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M Sandor

Publications and source records attributed to M Sandor.

At least 19 recordsLinked to original sources
PubMed1998

A regulatory role for Fcgamma receptors CD16 and CD32 in the development of murine B cells.

Early in development, murine B-lineage progenitor cells express two classes of IgG Fc receptors (FcgammaR) designated as FcgammaRII (CD32) and FcgammaRIII (CD16), but mature B lymphocytes only express FcgammaRII (CD32), which functions as an inhibitor of B-cell activation when it is induced to associate with mIgM. The functions of CD16 and CD32 on B-lineage precursor cells have not previously been investigated. To search for FcgammaR functions on developing B-lineage cells, normal murine bone marrow cells were cultured in the presence of 2.4G2, a rat monoclonal antibody that binds to CD16 and CD32, or in the presence of control normal rat IgG, and then the B-lineage compartment was analyzed for effects. Cultures that contained 2.4G2 showed enhanced growth and differentiation of B-lineage cells compared with control cultures. The enhancing effect of 2.4G2 also occurred when fluorescence-activated cell-sorted B-cell precursors (B220(+), sIgM-, HSAhigh, FcgammaR+) from normal bone marrow were cocultured with BMS2, a bone marrow stromal cell line, but not when they were cultured in BMS2-conditioned media. The enhancement of B-lineage development induced by 2.4G2 was CD16-dependent and CD32-dependent, because 2.4G2 did not effect B-lineage growth or differentiation in cultures of bone marrow from mice in which either the gene encoding CD16 or CD32 had been disrupted. Analysis of fresh bone marrow from the CD16 gene-disrupted mice showed normal numbers and distribution of cells within the B-cell compartment, but in CD32 gene-disrupted mice, the B-cell compartment was significantly enlarged. These experiments provide several lines of evidence that the FcgammaR expressed on murine B-cell precursors can influence their growth and differentiation.

Animals↗
PubMed1998

IL-6-deficient mice form granulomas in murine schistosomiasis that exhibit an altered B cell response.

IL-6 can play an important role in various biological activities. Using IL-6-deficient, 129 x C57BL/6 mice and normal littermate controls, we studied the role of IL-6 in granulomas of mice infected with schistosomiasis mansoni. Granulomas from IL-6(+/+) mice produced large quantities of IL-6, derived from T, B, and myeloid cells. Yet, IL-6 mutant mice generated normal-appearing granulomas of appropriate size. Multiple-parameter flow cytometric analysis of dispersed granuloma cells revealed no substantial differences. Granuloma cells and splenocytes were cultured in vitro to measure cytokine and immunoglobulin production. Compared to control cells, IL-6(-/-) granuloma cells secreted more IL-4, IL-5, and IL-10. However, splenocytes secreted cytokines comparably. In the IL-6(-/-) state, the granuloma cells released less IgE and substantially more IgM, although IgG1, IgG2a, and IgA secretion remained normal. ELISPOT assay showed that dispersed granuloma cells from IL-6-deficient animals had substantially more IgM-secreting B cells. Thus, schistosome granulomas make IL-6 that is not essential for most aspects of granuloma development. However, IL-6 deficiency results in some disturbance of granuloma cytokine and immunoglobulin expression.

Animals↗
PubMed1998

Homing of transgenic gammadelta T cells into murine vaginal epithelium.

The vaginal epithelium of normal mice contains lymphocytes of fetal thymic origin that express an invariant Vgamma4/Vdelta1 TCR. The apparent lack of other gammadelta TCR species suggests that a selection mechanism might operate to regulate the localization of gammadelta T cells at this anatomical site. Selection might be connected to the Vgamma4/Vdelta1 TCR or to some homing characteristic of the fetal thymic lineage that appears at day 17-18 of embryonic life. In the present studies, we investigated whether transgenic gammadelta cells expressing a TCR species characteristic of the subpopulation of gammadelta T cells found in the blood, spleen and lymph would translocate to the vaginal epithelium. We found that the transgenic Vgamma2 TCR+ cells did accumulate in the vagina of transgenic mice. Furthermore, like normal vaginal gammadelta T cells, the transgenic vaginal gammadelta T cells expressed the phenotype of recently activated memory/effector T cells (CD44(hi), CD62L-, CD45RB(lo), CD69+). Vaginal gammadelta T cells in normal mice do not express the CD2 and CD28 antigens, but both of these markers are present on transgenic vaginal gammadelta T cells. We observed that a small fraction of splenic transgenic gammadelta T cells had the same surface phenotype as the vaginal transgenic gammadelta T cells, raising the possibility that the gammadelta T cells present in the vaginal epithelium of transgenic mice originated from the peripheral lymphoid organs. Data in support of this possibility came from experiments in which co-incubation of splenic transgenic gammadelta T cells with vaginal epithelial cell suspensions induced the vaginal gammadelta phenotype on the splenic gammadelta T cells. The finding of transgenic gammadelta T cells in the vaginal epithelium suggests that homing of gammadelta T cells to this site is not restricted to gammadelta T cells that express the V4/NS1 invariant TCR. Furthermore, these findings imply that retention of gammadelta T cells in the vaginal epithelium of normal mice is affected by a Vgamma4/Vdelta1-specific mechanism. The finding of a significant level of apoptosis in the transgenic vaginal gammadelta T cells, but not in the normal vaginal gammadelta T cells, could reflect that the mechanism of retention of Vgamma4/Vdelta1 + in the vaginal epithelium involves selective survival at the site.

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PubMed1997

Ontogeny of thymic NK1.1+ cells.

Thymic NK1.1+ cells are a recently described lymphocyte subset whose biologic function is not well defined. There is some controversy as to whether thymic NK1.1+ cells mature in a thymic or an extrathymic pathway. In this study, we examined the ontogeny of murine thymic NK1.1+ cells utilizing direct examination of freshly obtained fetal thymi as well as fetal thymi established in organ cultures (FTOC). We found a reproducible peak (5-40%) of NK1.1+ cells, demonstrable in day 15 to 16 freshly obtained fetal thymi, which was markedly decreased by day 17 of gestation; this peak preceded the appearance of the CD4+ CD8+ thymocytes by 12 to 24 h. Reverse-transcriptase PCR analysis of NK1.1 demonstrated its presence as early as day 9 of gestation, thus placing it as one of the earliest lymphocytic genes to be transcribed. Utilizing FTOC, we found that: 1) day 12 fetal thymi contained a progenitor that can differentiate into an NK1.1+ CD4+ CD8+ lymphocyte; 2) NK1.1+ cells dwindle to <5% in FTOC established from day 14 thymi; 3) NK1.1+ cells dominate in FTOC supplemented with IL-2; and 4) most of the NK1.1+ cells seen in FTOC did not express CD3epsilon on their surface, except for the FTOC supplemented with IL-12. These findings suggest that NK1.1+ cells may play an important role in thymic maturation. Moreover, these findings suggest that fetal thymi contain several novel lymphocyte subsets that can be induced to overgrow the normal thymocytes upon exposure to certain cytokines.

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PubMed1997

Fc gammaRII (CD32) is linked to apoptotic pathways in murine granulocyte precursors and mature eosinophils.

Murine granulocytes and precursors express low-affinity IgG Fc receptors (Fc gammaR). We investigated the effects of FcyR ligation on the development of eosinophils in cultures of normal murine bone marrow. Eosinophilopoiesis was induced by culture of bone marrow cells in the presence of cytokines (granulocyte-macrophage colony-stimulating factor [GM-CSF], interleukin-3 [IL-3], and IL-5). Addition to the cultures of 2.4G2, a rat monoclonal antibody (mAb) that reacts with Fc gammaRII (CD32) and Fc gammaRIII (CD16), induced granulocyte apoptosis within 24 hours. Granulocytes in cultures that contained 2.4G2 showed chromatin condensation, binding of Annexin-V, and fas induction, and by electron microscopy, apoptosis was most commonly observed in cells of the eosinophil lineage. Since murine granulocytes can express both Fc gammaRII (CD32) and Fc gammaRIII (CD16), we investigated the effect of 2.4G2 on cultures of bone marrow obtained from Fc gammaRIII (CD16) gene-disrupted mice and found that the apoptosis induced with 2.4G2 was CD16-independent. Studies with bone marrow cultures from B6MLR-lpr/lpr and C3H/HEJ-gld/gld mice established that the Fc gammaRII (CD32)-triggered apoptosis was fas-fasL-dependent. When mature eosinophils isolated from hepatic granulomas of Schistosoma mansoni-infected mice were cultured in cytokines in the presence of 2.4G2, the eosinophils underwent apoptosis within 24 hours. These findings identify a previously unknown linkage between Fc gammaR on eosinophils and fas-mediated apoptosis, a connection that could be relevant to mechanisms by which eosinophils mediate tissue injury and antibody-dependent cellular cytotoxicity reactions.

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PubMed1997

Lack of Fc-epsilon receptors on murine eosinophils: implications for the functional significance of elevated IgE and eosinophils in parasitic infections.

Chronic infection with Schistosoma mansoni induces in humans and mice a Th2-dominant immune response in which eosinophils and IgE are conspicuously elevated. Human eosinophils express IgE receptors that participate in an IgE-dependent eosinophil-mediated ADCC reaction against Schistosomula larvae in vitro. To investigate the expression of IgE receptors on murine eosinophils, they were purified (>95% pure by Giemsa-stained cytospin preparations) from liver granulomas of Schistosoma-infected mice. Flow cytometric analysis showed the absence of the low-affinity IgE receptor Fc-epsilon RII (CD23) and Mac-2 and the absence of binding of murine IgE. Reverse transcription-polymerase chain reaction (RT-PCR) analysis of granuloma eosinophil mRNA did not detect transcripts for Fc-epsilon RII or the alpha-chain of the high-affinity IgE receptor Fc-epsilon RI, but did detect transcripts that encode Mac-2 and the low-affinity IgG receptors Fc-gamma RIIb2, Fc-gamma RIII, and the FcR-associated gamma-chain. In vitro stimulation of granuloma eosinophils with interleukin-4 (IL-4) did not induce IgE binding, surface expression of Mac-2, or the transcription of Fc-epsilon receptors (Fc-epsilon RI, Fc-epsilon RII/CD23). To investigate normal murine eosinophils, we cultured normal mouse bone marrow cells with recombinant IL-3, recombinant IL-5, and recombinant granulocyte-macrophage colony-stimulating factor, conditions that promote eosinophil differentiation. Flow cytometric analysis of bone marrow-derived eosinophils failed to detect IgE binding or cell surface expression of Fc-epsilon RII and Mac-2, and RT-PCR analysis of fluorescence-activated cell sorted bone marrow-derived eosinophils failed to detect transcripts that encode Fc-epsilon RI or Fc-epsilon RII. These findings show that, in contrast to human eosinophils, murine eosinophils do not express cell surface receptors that bind IgE. However, because IgG receptors (Fc-gamma RIIb2, Fc-gamma RII) were present on eosinophils purified from granulomas, we investigated whether they might be involved in eosinophil activation. We found that an oxidative burst in eosinophils could be triggered through their IgG receptors.

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PubMed1997

Gamma delta T cells of the murine vagina: T cell response in vivo in the absence of the expression of CD2 and CD28 molecules.

While little is known about their activation requirements and function, the intraepithelial T cells of the murine vagina express TCR complexes in which the antigen recognition components and the signaling components have unusual features. These vaginal T cells express an invariant V gamma 4/V delta 1 TCR and appear to be the only intraepithelial gamma delta T cells that exclusively use FcR gamma chains in their TCR complex. To further characterize the vaginal gamma delta T cells we isolated them from normal mice and from mice injected systemically with an activation-inducing dose of anti-TCR mAb. The isolated gamma delta T cells were examined by flow cytometry for their surface expression of a panel of adhesion, proteins, activation antigens and cellular interaction molecules (CD44, CD62L, CD45RB, LFA-1, CD2 and CD28). The patterns of expression observed indicate that the vaginal gamma delta T cells of normal mice show the phenotype of effector T cells. The adhesion/co-stimulatory molecules CD28 and CD2 were not detected on vaginal gamma delta T cells, an interesting finding since the absence of CD2 from other T cells has been suggested to result in anergy. However, vaginal gamma delta T cells are responsive to TCR-mediated signals since injection of normal mice with pan-anti-TCR antibody or stimulating anti-gamma delta TCR antibody resulted in an increase in cell number and increased expression of transferrin and IL-2 receptors. These results indicate that vaginal gamma delta T cells might utilize other co-stimulatory molecules, if any, in connection with TCR-induced activation and differentiation. While the physiological function of vaginal gamma delta T cells remains unknown, the expression of an invariant V gamma 4/V delta 1 TCR, their exclusive use of gamma chain homodimers in their TCR, and the absence of CD2 and CD28 co-stimulatory molecules are a novel combination of properties that suggests specialized functional properties. Although vaginal gamma delta T cells share some features in common with gamma delta T cells that reside in other epithelial tissues, such as skin and intestine, the present studies provide additional evidence that vaginal gamma delta T cells are a highly specialized and distinct T cell population.

Animals↗
PubMed1996

The granulomatous response in murine Schistosomiasis mansoni does not switch to Th1 in IL-4-deficient C57BL/6 mice.

IL-4 plays an important role in polarizing inflammation toward a Th2 response. It remains uncertain, however, whether IL-4 also serves to prevent expression of Th1 inflammation. Therefore, using a genetically pure C57BL/6 IL-4-deficient mouse, we studied the role of IL-4 in regulating the production of IFN-gamma and Th1 inflammation in the granulomas of mice infected with Schistosoma mansoni. In contrast to normal animals, IL-4 mutant mice generated smaller liver granulomas that contained fewer eosinophils and no mast cells. Collagenase-dispersed granuloma cells were analyzed by flow cytometry and cultured in vitro to measure cytokine and Ig production. Compared with control granuloma cells, IL-4-/- cells secreted only small quantities of IL-5 and IL-10. Also, there was impaired expression of the IL-4-dependent molecules IgE and IgG1 as well as B cell surface class II and CD23. Yet the granulomas of IL-4 -/- animals produced little IFN-gamma, IgG2a, or other molecules associated with Th1 inflammation even after Ag or anti-CD3 stimulation. Splenocytes from IL-4 -/- animals stimulated with schistosome Ag also failed to produce a Th1 response. Our data show that most aspects of the Th2 response in murine schistosomiasis are highly dependent on IL-4 production. But in the absence of IL-4, neither the natural local granulomatous response to schistosome ova nor the systemic response to soluble egg Ag switches to the type 1 phenotype. Thus the production of IL-4 early in the inflammatory response is not the only factor preventing Th1 expression in inflammation.

Animals↗
PubMed1996

T cell vasoactive intestinal peptide receptor subtype expression differs between granulomas and spleen of schistosome-infected mice.

Granulomas form in the liver and intestines of mice infected with the parasite Schistosoma mansoni. Vasoactive intestinal peptide (VIP) is a neurokine that can modulate aspects of the immune response by acting through receptors within the granuloma. Cloned are two novel VIP receptor (VIPR) mRNAs (VIPR1 and VIPR2) that also bind a second neurokine called pituitary adenylated cyclase-activating polypeptide (PACAP). The objective of this study was to determine if granulomas express either VIPR1 or VIPR2. Using a radioligand-binding assay, it was established that PACAP is as effective as VIP at displacing radiolabeled VIP from splenocytes and granuloma cells, and that most if not all VIPRs in the spleen and granulomas bind PACAP. PCR amplification of reverse transcribed RNA determined that granulomas express both VIPR1 and VIPR2 mRNAs. Gel electrophoresis and nucleotide sequencing confirmed the authenticity of the PCR products. Also, both receptor subtypes were amplified from several granuloma CD4+ T cell lines; yet reverse transcribed RNA from T cell-depleted, dispersed granuloma cells had only VIPR1 RNA. It is notable that reverse transcriptase-PCR detected only VIPR1 in the thymus and spleen, which are organs rich in T lymphocytes. Thus, the granulomas and spleens from mice with schistosomiasis contain cells that display authentic VIP/PACAP receptors. Moreover, these data suggest that T cells in different compartments vary in VIPR subtype expression. VIPR1 and VIPR2 may have different physiologic roles in inflammation.

Animals↗
PubMed1996

Local suppression of IFN-gamma in hepatic granulomas correlates with tissue-specific replication of Leishmania chagasi.

BALB/c mice are susceptible to infection with the visceralizing species of Leishmania, Leishmania chagasi. The parasite load initially rises in the liver and spontaneously subsides, whereas parasite multiplication begins later and remains lower in the spleen. To investigate whether this organ-specific multiplication of L. chagasi correlates with localized immune responses, we compared cytokine production by splenic vs hepatic immune cells. Livers from infected mice contained granulomas harboring intracellular L. chagasi amastigotes, whereas few amastigotes were present in the spleen. FACS analysis granuloma cells showed granuloma lymphocytes expressed a memory/effector phenotype. Granuloma cells cultured in vitro produced IL-10 and IL-6 but no detectable IFN-gamma, IL-4 or IL-5. In contrast, splenocytes from the same animals secreted IFN-gamma, IL-4, IL-6, and IL-10. T cells were depleted from granuloma cells by immune lysis, and the results indicated that IL-10 and IL-6 were derived at least in part from a non-T cell compartment. Paradoxically, FACS-purified Thy-1+ granuloma lymphocytes were able to produce IFN-gamma in the absence of other granuloma cells, suggesting IFN-gamma production might usually be inhibited by a granuloma-associated non-T cell element. Coculture of splenocytes with either granuloma cells or supernatants from granuloma cultures inhibited the usual splenocyte production of IFN-gamma and IL-4 but not IL-10. Thus, there may be a unique granuloma-associated suppressive factor accounting for the absence of IFN-gamma in hepatic granuloma cultures. It may be the absence of IFN-gamma in the liver and presence in the spleen that allows or inhibits parasite survival, respectively, in these different locations.

Animals↗
PubMed1996

Editorial

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Journal Article↗
PubMed1996

Substance P receptor antagonist inhibits murine IgM expression in developing schistosome granulomas by blocking the terminal differentiation of intragranuloma B cells.

Schistosome granulomas make substance P (SP). CP96,345 is a nonpeptide SP receptor antagonist active in vivo. Granulomas that form in the presence of SP receptor blockade produce little IgM as compared to normal lesions. The objective of this study was to determine how CP96,345 modulates granuloma IgM production. Schistosome ova were embolized to the lungs of infected mice to induce granulomas of synchronous age. Animals received CP96,345 (50 mg/kg/day) for 4 days following egg embolization. Then granulomas were isolated from tissue and dispersed into single-cell preparations. The dispersed granuloma cells were cultured in vitro to measure IgM and cytokine secretion. Also, granuloma B cells were studied using an IgM ELISPOT assay and flow cytometry. As expected, mice treated with CP96,345 formed granulomas that secreted little IgM. Granulomas from CP96,345-treated mice, as compared to buffer-treated animals, contained few IgM-secreting B lymphocytes, but had appropriate numbers of B cells expressing surface IgM. Also decreased was the capacity of the granulomas to make IFN-gamma, IL-4, IL-5 and IL-6. CP96,345 treatment did not affect splenocyte IgM or cytokine synthesis. These data suggest that CP96,345 inhibits granuloma IgM secretion by blocking intragranuloma B cell maturation at a terminal stage of B cell differentiation. Moreover, SP receptor antagonist affects a variety of cytokine circuits that could influence IgM B cell maturation in vivo.

Animals↗
PubMed1996

Activation features of intraepithelial gamma delta T-cells of the murine vagina.

The epithelium of the murine vagina contains a resident population of gamma delta T-cells that expresses a homogenous Vgamma4/Vdelta1 TCR lacking N-region junctional diversity, implying that these T-cells recognize a very limited array of antigenic structures. The vaginal gamma delta T-cells express a pattern of surface markers characteristic of memory/effector T-cells that have previously been activated. Although vaginal gamma delta T-cells do not express the major costimulatory molecules CD28 and CD2, they do proliferate in response to a systemically delivered anti gamma delta TCR stimulus. Vaginal gamma delta T-cells contain mRNA that encodes the keratinocyte growth factor raising the possibility that these cells play a role in the repair of vaginal epithelium following injury. While the antigen recognized by the vaginal gamma delta TCR is unknown, a model is proposed which attempts to relate some of the unusual phenotypic features of vaginal gamma delta T-cells to the physiological injury and shedding of vaginal epithelium that occurs during the estrous cycle.

Animals↗
PubMed1996

Impaired IgG-dependent anaphylaxis and Arthus reaction in Fc gamma RIII (CD16) deficient mice.

The family of receptors for IgG (Fc gamma R) plays an essential role in antibody-mediated effector functions of the immune system. However, the specific contribution of each of the Fc gamma R classes to in vivo immune reactions is still unclear. Here, we demonstrate that mice deficient for the ligand-binding alpha chain of Fc gamma RIII lack NK cell-mediated antibody-dependent cytotoxicity and phagocytosis of IgG1-coated particles by macrophages. Strikingly, these mice lack IgG-mediated mast cell degranulation, are resistant to IgG-dependent passive cutaneous anaphylaxis, and exhibit an impaired Arthus reaction. These results indicate a prominent role for Fc gamma RIII in inflammatory and anaphylactic responses, making this receptor a potential target in immunotherapy.

Animals↗
PubMed1996

Cytokine secretion and adhesion molecule expression by granuloma T lymphocytes in Mycobacterium avium infection.

Mice experimentally infected with Mycobacterium avium develop a chronic disease characterized by widespread noncaseating granulomas. In this report, we describe the phenotype and cytokine secretion profile of these granuloma-infiltrating effector T lymphocytes. In response to specific antigen, granuloma T cells and, to a lesser extent, spleen cells secrete interferon-gamma, but no interleukin-4 or -5. The importance of this Th1-like response to the host was demonstrated by the massively increased bacterial load and lethal disease in interferon-gamma knockout mice. One function of localized cytokine secretion is to recruit inflammatory T cells bearing surface adhesion molecules complementary to counter-receptors on vascular endothelial cells. Granuloma T cells express high levels of these pro-inflammatory adhesion molecules but have down-regulated their expression of L-selectin (CD62L). The expression of these adhesion molecules on granuloma-infiltrating T lymphocytes would alter the migration pathway of these cells and is likely to be important in facilitating the traffic of effector T cells to the granulomatous inflammatory site. In addition, T cells from Schistosoma mansoni granulomas express the same set of adhesion molecules, showing that this phenotype is not specifically dependent upon the Th1 pattern of cytokine secretion.

Animals↗
PubMed1995

Two waves of gamma delta T cells expressing different V delta genes are recruited into schistosome-induced liver granulomas.

Isolated granulomas provide a unique model to study T cells in the site of inflammation. Schistosoma mansoni-infected mice develop liver granulomas in response to schistosome egg deposition and the granulomas contain gamma delta T cells that appear to be activated (Pgp-1high and L-selectin low). Analysis of kinetics and TCR gene usage of granuloma gamma delta T cells revealed a limited TCR repertoire restricted to V gamma 1.1, V delta 4, and V delta 6 genes, suggesting that the occurrence of gamma delta T cells in the granuloma is influenced by TCR V gene usage. The V delta 4+, but not the V delta 6+, gamma delta T cells expressed CD69, a marker of recent activation. To determine if there was a preferred order of accumulation of the gamma delta T cells in granulomas, s.c. sponge grafts were implanted into schistosome-infected mice, schistosome eggs were injected into the grafts, and accumulated T cells were sequentially analyzed. The earliest gamma delta T cell immigrants expressed V delta 6 and later immigrants expressed V delta 4 V genes. Additional evidence for a role of TCR specificity in the accumulation of gamma delta T cells in granulomas is their absence from schistosome granulomas in TCR transgenic mice that express only a single MHC-specific gamma delta TCR. Finally, gamma delta T cell recruitment into the granulomas did not require beta 2-microglobulin, since gamma delta T cells were present in liver granulomas of beta 2-microglobulin gene-disrupted mice. The analysis of the influx of gamma delta T cells into schistosome-induced, liver granulomas and schistosome egg-containing sponges provides a model system to investigate the role, if any, of gamma delta T cells in schistosome infections.

Animals↗
PubMed1995

The Fc epsilon RII/CD23 gene is actively transcribed during all stages of murine B-lymphocyte development.

It is generally accepted that the expression of Fc epsilon RII/CD23 on the surface of the B-lineage cells is restricted to the stage of the resting, mature (sIgM+/sIgD+) B-lymphocyte. However, it is unknown whether activation of the Fc epsilon RII/CD23 gene is also restricted to the stage of the mature B-lymphocyte. To address this question we investigated a panel of B-lineage cell lines for the presence of transcripts encoding Fc epsilon RII/CD23. We detected transcripts in 16 of 26 B-lineage cell lines representing the entire spectrum of B-cell development. In most cases (13 of 16) active transcription of the murine Fc epsilon RII/CD23 gene was not coupled with the expression of cell surface Fc epsilon RII/CD23 expression did not hold for all murine B-cell lines. One post-switch B-cell line (sIgM-/sIgG+) expressed Fc epsilon RII/CD23 on the cell surface and another could be induced with IL-4 and LPS to express surface Fc epsilon RII/CD23. Transcription of the murine CD23 gene in the absence of cell surface expression of Fc epsilon RII/CD23 does not appear to simply be an aberrant feature of transformed B-cells since we found transcripts, but not surface expression, in some normal splenic and peritoneal B-lymphocytes. Our findings suggest that the potential for expression of Fc epsilon RII/CD23 may occur over a much broader development window of the B-lineage than previously suspected. Transcription of the Fc epsilon RII/CD23 gene, in the absence of detectable cell surface protein expression in B-lineage cell lines, and in sort-purified B-lymphocyte subpopulations, implies that in addition to regulatory mechanisms already known, murine CD23 is also regulated through post-transcriptional mechanisms that have not yet been characterized.

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