scholarly journals Pyrophosphatase of the Roundworm Ascaris suum Plays an Essential Role in the Worm's Molting and Development

2005 ◽  
Vol 73 (4) ◽  
pp. 1995-2004 ◽  
Author(s):  
M. Khyrul Islam ◽  
Takeharu Miyoshi ◽  
Manabu Yamada ◽  
Naotoshi Tsuji
Keyword(s):  
Rna Interference ◽  
Active Sites ◽  
Ascaris Suum ◽  
Critical Role ◽  
Interleukin 2 ◽  
Pcr Analysis ◽  
Mrna Levels ◽  
Molting Process ◽  
Third Stage

ABSTRACT Previous studies indicated that inorganic pyrophosphatase of Ascaris suum (AsPPase) plays an important role in larval survival in the host. Here we describe a precise role for AsPPase in larval molting and development and also describe the potential role of recombinant AsPPase (rAsPPase) in protective immunity to A. suum infection. Using reverse transcriptase PCR analysis, we found that disruption of AsPPase gene function by RNA interference resulted in suppression of AsPPase mRNA levels. RNA interference also caused inhibition of molting of third-stage larvae (31%) and suppression of native protein expression, as demonstrated by a 56% reduction in enzyme activity and quantified by immunoblot and immunofluorescence analyses, suggesting that AsPPase has a role in the molting process. The anatomic location of the AsPPase native enzyme in the hypodermis of larvae along with its elevated expression prior to and during the molting process supports such a role. Anti-rAsPPase immunoglobulin G (IgG) also resulted in 57% inhibition of molting of A. suum lung-stage third-stage larvae to fourth-stage larvae in vitro with developmental arrest. Antigenic epitopes of AsPPase overlapped the enzyme active sites. Mice immunized with rAsPPase exhibited high antigen-specific IgG antibody responses and were protected (>70%) against a challenge A. suum migratory-phase infection. Splenic T cells from rAsPPase-immunized mice produced low levels of T helper 1-type cytokines (gamma interferon and interleukin-2) in vitro but exhibited an elevated interleukin-10 response. A significantly high level of IgG1 subclass antibodies was found in immunized mice. Our results establish that AsPPase has a critical role in the molting and development of Ascaris roundworms and suggest the potential of AsPPase for use as a candidate vaccine against ascariasis.

scholarly journals Tendon Extracellular Matrix Remodeling and Defective Cell Polarization in the Presence of Collagen VI Mutations

Cells ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 409 ◽  
Author(s):  
Manuela Antoniel ◽  
Francesco Traina ◽  
Luciano Merlini ◽  
Davide Andrenacci ◽  
Domenico Tigani ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Critical Role ◽  
Active Form ◽  
Congenital Muscular Dystrophy ◽  
Cell Polarization ◽  
Pcr Analysis ◽  
Matrix Remodeling ◽  
Collagen Vi

Mutations in collagen VI genes cause two major clinical myopathies, Bethlem myopathy (BM) and Ullrich congenital muscular dystrophy (UCMD), and the rarer myosclerosis myopathy. In addition to congenital muscle weakness, patients affected by collagen VI-related myopathies show axial and proximal joint contractures, and distal joint hypermobility, which suggest the involvement of tendon function. To gain further insight into the role of collagen VI in human tendon structure and function, we performed ultrastructural, biochemical, and RT-PCR analysis on tendon biopsies and on cell cultures derived from two patients affected with BM and UCMD. In vitro studies revealed striking alterations in the collagen VI network, associated with disruption of the collagen VI-NG2 (Collagen VI-neural/glial antigen 2) axis and defects in cell polarization and migration. The organization of extracellular matrix (ECM) components, as regards collagens I and XII, was also affected, along with an increase in the active form of metalloproteinase 2 (MMP2). In agreement with the in vitro alterations, tendon biopsies from collagen VI-related myopathy patients displayed striking changes in collagen fibril morphology and cell death. These data point to a critical role of collagen VI in tendon matrix organization and cell behavior. The remodeling of the tendon matrix may contribute to the muscle dysfunction observed in BM and UCMD patients.

scholarly journals Transendothelial movement of adiponectin is restricted by glucocorticoids

2017 ◽  
Vol 234 (2) ◽  
pp. 101-114 ◽  
Author(s):  
Thanh Q Dang ◽  
Nanyoung Yoon ◽  
Helen Chasiotis ◽  
Emily C Dunford ◽  
Qilong Feng ◽  
...  
Keyword(s):  
Critical Role ◽  
Endothelial Permeability ◽  
The Body ◽  
Diabetic Rat ◽  
Mrna Levels ◽  
Endothelial Monolayers ◽  
Basolateral Side ◽  
Induced Changes

Altered permeability of the endothelial barrier in a variety of tissues has implications both in disease pathogenesis and treatment. Glucocorticoids are potent mediators of endothelial permeability, and this forms the basis for their heavily prescribed use as medications to treat ocular disease. However, the effect of glucocorticoids on endothelial barriers elsewhere in the body is less well studied. Here, we investigated glucocorticoid-mediated changes in endothelial flux of Adiponectin (Ad), a hormone with a critical role in diabetes. First, we used monolayers of endothelial cells in vitro and found that the glucocorticoid dexamethasone increased transendothelial electrical resistance and reduced permeability of polyethylene glycol (PEG, molecular weight 4000 Da). Dexamethasone reduced flux of Ad from the apical to basolateral side, measured both by ELISA and Western blotting. We then examined a diabetic rat model induced by treatment with exogenous corticosterone, which was characterized by glucose intolerance and hyperinsulinemia. There was no change in circulating Ad but less Ad protein in skeletal muscle homogenates, despite slightly higher mRNA levels, in diabetic vs control muscles. Dexamethasone-induced changes in Ad flux across endothelial monolayers were associated with alterations in the abundance of select claudin tight junction (TJ) proteins. shRNA-mediated knockdown of one such gene, claudin-7, in HUVEC resulted in decreased TEER and increased adiponectin flux, confirming the functional significance of Dex-induced changes in its expression. In conclusion, our study identifies glucocorticoid-mediated reductions in flux of Ad across endothelial monolayers in vivo and in vitro. This suggests that impaired Ad action in target tissues, as a consequence of reduced transendothelial flux, may contribute to the glucocorticoid-induced diabetic phenotype.

scholarly journals BCL-6 expression during B-cell activation

Blood ◽  
1996 ◽  
Vol 87 (12) ◽  
pp. 5257-5268 ◽  
Author(s):  
D Allman ◽  
A Jain ◽  
A Dent ◽  
RR Maile ◽  
T Selvaggi ◽  
...  
Keyword(s):  
B Cells ◽  
T Lymphocytes ◽  
Germinal Center ◽  
Cell Activation ◽  
Interleukin 2 ◽  
Large Cell ◽  
Cd40 Ligand ◽  
Mrna Levels ◽  
Coding Region

Translocations involving the BCL-6 gene are common in the diffuse large cell subtype of non-Hodgkin's lymphoma. Invariably, the BCL-6 coding region is intact, but its 5′ untranslated region is replaced with sequences from the translocation partner. The present study shows that BCL-6 expression is regulated in lymphocytes during mitogenic stimulation. Resting B and T lymphocytes contain high levels of BCL-6 mRNA. Stimulation of mouse B cells with anti-IgM or IgD antibodies, bacterial lipopolysaccharide, phorbol 12-myristate 13-acetate plus ionomycin, or CD40 ligand led to a five-fold to 35-fold decrease in BCL-6 mRNA levels. Similar downregulation of BCL-6 mRNA was seen in human B cells stimulated with Staphylococcus aureus plus interleukin-2 or anti-IgM antibodies and in human T lymphocytes stimulated with phytohemagglutinin. BCL-6 mRNA levels began to decrease 8 to 16 hours after stimulation, before cells entered S phase. Although polyclonal activation of B cells in vitro invariably decreased BCL-6 MRNA expression, activated B cells from human germinal centers expressed BCL-6 mRNA at levels comparable to the levels in resting B cells. Despite these similar mRNA levels, BCL-6 protein expression was threefold to 34-fold higher in germinal center B cells than in resting B cells, suggesting that BCL-6 protein levels are controlled by translational or posttranslational mechanisms. These observations suggest that the germinal center reaction provides unique activation signals to B cells that allow for continued, high-level BCL-6 expression.

The B-Cell Chemoattractant Factor CXCL13 Is Expressed in the Malignant Lymphocyte of the Sezary Syndrome.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 2292-2292
Author(s):  
Maria Grazia Narducci ◽  
Maria Cristina Picchio ◽  
Cristina Lazzeri ◽  
Irene Angelucci ◽  
Enrico Scala ◽  
...  
Keyword(s):  
B Cell ◽  
Critical Role ◽  
Pcr Analysis ◽  
Low Grade ◽  
Mrna Levels ◽  
Healthy Controls ◽  
Qrt Pcr ◽  
Cellular Recruitment ◽  
Skin Biopsies ◽  
Infiltrating Lymphocytes

Abstract Sézary Syndrome (SS) is a rare and aggressive form of Cutaneous T-Cell Lymphoma (CTCL) characterised by a distinct metastatic pattern mainly involving blood and skin. Our expression analyses performed by microarrays demonstrated that many chemokines resulted up-regulated in this type of lymphoma. Since these chemoattractant molecules play a critical role in cellular recruitment and homing to tissues and in the metastatic process of several tumors, we focused our attention on one of them named CXCL13, a lymphoid chemokine involved in B-cell compartmental homing within secondary lymphoid organs. Peripheral Blood Mononuclear cells (PBMCs) were isolated from blood obtained from SS patients and controls by Ficoll-Hypaque density gradient centrifugation (Sigma Aldrich). SS cells and healthy resting CD4+ lymphocytes were purified by positive selection using an anti-human-CD4 conjugated dynabeads (Oxoid). Total RNA was extracted using the Trizol reagent (Life Technologies). Quantitative-Real Time RT-PCR analysis was performed on CD4+ sorted from 14 SS patients and 3 controls. CXCL13 primers were designed by means of the Primer Express software package (Applied Biosystems). The qRT-PCR were performed with a SYBR Green I dye chemistry and AmpliTaq Gold DNA Polymerase on an ABI PRISM 7000 machine (Applied Biosystems). Immunohistochemistry analyses for CXCL13 were performed on formalin-fixed, paraffin-embedded skin biopsies from 15 SS, 15 MF, 6 MF-B cell rich patients using streptoavidin-biotin peroxidase labeling method (DAKO). Sections were counterstained with hematoxylin. Plasma CXCL13 levels were determined using a CXCL13 ELISA kit (BD Pharmingen). Results can be summarized as follow: qRT-PCR analysis revealed that 6 out 13 of SS patients showed an high mRNA levels of CXCL13; Immunohistochemistry analysis showed that CXCL13 is abundantly expressed by neoplastic skin-infiltrating lymphocytes of 9 out 15 SS skin biopsies. Conversely, CXCL13 is weakly expressed on scattered neoplastic skin-infiltrating lymphocytes of 1 out 15 MF and 1 out 6 MF-B cell rich biopsies. Plasma CXCL13 concentrations in SS patients (n = 10) were 1362 ± 134 pg/mL. Conversely, those in MF patients (n = 10) and healthy donors (n = 5) were 70 ± 43 and 13 ± 10 pg/mL, respectively. Compared with healthy controls, plasma CXCL13 levels were significantly higher in patients with SS (p<0.001) and with MF (p=0.04). In this study we report that both circulating and skin-infiltrating neoplastic lymphocytes of SS patients abundantly express CXCL13. Furthermore, this chemokine is also detectable at high level on plasma of SS patients. Conversely, CXCL13 is not observable in healthy controls as well as in Mycosis Fungoides, a variant of low grade of CTCL. These findings indicate that CXCL13 could play a role in pathobiology of Sézary Syndrome and that the expression of this chemokine could be used as diagnostic marker for this kind of tumor

Trans-resveratrol modulates the catalytic activity and mRNA expression of the procarcinogen-activating human cytochrome P450 1B1

2000 ◽  
Vol 78 (11) ◽  
pp. 874-881 ◽  
Author(s):  
Thomas KH Chang ◽  
Wendy BK Lee ◽  
Hin Hin Ko
Keyword(s):  
Gene Expression ◽  
Cytochrome P450 ◽  
Catalytic Activity ◽  
Pcr Analysis ◽  
Mrna Levels ◽  
Toxic Response ◽  
Cytochrome P450 1B1 ◽  
Cyp1b1 Mrna ◽  
Mcf 7

The present study was performed to determine if trans-resveratrol (3,5,4'-trihydroxy-trans-stilbene) modulates the catalytic activity and gene expression of cytochrome P450 1B1 (CYP1B1). In vitro, trans-resveratrol decreased human recombinant CYP1B1-catalyzed 7-ethoxyresorufin O-dealkylation activity, with an IC50 value of 1.4 ± 0.2 µM (mean ± SEM). Enzyme kinetic analysis indicated that trans-resveratrol inhibited CYP1B1 enzyme activity by a mixed-type inhibition and the apparent Ki was 0.75 ± 0.06 µM. To determine if trans-resveratrol modulates constitutive CYP1B1 gene expression, cultured MCF-7 human breast carcinoma cells were treated with trans-resveratrol. As indicated by RT-PCR analysis, treatment of MCF-7 cells with 10 µM trans-resveratrol decreased relative CYP1B1 mRNA levels after 5 h, but not after 1.5 or 3 h, of exposure. trans-Resveratrol treatment at 5, 7.5, 10, or 20 µM for 5 h produced a concentration-dependent decrease in CYP1B1 mRNA levels. The extent of suppression was ~50% at 20 µM concentration. The suppressive effect was not a consequence of a toxic response to the compound as assessed by a cell proliferation assay. Overall, our novel finding that trans-resveratrol inhibits the catalytic activity and suppresses the constitutive gene expression of CYP1B1 leads to the possibility that this nutraceutical confers protection against toxicity and carcinogenicity induced by compounds that undergo CYP1B1-catalyzed bioactivation.Key words: cytochrome P450, CYP1B1, 7-ethoxyresorufin, nutraceutical, trans-resveratrol.

scholarly journals Expression and homologous regulation of GH secretagogue receptor mRNA in rat adrenal gland

2002 ◽  
pp. 677-688 ◽  
Author(s):  
ML Barreiro ◽  
L Pinilla ◽  
E Aguilar ◽  
M Tena-Sempere
Keyword(s):  
Biological Effects ◽  
Biologically Active ◽  
Pcr Analysis ◽  
Mrna Levels ◽  
R Gene ◽  
Rt Pcr ◽  
Short Term ◽  
Opposite Pattern ◽  
Corticosterone Secretion

OBJECTIVE: GH secretagogues (GHSs) elicit a variety of biological effects in several endocrine and non-endocrine target tIssues, including activation of the hypothalamic-pituitary-adrenal axis. The latter is mainly carried out through a central hypothalamic action; yet the possibility of additional effects directly at the adrenal level cannot be ruled out. The aims of this study were to evaluate the expression and homologous regulation of the GHS-receptor (GHS-R) gene in rat adrenal and to assess the effects of synthetic (GH releasing peptide-6 - GHRP-6) and natural (ghrelin) ligands of GHS-R upon basal and ACTH-stimulated corticosterone secretion in vitro. DESIGN AND METHODS: Analysis of adrenal expression of target mRNAs (GHS-R, GHS-R1a, ghrelin, and several steroidogenic factors) was conducted by means of primer-specific, semi-quantitative RT-PCR. Evaluation of corticosterone secretion by incubated adrenal tIssue was carried out by specific RIA. RESULTS: RT-PCR analysis demonstrated expression of the GHS-R gene, but not of the gene encoding the cognate ligand ghrelin, in rat adrenal. Moreover, expression of the mRNA coding for the type 1a GHS-R (GHS-R1a), i.e. the biologically active receptor form, was demonstrated. The adrenal expression of the GHS-R message appeared under the regulation of homologous signals in vitro, as short-term incubation of adrenal samples in serum-free medium induced a significant increase in GHS-R mRNA levels that was inhibited by exposure to different doses of GHRP-6 (10(-9)-10(-5) mol/l) or ghrelin (10(-7) mol/l). Notably, an opposite pattern of homologous regulation of GHS-R gene expression was observed at the pituitary. Finally, short-term stimulation with increasing concentrations of GHRP-6 (10(-9)-10(-5) mol/l) or ghrelin (10(-7) mol/l) failed to alter basal and ACTH-stimulated corticosterone secretion in vitro, neither did it modify ACTH-stimulated mRNA expression levels of several upstream elements in the steroidogenic route: the steroidogenic acute regulatory (StAR) protein, and the enzymes P450 cholesterol side-chain cleavage (P450scc) and 3beta-hydroxysteroid dehydrogenase (3beta-HSD). CONCLUSIONS: Our study provides novel evidence for the expression and homologous regulation of the GHS-R gene in rat adrenal. However, our results cast doubts on the possibility of direct adrenal actions of ligands of the GHS-R in the regulation of corticosterone secretion in the rat.

scholarly journals Single-Cell Sequencing Reveals the Transcriptome and TCR Characteristics of pTregs and in vitro Expanded iTregs

2021 ◽  
Vol 12 ◽  
Author(s):  
Zhenzhen Hui ◽  
Jiali Zhang ◽  
Yu Zheng ◽  
Lili Yang ◽  
Wenwen Yu ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Single Cell ◽  
Cancer Patients ◽  
Peripheral Blood ◽  
Critical Role ◽  
Interleukin 2 ◽  
Treg Cells ◽  
Single Cell Sequencing ◽  
Colorectal Cancer Patients

Regulatory T cells (Tregs) play a critical role in the maintenance of immune tolerance and tumor evasion. However, the relative low proportion of these cells in peripheral blood and tissues has hindered many studies. We sought to establish a rapamycin-based in vitro Treg expansion procedure in patients diagnosed with colorectal cancer and perform single-cell sequencing to explore the characteristics of Treg cells. CD25+ cells enriched from peripheral blood mononuclear cells (PBMC) of colorectal tumor patients were cultured in X-VIVO15 medium, supplemented with 5% human AB serum, L-glutamine, rapamycin, interleukin-2 (IL-2), and Dynabeads human Treg expander for 21 days to expand Tregs. Treg cells with satisfactory phenotype and function were successfully expanded from CD4+CD25+ cells in patients with colorectal cancer. The median expansion fold was 75 (range, 20–105-fold), and &gt;90.0% of the harvest cells were CD4+CD25+CD127dim/− cells. The ratio of CD4+CD25+Foxp3+ cells exceeded 60%. Functional assays showed that iTregs significantly inhibited CD8+T cell proliferation in vitro. Single-cell sequencing showed that the transcriptome of pTreg (CD4+CD25+CD127dim/− cells isolated from PBMC of colorectal cancer patients) and iTreg (CD4+CD25+CD127dim/− cells expanded in vitro according to the above regimen) cells were interlaced. pTregs exhibited enhanced suppressive function, whereas iTregs exhibited increased proliferative capacity. TCR repertoire analysis indicated minimal overlap between pTregs and iTregs. Pseudo-time trajectory analysis of Tregs revealed that pTregs were a continuum composed of three main branches: activated/effector, resting and proliferative Tregs. In contrast, in vitro expanded iTregs were a mixture of proliferating and activated/effector cells. The expression of trafficking receptors was also different in pTregs and iTregs. Various chemokine receptors were upregulated in pTregs. Activated effector pTregs overexpressed the chemokine receptor CCR10, which was not expressed in iTregs. The chemokine CCL28 was overexpressed in colorectal cancer and associated with poor prognosis. CCR10 interacted with CCL28 to mediate the recruitment of Treg into tumors and accelerated tumor progression. Depletion of CCR10+Treg cells from tumor microenvironment (TME) could be used as an effective treatment strategy for colorectal cancer patients. Our data distinguished the transcriptomic characteristics of different subsets of Treg cells and revealed the context-dependent functions of different populations of Treg cells, which was crucial to the development of alternative therapeutic strategies for Treg cells in autoimmune disease and cancer.

scholarly journals Downregulation of decidual SKP2 is associated with human recurrent miscarriage

2021 ◽  
Author(s):  
Shijian Lv ◽  
Mei Liu ◽  
Lizhen Xu ◽  
Cong Zhang
Keyword(s):  
Stromal Cells ◽  
Recurrent Miscarriage ◽  
Aerobic Glycolysis ◽  
Critical Role ◽  
Protein S ◽  
Pcr Analysis ◽  
Endometrial Stromal Cells ◽  
Downstream Target ◽  
F Box Protein

Abstract Background: Recurrent miscarriage (RM) is a very frustrating problem for both couples and clinicians. To date, the etiology of RM remains poorly understood. Decidualization plays a critical role in implantation and the maintenance of pregnancy, and its deficiency is closely correlated with RM. The F-box protein S-phase kinase associated protein 2 (SKP2) is a key component of the SCF-type E3 ubiquitin ligase complex, which is critically involved in ErbB family-induced Akt ubiquitination, aerobic glycolysis and tumorigenesis. SKP2 is pivotal for reproduction, and SKP2-deficient mice show impaired ovarian development and reduced fertility.Methods: Here, we investigated the expression and function of SKP2 in human decidualization and its relation with RM. A total of 40 decidual samples were collected. Quantitative PCR analysis, western blot analysis and immunohistochemistry analysis were performed to analyze the differential expression of SKP2 between RM and control cells. For in vitro induction of decidualization, both HESCs (human endometrial stromal cells) cell line and primary ESCs (endometrial stromal cells) were used to analyze the effects of SKP2 on decidualization via siRNA transfection.Results: Compared to normal pregnant women, the expression of SKP2 was reduced in the decidual tissues from individuals with RM. After in vitro induction of decidualization, knockdown of SKP2 apparently attenuated the decidualization of HESCs and resulted in the downregulation of HOXA10 and FOXM1, which are essential for normal human decidualization. Moreover, our experiments demonstrated that SKP2 silencing reduced the expression of its downstream target GLUT1.Conclusions: Our study indicates a functional role of SKP2 in RM: downregulation of SKP2 in RM leads to impaired decidualization and downregulation of GLUT1 and consequently predisposes individuals to RM.

scholarly journals Transcriptome-Wide Analysis Reveals a Role for Extracellular Matrix and Integrin Receptor Genes in Otic Neurosensory Differentiation from Human iPSCs

2021 ◽  
Vol 22 (19) ◽  
pp. 10849
Author(s):  
Lejo Johnson Chacko ◽  
Hanae Lahlou ◽  
Claudia Steinacher ◽  
Said Assou ◽  
Yassine Messat ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Inner Ear ◽  
Cell Fate ◽  
Time Course ◽  
Critical Role ◽  
Pcr Analysis ◽  
Sensory Cells ◽  
Gene Markers ◽  
Human Ipscs

We analyzed transcriptomic data from otic sensory cells differentiated from human induced pluripotent stem cells (hiPSCs) by a previously described method to gain new insights into the early human otic neurosensory lineage. We identified genes and biological networks not previously described to occur in the human otic sensory developmental cell lineage. These analyses identified and ranked genes known to be part of the otic sensory lineage program (SIX1, EYA1, GATA3, etc.), in addition to a number of novel genes encoding extracellular matrix (ECM) (COL3A1, COL5A2, DCN, etc.) and integrin (ITG) receptors (ITGAV, ITGA4, ITGA) for ECM molecules. The results were confirmed by quantitative PCR analysis of a comprehensive panel of genes differentially expressed during the time course of hiPSC differentiation in vitro. Immunocytochemistry validated results for select otic and ECM/ITG gene markers in the in vivo human fetal inner ear. Our screen shows ECM and ITG gene expression changes coincident with hiPSC differentiation towards human otic neurosensory cells. Our findings suggest a critical role of ECM-ITG interactions with otic neurosensory lineage genes in early neurosensory development and cell fate determination in the human fetal inner ear.

scholarly journals Increased Capacity for Interleukin-2 Synthesis Parallels Disease Progression in Mice Infected withLeishmania major

1998 ◽  
Vol 66 (9) ◽  
pp. 4537-4540 ◽  
Author(s):  
Frederick P. Heinzel ◽  
Ronald M. Rerko ◽  
Andrea M. Hujer ◽  
Richard A. Maier
Keyword(s):  
Lymph Node ◽  
Disease Progression ◽  
Functional Significance ◽  
Interleukin 2 ◽  
Gamma Interferon ◽  
Mrna Levels ◽  
Lymph Node Cells

ABSTRACT Lymph node cells of BALB/c mice with progressive leishmaniasis produced sixfold more interleukin-2 (IL-2) in culture than those of healing C57BL/6 mice. IL-2 synthesis also increased in C57BL/6 mice made susceptible by IL-12 or gamma interferon deficiency. However, IL-2 mRNA levels in vivo did not reflect IL-2 production in vitro. Because IL-2 contributes to the pathogenesis of progressive leishmaniasis, the functional significance of these findings should be further explored.

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