADA), during and after treatment of the reactions, using a standard technique, in order to establish its pattern and if possible, its value in assessing the course of reactions. The results were compared with those from 30 control subjects, comprising 10 normal healthy adults, 10 patients with borderline tuberculoid (BT) leprosy, four patients with borderline lepromatous (BL) leprosy and six patients with lepromatous (LL) leprosy. The level of L-ADA in the leprosy controls was higher than that of normal healthy subjects. The L-ADA values in patients with different types of reactions were about 10-fold higher than those obtained from leprosy controls, emphasizing a possible role in assessing reactions in leprosy. However, there was no significant variation in L-ADA levels, either between the various leprosy controls or reaction groups, before and after treatment.

Adenosine Deaminase and Purine Phosphorylase Activities in Lymphocytes and Red Blood Cells of Patients with Carcinoma of the Larynx

Lymphocytes from patients with cancer of the larynx have been characterized by the activity of two enzymes involved in purine metabolism--adenosine deaminase and purine nucleoside phosphorylase. It has been shown that purine nucleoside phosphorylase activity was 1.5-fold higher in lymphocytes of patients in comparison with a group of healthy individuals. Adenosine deaminase activity in lymphocytes was elevated three to four-fold. The authors suggest that especially the estimation of adenosine deaminase activity in lymphocytes would be a useful laboratory test in the study of immune responsiveness of patients with cancer of the larynx.

IMMUNOPURINOGENIC ENZYMATIC ACTIVITY IN THE ACQUIRED IMMUNODEFICIENCY SYNDROME: 132

Deficiencies of the purine catabolic enzymes adenosine deaminase (ADA) and purine nucleoside phosphorylase (PNP) have been described in association with severe combined immunodeficiency disease and selective T-cell immunodeficiency disease respectively. Recently a selective T-cell acquired immunodeficiency syndrome has been described in homosexuals, drug addicts,Haitians and hemophiliacs. In an attempt to explore further metabolic mechanisms to account for this disorder we have quantitated erythrocyte and lymphocyte ADA and PNP activities using highly sensitive radiochemical methods in controls and seven patients with AIDS. Our results are as follows: 1) Erythrocyte ADA activity in controls and AIDS patients was 0.66 n mol/min/mg protein and 0.80 n mol/min/mg protein respectively. 2) Lymphocyte ADA activity was 6.86 n mol/min/mg protein for controls and 5.57 n mol/min/mg protein in AIDS. 3)Erythrocyte PNP activity was 2680 n mol/hr/mg protein for controls and 1618 n mol/hr/mg protein in the patients (p<.0005) 4)Lymphocyte PNP activity was 5892 n mol/hr/mg protein and 2740 n mol/hr/mg protein for controls and AIDS patients respectively (P<.0025). We conclude that: (1) Abnormalities in purine catabolic enzymes should be included in the disease spectrum of AIDS. (2) The causal relationship of decreased PNP activity in perpetuating the abnormal T-cell function in these patients remains to be determined (3) Alternatively the decreased PNP activity in AIDS may be secondary to the profound selective T-cell lymphopenia in this syndrome.

Alteration of adenosine deaminase levels in peripheral blood lymphocytes of patients with gastric cancer.

The present study was undertaken to determine the adenosine deaminase (ADA) activity of peripheral lymphocytes in patients with gastric cancer, with respect to the cancer progression, the effect of surgery and/or immunotherapy. The gastric cancer patients showed lower lymphocyte ADA activity than did the normal control. The lymphocyte ADA activity did not decrease with the cancer progression. There was a significant correlation between lymphocyte ADA activity and blastogenesis of lymphocyte by phytohemaglutinin or concanavalin A. Six months following gastrectomy, the lymphocyte ADA activity was increased, as compared with the preoperative value. The ADA activity of patients on post-operative OK-432 showed a greater increase, as compared to that of patients not given this treatment. In conclusion, decreased lymphocyte ADA activity in gastric cancer patients might be due to either the cancer bearing status or to the immunological suppression.

Aldolase and adenosine deaminase activity in lymphocytes of patients with glomerulonephritis.

Studies on the adenosine deaminase (ADA) and aldolase activities in lymphocytes were performed in 67 patients with glomerulonephritis (gn) and in 20 healthy individuals from the control group to get an insight into the lymphocyte metabolism. Statistically significant decrease of ADA activity was found in the groups of patients with chronic proliferative gn, membranoproliferative gn, membranous gn and lupus nephritis in comparison with the healthy individuals from the control group. As far as decrease of aldolase activity is concerned it has reached statistical significance in patients with mesangial gn, membranoproliferative gn, membranous gn and lupus nephritis. The lymphocyte metabolism did not show any abnormalities in the enzymatic indicators only in patients with acute proliferative gn and submicroscopic gn. The activity comparison between both enzymes in the lymphocytes, contrasted on the basis of high and low clinical dynamics of gn, revealed a tendency to lower ADA and aldolase activities in patients with high clinical dynamics. However, this difference was at the limit of statistical significance (p less than or equal to 0.10).

Adenosine and deoxyadenosine metabolism in horse erythrocytes and lymphocytes

1. 1. Horse erythrocytes are essentially devoid of adenosine deaminase activity, but phosphorylate both adenosine and deoxyadenosine. 2. 2. In horse lymphocytes, deamination of adenosine and deoxyadenosine is equal or greater than the rate of phosphorylation. 3. 3. Horse lymphocyte adenosine deaminase activity is 5-fold more labile than the human activity at 60°C. 4. 4. On sucrose density gradients, there are distinct adenosine and deoxyguanosine kinase activities and a co-sedimenting deoxyadenosine-deoxycytidine kinase activity.

Adenosine deaminase deficiency: disappearance of adenine deoxynucleotides from a patient's erythrocytes after successful marrow transplantation.

Accumulation of adenine deoxynucleotides (dATP and dADP) in the erythrocytes of a patient with adenosine deaminase (ADA) deficiency was confirmed. The patient, now 18 mo old, was treated with a bone marrow transplantation from his HLA identical sister at 7 mo of age. Before and after the transplant, his erythrocyte and lymphocyte ADA activities, as well as his erythrocyte nucleotide profiles, were measured. 10 wk after the marrow transplant, no ADA activity could be detected in his erythrocytes, whereas there was a mixture of donor and patient lymphocytes as measured by ADA assays and karyotyping. At the same time, both dATP and dADP had disappeared from his erythrocytes, which were entirely of patient origin. These findings indicate that partial engraftment of donor lymphocytes into an ADA-deficient patient is capable of "correcting" alterations of deoxynucleotide concentrations in the patient's ADA-deficient erythrocytes.

Adenosine Deaminase Activity in Patients with Carcinoma of the Bladder

Adenosine deaminase is an important enzyme in purine metabolism, and patients with abnormal lymphocyte and erythrocyte adenosine deaminase levels have been shown to have impaired immune competence. Since immune factors have been shown to be important in patients with transitional cell carcinoma of the bladder we studied adenosine deaminase activity in the hemic cells of 48 patients with this tumor. Lymphocyte adenosine deaminase levels were elevated in patients with transitional cell carcinoma and correlated with stage, activity, clinical course and tumor resection but not with tumor grade. Erythrocyte adenosine deaminase levels also were elevated in patients with transitional cell carcinoma but did not correlate with other disease parameters. Lymphocyte adenosine deaminase activity in patients with transitional cell carcinoma may be a sensitive indicator of disease activity and further studies may provide insight into the host-tumor relationship at the enzyme level.

Adenosine deaminase activity in lymphocytes of normal persons, leukemic patients, and kidney-transplant recipients.

We determined the activity of adenosine deaminase in normal lymphocytes from peripheral blood, leukemic cells from patients with various hematologic malignancies, and mononuclear cells from kidney-transplant patients, by adapting the method of Hopkinson et al. [Ann. Hum. Genet. 32, 361 (1969)] to the centrifugal analyzer. Normal lymphocytes separated on Ficoll-Hypaque from peripheral blood had a mean activity of 1.42 U/10(9) cells (SD = 0.57; N = 33). Cells similarly isolated from patients with acute lymphoproliferative and myeloproliferative disease generally showed greater values, but the ranges overlapped. Cells from patients with chronic lymphocytic leukemia had activities that were within or below the normal range. Mononuclear cells isolated from the peripheral blood of 15 stable renal allograft recipients showed a mean activity of 1.90 U/10(9) cells (SD = 0.59), not significantly different from normal. In contrast, cells from five patients with biopsy-proven allograft rejection showed a mean activity of 12.84 U/10(9) cells (SD = 10.10), which was significantly different from that of the stable patients.

ADENOSINE DEAMINASE ACTIVITY IN LYMPHOCYTES

British Journal of HaematologyVolume 37, Issue 1 p. 157-158 Free Access ADENOSINE DEAMINASE ACTIVITY IN LYMPHOCYTES J. L. Sullivan, J. L. Sullivan Department of Pediatrics, University of Washington School of Medicine, Seattle, Washington 98195, U.S.A.Search for more papers by this authorW. R. A. Osborne, W. R. A. Osborne Department of Pediatrics, University of Washington School of Medicine, Seattle, Washington 98195, U.S.A.Search for more papers by this authorR. J. Wedgwood, R. J. Wedgwood Department of Pediatrics, University of Washington School of Medicine, Seattle, Washington 98195, U.S.A.Search for more papers by this author J. L. Sullivan, J. L. Sullivan Department of Pediatrics, University of Washington School of Medicine, Seattle, Washington 98195, U.S.A.Search for more papers by this authorW. R. A. Osborne, W. R. A. Osborne Department of Pediatrics, University of Washington School of Medicine, Seattle, Washington 98195, U.S.A.Search for more papers by this authorR. J. Wedgwood, R. J. Wedgwood Department of Pediatrics, University of Washington School of Medicine, Seattle, Washington 98195, U.S.A.Search for more papers by this author First published: September 1977 https://doi.org/10.1111/j.1365-2141.1977.tb08825.xCitations: 49AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article. References Fu, S.M., Winchester, R.J. & Kunkel, H.G. (1975) The occurrence of the HL-B alloantigens on the cells of unclassified acute lymphoblastic leukemias. Journal of Experimental Medicine, 142, 1334. Kaplan, J., Ravindranath, Y. & Peterson, W.D. (1977) T and B lymphocyte antigen-positive null cell leukemias. Blood, 49, 371. Nilsson, K. (1976) Establishment of permanent human lymphoblastoid cell lines in vitro. In Vitro Methods in Cell Mediated and Tumor Immunity, p 713. Academic Press, London . Ramot, B., Brok-Simoni, F., Barnea, N., Banik, I. & Holtzman, F. (1977) Adenosine deaminase (ADA) activity in lymphocytes of normal individuals and patients with chronic lymphatic leukaemia. British Journal of Haematology, 36, 67. Royston, I., Pitts, R.B., Smith, R.W. & Graze, P.R. (1975) In vitro immunization against cultured human B and T lymphoblastoid cell lines. Transplantation Proceedings, 7 (Suppl. 1), 531. Tung, R., Silber, R., Quagliata, F., Conklyn, M., Gottesman, J. & Hirschhorn, R. (1976) Adenosine deaminase activity in chronic lymphocytic leukemia. Journal of Clinical Investigation, 57, 756. Citing Literature Volume37, Issue1September 1977Pages 157-158 ReferencesRelatedInformation

ADENOSINE DEAMINASE ACTIVITY IN LYMPHOCYTES

ADENOSINE DEAMINASE ACTIVITY IN LYMPHOCYTES