Biomedical subjects

H Ben-Bassat

Publications and source records attributed to H Ben-Bassat.

At least 37 records · Page 2Linked to original sources

PubMed1998

Early nonsurgical removal of chemically injured tissue enhances wound healing in partial thickness burns.

Chemical burns are slow healing injuries and their depth is difficult to assess. Tissue destruction continues as long as active material is present in the wound site. The routine therapy for treatment of full thickness chemical burns is early excision; it shortens hospitalization and reduces morbidity. However, presently there is no specific treatment for chemical burns of partial thickness. This study examined several treatment modalities for partial thickness chemical burns: surgical excision; laser ablation and chemical debridement with Debridase or trypsin-linked to gauze. Chemical burns were inflicted with nitrogen mustard (NM -- a nitrogen analog to sulfur mustard -- mustard gas) in an experimental guinea pig model. Debridase was most effective and reduced significantly lesion area of burns after 'humid' exposure to 2 mg NM. The healing action of Debridase was also evident in the significantly higher histopathological score of biopsies from local tissue obtained on day 5. Laser ablation was most effective and accelerated healing of burn lesions after 'dry' exposure to 5 mg NM. The histopathology score of the laser treated burns was higher on day 4 compared to untreated controls. It is concluded that for partial thickness chemical burns early nonsurgical removal of the damaged tissues accelerates wound healing.

Administration, Topical↗

PubMed1998

P53 gene mutation in a T-acute lymphoblastic leukemia cell line (loucy) with t(16:20) and 5q- chromosomal aberrations.

A human T-acute lymphoblastic leukemia (ALL) cell line (Loucy), derived from cells from a patient with resistant ALL with a t(16:20) and 5q- chromosomal aberrations was evaluated for p53 gene alterations and expression. Western blot analysis of p53 showed elevated levels of the protein. Reverse transcriptase-polymerase chain reaction (RT-PCR) analysis and direct sequencing identified a point mutation at codon 272 (GTG --> ATG) of the p53 gene. Possible molecular mechanisms underlying these alterations and their role in the establishment of this cell line and in leukemogenesis in general are discussed.

Blotting, Western↗

PubMed1997

Inhibitors of epidermal growth factor receptor kinase and of cyclin-dependent kinase 2 activation induce growth arrest, differentiation, and apoptosis of human papilloma virus 16-immortalized human keratinocytes.

Human papilloma virus 16 (HPV 16) is associated with cervical cancer and is therefore considered a major health risk for women. Immortalization of keratinocytes induced by HPV infection is largely due to the binding of p53 and Rb by the the viral oncoproteins E6 and E7, respectively, and is driven to a large extent by a transforming growth factor alpha/amphiregulin epidermal growth factor receptor autocrine loop. In this study, we show that the growth of HPV 16-immortalized human keratinocytes can be blocked by a selective epidermal growth factor receptor kinase inhibitor, AG 1478, and by AG 555, a blocker of cyclin-dependent kinase 2 (Cdk2) activation. AG 1478 induces a massive increase in the Cdk2 protein inhibitors p27 and p21, whereas AG 555 appears to have a different mechanism of action, inhibiting the activation of Cdk2. Growth arrest induced by AG 1478 and AG 555 is accompanied by up to 20% of cells undergoing apoptosis. Following AG 1478 treatment but not AG 555 treatment, up to 50% of cells undergo terminal keratinocyte differentiation as determined by filaggrin expression and by the decline in the expression of cytokeratin 14. The growth-arresting properties of AG 1478 and AG 555 identifies them as possible lead antipapilloma agents.

Antibodies↗

PubMed1997

Opposing effects of tyrosine kinase inhibitors on mineralization of normal and tumor bone cells.

Induction of matrix maturation and mineralization in calcified tissues is important for patients with primary bone tumors and other bone deficiencies, e.g., osteoporosis. For the former it signifies a better prognosis in osteosarcoma, and for the latter it might improve bone remodeling. In the present study we exposed osteosarcoma cells (Saos2), normal bone cells, and marrow stroma to two different tyrosine kinase (TK) inhibitors: AG-555 and AG-1478. These tyrphostins differ in their effect on signal transduction downstream to the TK receptor (RTK): AG-1478 inhibits src family TKs whereas AG-555 inhibits nuclear TKs. We found that both tyrphostins at 50 microM increased specific alkaline phosphatase (ALP) activity in Saos2 cells. AG-555 abrogated mineralization whereas AG-1478 increased it. Similarly, in human bone-derived cell cultures the same dose of tyrphostins had an opposing effect on mineralization but, in contrast to AG-555, AG-1478 positively selected cells with ALP activity. These tyrphostins also differed in their effect on rat marrow stromal cells. AG-555 decreased cell counts unselectively, whereas the decreased cell counts by AG-1478 resulted in selection of osteoprogenitor cells as indicated by a concordant increase in specific ALP activity. The effect of a lower dose of AG-1478, 5 microM, on the increase in mineralization exceeded its own efficiency in selecting cells with specific ALP activity. Our results indicate that AG-1478 selects and preserves the osteoblastic phenotype, at doses moderately higher than those required to induce mineralization, and substantially higher than the doses required for RTK inhibition. Identification of downstream molecular targets for AG-1478, in marrow stromal cells, might prove useful in designing more selective drugs, capable of separating proliferative from differentiation-inducing activities.

Alkaline Phosphatase↗

PubMed1997

Interleukin-2 (IL-2) receptor alpha, beta and gamma subunit expression as a function of B-cell lineage ontogeny: the use of IL-2-PE66(4Glu) to characterize internalization via IL-2 receptor subunits.

Interleukin-2 (IL-2) is a pluripotent cytokine which plays a crucial role in the immune system response. Although the IL-2/IL-2 receptor (IL-2R) system has been well characterized in cells of the T lineage it is less known in B lymphocytes. The authors therefore studied the expression of the IL-2R alpha, beta and gamma subunits in human B-cell lines at different stages of maturation, by the polymerase chain reaction technique. The authors found that the alpha and beta subunits are expressed in the final stages of B-cell lineage maturation, whereas the gamma subunit is constitutively expressed during B-lymphocyte differentiation. The results indicate that the IL-2/IL-2R system, most probably, does not have a role in the early stages of B-cell differentiation, but may be involved only in the final stages of B-cell lineage ontogeny. Moreover, the ability of the different forms of IL-2R to internalize the IL-2 ligand was investigated, using the chimeric protein IL-2-PE66(4Glu). Cell lines bearing the alphagamma, betagamma and alpha betagamma forms of IL-2R were inhibited by the chimeric protein, while those bearing the gamma subunit alone did not respond to the chimera. Thus, internalization of IL-2 is most likely mediated via the alphagamma form of the IL-2R, as shown here for the first time, as well as through the betagamma and alpha betagamma IL-2R forms. However, IL-2 cannot be internalized through the IL-2R gamma subunit alone.

B-Lymphocytes↗

PubMed1997

Cyclosporin A and its non-immunosuppressive derivative exhibit a differential effect on cell-mediated mineralization in culture.

Chronic immunosuppressive treatment with cyclosporin A (CsA) is associated with decreased bone density. However, in culture, CsA inhibits osteoclast differentiation and bone resorption. This raises the question as to whether CsA also affects osteoblast function. Immunophilin, one of the CsA-binding cyclophilins that is implicated in the immunosuppressive action of CsA via calcineurin, is a peptidyl prolyl cis-trans isomerase (PPl). CsA also binds a mitochondrial membrane PPl which is implicated in controlling permeability transition pores. Therefore, in the present study we tested the effect of CsA on cell mediated mineralization in parallel with mitochondrial rhodamine retention as an indicator of mitochondrial membrane potential Rat marrow stromal cells were grown in dexamethasone (DEX) medium to stimulate mineralization in culture, and CsA was added to various cultures using different treatment schedules. Low dose (0.1 microM) CsA inhibited mineralization, compared to controls, when present in the cultures during days 3-11 of DEX stimulation. Contrarily, high dose CsA (1.0 microM) resisted the inhibitory effect of the low dose. SDZ 220-384 (SDZ), a non-immunosuppressive derivative of CsA which is known, like CsA, to bind to mitochondrial cyclophilin but does not inhibit calcineurin, was also tested. Both high and low doses of SDZ decreased mineralization when present in the cultures from day 3 or from day 0. The similar effect of the low CsA dose and SDZ on mineralization is in accord with their ability to block permeability transition pores. The differential effect, on day 21 mineralization, between high CsA dose and SDZ took place in parallel to their opposing effects on mitochondrial membrane potential. On days 4-8, mitochondrial rhodamine retention was higher under CsA than under SDZ. Under these conditions there was no significant difference between the effects of these drugs on cell proliferation measured on day 11; there was a minor decrease in specific alkaline phosphatase activity by SDZ, too small to explain the extent of mineralization inhibition by SDZ. These results suggest that permeability transition pores might be involved in controlling mineralization. Unlike SDZ, CsA exhibits an additional effect on the mitochondrial membrane potential and on mineralization when applied at a high dose on day 3. Therefore identifying the additional activity of high dose CsA, which is missing in SDZ, may be beneficial. Such activity is expected to resist changes in rhodamine retention and decreased mineralization induced by SDZ, and yet enable preservation of immunosuppressive activity of CsA.

Alkaline Phosphatase↗

PubMed1996

Cell-mediated mineralization in culture at low temperature associated with subtle thermogenic response.

In both the growth plate and in marrow stromal cell cultures cell-mediated mineralization is preceded by characteristics of anaerobic and low efficiency energy metabolism. Reagents that increase mineralization like malonate and dexamethasone (DEX) also increase the mitochondrial membrane potential (MtMP) especially 1 week after DEX stimulation. Contrarily, levamisole, which decreases mineralization, also decreases MtMP. Modulation of MtMP and energy metabolism could be linked to regulation of mineralization by the uncoupling of oxidative phosphorylation. This uncoupling should be associated with thermogenesis in cells that induce mineralization. We examined whether cold temperature affects mineralization, and whether cellular thermogenesis takes place at cold temperature in parallel to changes in MtMP. Osteoprogenitor cells (OPC) induced, in DEX stimulated rat marrow stroma, higher mineralization at 33 degrees C than at 37 degrees C. Increased mineralization by cold temperature required long incubation since incubation in the cold during short intervals, 3-4 days, did not increase mineralization relative to (37 degrees C) controls. Marrow stromal cells in the presence of valinomycin responded to incubation at 33 degrees C by retaining all the vital dye after 4 h, unlike the cells at 37 degrees C; however, after 24 h the level of dye retention at 33 degrees C was the same as at 37 degrees C. The delayed response of the temperature-dependent (> 37 degrees C) K+ ionophor to incubation in the cold indicated that certain cells may respond to low temperature by local intracellular heating, and by heat conduction to the plasma membrane. DEX-stimulated stromal cells, unlike unstimulated cells, showed increased mitochondrial rhodamine 123 retention in the presence of valinomycin after 24 h in the cold, which corresponds to day 4 of OPC induction. This is consistent with the concept that valinomycin-induced cell damage is mediated by (cold-induced) local heating. The mechanism of this cell damage should selectively prefer nonthermogenic (rhodamine retaining) over thermogenic (rhodamine leaking) cells such as OPC. At cold temperature DEX-stimulated stromal cells showed the best anti-OPC selection under exposure to valinomycine between days 3-7, concurrent with the period of rhodamine leakage from the mitochondria. These results indicate that thermogenesis is enhanced during the period of low MtMP in mineralizing cells, and prolonged exposure to cold increases mineralization also due to induction of subtle thermogenesis.

Animals↗

PubMed1996

Opposing effects on mitochondrial membrane potential by malonate and levamisole, whose effect on cell-mediated mineralization is antagonistic.

The act of chondrocyte preparation for primary, enchondral, mineralization is associated with a decline in mitochondrial respiration toward the end of the proliferative zone and the hypertrophic zone in the growth plate. Dexamethasone (Dex)-stimulated cultures of rat marrow stroma constitute a differentiation model simulating, in its energy metabolism, chondrocyte mineralization. In this model, early inhibition of succinate dehydrogenase (SDH) enriches the culture with mineralizing cells, whereas levamisole inhibits mineralization. Dex also increases mitochondrial membrane potential in stromal cells, especially on days 7-8 of stimulation. In the present study, suicide inhibition of SDH, by nitropropionic acid (NPA), in Dex-stimulated cells showed a dose-dependent increase in day 21 mineralization; the maximal effect was induced on days 2-4 of stimulation. Mineralization under 2-day-long exposure to NPA showed a similar trend to the previously studied effect of continuous exposure to malonate applied between days 3-11. Unlike malonate, the effect of NPA required its presence in the cultures for only 2 days and resulted in higher mineralization than that seen under 8 days of malonate. NPA delineated a period, days 2/4 to 7/9, in which inhibition of succinate oxidation is necessary to augment mineralization. During this period, NPA also exhibited OPC selection capacity. Early application of levamisole, under conditions previously shown to decrease day 21 mineralization, maintained mitochondrial membrane potential at the beginning of Dex stimulation but decreased or had little effect on it during days 5-10. By contrast, malonate previously found to increase day 21 mineralization decreased the membrane potential at the beginning of Dex stimulation but increased it later on day 7, or during days 5-10. These results indicate that during osteoprogenitor differentiation, before the mineralization stage, a surge in mitochondrial inner membrane potential during late matrix maturation may be a marker that heralds the extracellular matrix mineralization.

Alkaline Phosphatase↗

PubMed1996

Differential induction of cell-mediated mineralization in rat marrow stroma by sera from women of low and high risk for vertebral fracture.

The purpose of this study was to analyze the ability of sera to reflect the state of bone metabolism by testing the osteogenic response of mesenchymal cells in culture. Sera of 20 peri- and postmenopausal women were tested before the initiation of hormone replacement therapy. The responding cells were osteoprogenitors (OPC) of rat marrow stroma which normally respond to dexamethasone (DEX) and beta-glycerophosphate (beta GP) by proliferation, differentiation, and mineralization in culture. Instead of DEX, diluted sera (1:50) were applied to rat stromal cell cultures for analysis of their ability to affect cell proliferation, specific alkaline phosphatase (ALP) activity, and cell-mediated mineralization. The results were compared individually with the respective values of vertebral bone mineral density (BMD), expressed as the number of standard deviations above or below the mean BMD of reference populations (positive or negative Z-score). Serum donors were divided in two; the group with positive Z-scores was considered to have a low risk, and that with negative Z-scores was considered to have a higher risk for vertebral fractures. No significant difference was found between the two groups in the ability of their sera to induce cell proliferation or specific ALP activity. However, sera representing negative Z-scores induced sixteenfold less mineralization than those of positive Z-scores. The scatter of individual mineralization values was highly discriminatory between the two groups (alpha < 0.00). These results indicate that the serum-induced, cell-mediated mineralization in culture might be suitable for initial evaluation of fracture risk and thus deserve further investigation.

Alkaline Phosphatase↗

PubMed1996

Molecular characterization of an unusual non-Hodgkin's B-lymphoma cell line ("Farage") lacking the ability to produce immunoglobulin polypeptide chains.

"Farage" is a cell line derived from a patient who had a diffuse and mixed type malignant lymphoma. In a previous study it was shown that Farage cells expressed B-cell markers, but not membrane IgM. Karyotypic analysis showed that in contrast to most follicular cell lymphomas, Farage did not have the 14;18 chromosomal translocation. In the present work Farage was further characterized by Southern and Northern blot analyses. Two rearranged heavy chain alleles and one rearranged kappa chain gene were detected. The cells expressed both mu and kappa mRNA, even though at a 3-7 fold lower level than that found in the control Daudi and DG-75 Burkitt lymphomas. Farage cells did not express the terminal deoxynucleotydyl transferase gene (TdT), nor the recombination activating genes RAG-1 and RAG-2, known as markers of the pre-B cell stage. These results show that Farage represents a mature B-cell rather than a pre-B cell. Despite the presence of C kappa and C mu RNAs, no Ig polypeptide chains were produced by Farage as judged by immunoblotting and biosynthesis labeling assays. Ig mRNAs were detected on the polysomal fraction, but at a lower level relative to Daudi cells. Our combined results suggest that in Farage cells translation of Ig mRNA is not fully blocked at the stage of translation initiation. Farage cells may express "germline" or mutated variants of Ig mRNAs. The unusual phenotype of Farage may reflect a normal as yet unknown stage of B-cell differentiation, or it may be due to an aberrant expression developed after malignant transformation.

Animals↗

PubMed1995

Analysis of cell-mediated mineralization in culture of bone-derived embryonic cells with neurofibromatosis.

von Recklinghausen neurofibromatosis (NF1) is an autosomal dominant genetic disorder associated with congenital pseudoarthrosis and with short stature. To examine whether the NF1 phenotype includes functional osteogenic defects, embryonic bone-derived cells affected with NF1 were tested in culture for specific alkaline phosphatase (ALP) activity and cell-mediated mineralization and compared with other embryonic bone derived cells. NF1 showed a relatively higher specific ALP activity, which has further increased in response to dexamethasone + beta-glycerophosphate (beta GP) (Dex medium) coordinately with a decrease in cell proliferation. In In the control group, two samples showed increased ALP activity, one showed decreased activity and the forth one did not show any change in ALP. NF1 cells were distinguished from other cells regarding day 21 mineralization, they did not mineralize when cultured with ascorbate alone in the absence of Dex medium, whereas control cells did mineralize. Adding beta GP resulted in mineralization by NF1 cells but less than in other cells. In addition, NF1 cells responded to dexamethasone by increasing the beta GP-induced mineralization, as opposed to cells from other embryonic bones, which either did not respond or have even decreased mineralization under dexamethasone. Upon cis-hydroxyproline exposure, Dex medium has also distinguished NF1 cell ALP activity from that of other cell origins. Inhibition of respiratory complex II by malonate showed that most embryonic bone-derived cells of 12 weeks gestation are malonate resistant; thus, malonate selection was ineffective. This is in contrast to rat marrow stromal cells previously shown to undergo mineralizing cell enrichment in response to malonate. Exposure to levamisole, of Dex-treated cells, at days 0-11 has inhibited day 21 mineralization in all tested cultures in spite of the increase in day 11-specific ALP activity. Both malonate and levamisole did not distinguish NF1 cells from the osteogenic phenotype of other cells. Essentially embryonic bone-derived cells from 12 weeks gestation, cultured in the absence of beta GP, retained their mineralization capacity, which does not increase under dexamethasone, as distinguished from NF1 cells which require beta GP for mineralization and positively respond to dexamethasone. Therefore, bone-derived NF1 cells may be useful for studying the regulation of the mineralization process.

Alkaline Phosphatase↗

PubMed1995

Tyrphostins suppress the growth of psoriatic keratinocytes.

Tyrosine kinase inhibitors of the tyrphostin family which block EGF receptor kinase are reported to arrest the growth of psoriatic keratinocytes in vitro. Three tyrphostins with the potency ratio AG555 >> AG18 >> AG814 were found to arrest growth with no adverse cytotoxic effects. The potency ratio to inhibit keratinocyte proliferation follows their potency to inhibit EGF receptor kinase activity in vitro. These compounds represent novel leads for the therapy of psoriasis.

Benzylidene Compounds↗

PubMed1995

Demonstration of thymopoietin transcripts in different hematopoietic cell lines.

We have cloned and characterized the human thymopoietin (TP) coding region and studied the mRNA expression of this gene in different hematopoietic cell lines. The 150-bp PCR fragment that encodes the 49-amino-acid human TP peptide was isolated from genomic placental DNA. Its colinearity with the cDNA sequence suggests lack of introns within the coding region. TP mRNA expression was demonstrated in lymphocytes from all the differentiation stages investigated, as well as in a myeloid cell line (K-562). These findings suggest a further expansion of the proposed TP functions.

Amino Acid Sequence↗

PubMed1995

Tibial implant mineralization in rats is inversely related to serum osteogenic capacity.

In this study, the correlation between the mineralization of healing bone defects and the osteogenic capacity of the serum was tested in rats. The purpose of the study was to test the hypothesis that during callus formation, some serum factors are consumed. The bone defects in the tibia contained two different implant types, and all sustained juxta-implant fractures. One implant type was the coral Porites and the other was its recrystallized version (Interpore-200), which exhibit different mineralization rates during fracture healing. Use of these two implant types permitted generation of an expanded mineralization spectrum suitable for regression analysis. Mineralization was assessed by measuring the mineral content change (MCC) using dual-energy X-ray absorptiometry. Osteogenic capacity of sera of the implanted rats was assessed by its ability to increase specific alkaline phosphatase (ALP) activity in stromal cell cultures. The MCC was followed for 5 weeks in the Porites and Interpore-200 implants, and it was found that the MCC in Interpore-200 implants exceeded that of the Porites implants. Thus, the two implant types generated a wide mineralization spectrum. Induction of ALP in stromal cell culture was lower for sera derived from rats implanted with Interpore-200 than for sera derived from rats implanted with Porites. Two weeks after implantation, the change in serum ALP induction correlated inversely with the MCC of bone defects. This indicates that during callus formation, the mineralization rate is reciprocally related to the serum osteogenic capacity. The decreased serum osteogenic capacity may be interpreted by the hypothesis that callus formation consumes certain serum osteogenic factors.

Alkaline Phosphatase↗

PubMed1994

Cyclosporin A treatment failed to extend skin allograft survival in two burn patients.

Prolongation of skin allograft survival by immunosuppression of burn casualties has been reported sporadically during the past two decades. Recently cyclosporin A (CycA) has been used effectively for such an indication. We report here two paediatric patients with extensive burns (85-95 per cent BSA) treated with fresh, family-related skin allografts that were rejected during CycA treatment after 14-18 days. One of these children survived while the other died with candida sepsis.

Burns↗

PubMed1994

Familial hyperinsulinism maps to chromosome 11p14-15.1, 30 cM centromeric to the insulin gene.

Familial hyperinsulinism (HI) is the most common cause of persistent neonatal hyperinsulinaemic hypoglycemia. Linkage analysis in 15 families (12 Ashkenazi Jewish, 2 consanguineous Arab, 1 non-Jewish Caucasian) mapped HI to chromosome 11p14-15.1 (lod score = 9.5, theta = 0 at D11S921). Recombinants localized the disease locus to the 6.6 cM interval between D11S926 and D11S928. In Jewish families, association (p = 0.003) with specific D11S921/D11S419 haplotypes suggested a founder effect. This locus, which is important for normal glucose-regulated insulin secretion, represents a candidate gene for studies of other diseases of beta-cell dysfunction including non-insulin-dependent diabetes mellitus (NIDDM).

Chromosome Mapping↗

PubMed1993

Cross-reactions of anti-DNA autoantibodies with cell surface proteins.

Anti-DNA autoantibodies are thought to play a major role in the pathogenesis of systemic lupus erythematosus. However, the mechanism(s) by which they participate in tissue and organ damage is not well understood. It has been suggested that these antibodies combine with DNA or DNA-histone complexes to produce circulating immune complexes which may deposit in various tissues. Alternatively, anti-DNA autoantibodies could interact directly with tissue components by way of immunological cross-reaction. In this study we have used a panel of mouse monoclonal autoantibodies with anti-nuclear specificity and measured their binding to membrane proteins of several tissues and cell lines. We show that the anti-DNA antibodies, but not anti-RNA or anti-histone antibodies bind to membrane proteins of molecular weights 102, 80, 42, 35 and 31 kDa, which are expressed in different combinations on several cell types. The binding of anti-DNA antibodies to these cell surface proteins was not affected by DNase treatment of the target cells, was increased by DNase treatment of the antibody preparations and was completely inhibited by DNA, indicating a true cross-reaction and not an indirect interaction of antibody and membrane proteins through a DNA bridge. Our results suggest that direct binding of anti-DNA autoantibodies to cell surface membrane proteins may play an important role in the induction of the pleomorphic tissue damage in systemic lupus erythematosus.

Animals↗

PubMed1993

The effect of IL-4 on the phenotype of a human B-cell lymphoma line (Farage) lacking immunoglobulin expression.

Farage cells do not express surface immunoglobulins (sIg) but display a high level of CD19, CD21, CD22, CD23, CD39, CD40 B-cell antigens, and various adhesion proteins, such as CD11a (LFA-1), CD29 (VLA-4), CD44, CD54 (ICAM-1), and CD58 (LFA-3). The phenotype of Farage resembled that of EBV-LCL but differed from the phenotype of Burkitt's lymphoma lines, which were CD39- CD44-, expressed a high level of CD38, and either lacked CD21 or were weakly positive. Exposure to IL-4 augmented the concentrations of CD23 and of adhesion proteins on the surface of Farage cells but diminished the expression of CD21, CD22, and CD38. IL-4 did not induce the expression of sIg on Farage cells and failed to affect the level of HLA-DR. IL-2 and TPA did not alter the level of CD21 and adhesion proteins on Farage cells. Although IL-4 induced unique changes of the antigenic pattern in Farage, no significant effect on the phenotype of Burkitt's lymphoma lines was detected after IL-4 treatment. The present study indicates that the responsiveness of B cells to IL-4 is not determined by the expression of sIg but rather is associated with the antigenic profile characteristic for non-germinal center B lymphocytes.

Antibodies, Monoclonal↗