Biomedical subjects

T Uede

Publications and source records attributed to T Uede.

At least 181 records · Page 10Linked to original sources

PubMed1987

[Vascular compression neuropathy of the optic nerve by sclerotic internal carotid artery].

Although mechanical compression of the optic nerve by a dilated and/or tortuous sclerotic intracranial internal carotid artery is occasionally reported as an etiology for impairment of vision and visual field, early diagnosis of such condition has been hampered by the lack of characteristic neuro-ophthalmological and neuroradiological findings. The review of 35 previously reported cases (60 eyes) including ours showed that 41% out of the 34 operated eyes were improved neurologically by the decompressive procedure, while it was in 27% out of the 26 undecompressed or non-operated eyes. These unsatisfactory operative results are considered mainly due to the failure of early diagnosis. In order to investigate the relationship between the carotid artery and optic nerve, we proposed a method of angiographical projection consisting of the straight view along the long axis of the optic canal. By this projection, it is possible to detect a supero-medial enlargement and/or dislocation of the cisternal portion of the internal carotid artery. The addition of metrizamide CT cisternography which clarifies the relationship of the optic nerve, chiasm and internal carotid artery in the supersellar cistern may further provide an useful clue for the diagnosis of this condition.

Aged↗

PubMed1986

Construction of rat-mouse T cell hybridomas that express regulatable rat interleukin 2 receptor.

Spleen cells obtained from Lewis rats were cultured with 4 micrograms/ml Con A for 96 hr, and activated cells were fused with BW5147 mouse T lymphoma cells. Seven clones obtained by fusion expressed rat IL 2R. The expression of rat IL 2R on those hybrid cells could be up-regulated by IL 2 itself, ATL-derived factor, and TPA and CA++ ionophore. Those IL 2R could be down-regulated by murine MoAb ART-18 that detects rat IL 2R. All hybrid clones produced IL 2 constitutively. IL 2 produced by hybrid cells bound to its receptor and promoted the proliferation of hybrid cells in some clones. Incubation of cells with exogenous IL 2 resulted in the proliferation of hybrid cells, whereas the proliferation of some clones was inhibited by exogenous IL 2, indicating that IL 2 had bifunctional properties on cell growth. Rat IL 2R from 6H2-F9 hybrid cells was studied by both one- and two-dimensional SDS-PAGE with ART-18. The IL 2R derived from 6H2-F9 cells had 72,000 to 77,000 and 40,000 to 48,000 m.w. major components under nonreducing conditions, and had 50,000 to 56,000 m.w. major and 35,000 to 38,000 m.w. minor components under reducing conditions. The 110,000 m.w. component, the third component of IL 2R, was constantly observed in 6H2-F9 hybrid cells.

Animals↗

PubMed1986

5C6-F4, a novel 100,000-dalton rat lymphocyte activation antigen defined by monoclonal antibody.

Con A-activated rat thymocytes were used to immunize mice, and immune spleen cells were fused with NS/1 myeloma cells. One clone, designated 5C6-F4, reacted strongly with Con A-activated rat thymocytes and some LPS-activated rat spleen cells but not with normal thymocytes, spleen cells, or bone marrow cells of rat origin. The 5C6-F4 did not react with Con A-activated thymocytes of mouse origin. Immunoprecipitation of 5C6-F4 antigen from surface-iodinated Con A-activated rat thymocytes or LPS-activated rat spleen cells revealed its m.w. to be approximately 100,000. The kinetic studies of the expression of 5C6-F4 antigen revealed that 5C6-F4 antigen was detectable at 6 hr after Con A stimulation of rat spleen cells, whereas IL 2 receptor (IL 2R) was detectable at 12 hr. The appearance of 5C6-F4 antigen and IL 2R precede the onset of DNA synthesis of Con A-activated spleen cells. Thus, 5C6-F4 antigen is classified as early activation antigen. The 5C6-F4 inhibits the lymphocyte proliferation induced by mitogen and the IL 2-driven rat T cell proliferation. Sequential immunoprecipitation study as well as binding inhibition study indicated that the 5C6-F4 antigen is distinct from IL 2R molecule. The 5C6-F4 antigen appears to be a novel rat lymphocyte activation antigen that exhibits immunoregulatory function and also may serve as a useful marker of T cell activation.

Animals↗

PubMed1986

Adherence of Lyme disease spirochetes to rat lymphocytes.

In the present work, the capacity of Lyme disease (LD) Spirochetes to spontaneously adhere to rat lymphocytes has been evaluated. Borrelia organisms adhere to thymus, spleen, Payer's patches and peripheral blood lymphocytes in a higher frequency than that observed with Salmonella minnesota R345 (Rb) used as reference strain. Employing enriched splenic T and B cell populations, Spirochete binding to B lymphocytes is more elevated than that obtained with Salmonella, while similar percentage of T cells forms rosettes with both microorganisms. Taken together, these findings provide evidence for a novel mode of interaction between LD Spirochetes and host immune system.

Animals↗

PubMed1986

Immunobiological and biochemical characterization of solubilized rat gliosarcoma cell tumor-associated transplantation antigens.

Tumor-associated transplantation antigen (TATA) was solubilized with n-butanol from rat gliosarcoma cells (T-9). Under the conditions used for the solubilization of TATA, the viability of T-9 cells was maintained above 85%, suggesting that the contamination of TATA with cytoplasmic protein is minimal. Normal Fischer rats were treated with 500 micrograms of n-butanol extract and inoculated with 2 X 10(6) viable T-9 cells. At 8 weeks after the inoculation of viable tumor cells, the tumor diameter was significantly smaller than that in control untreated rats. Rats treated with 770 micrograms of n-butanol extract from T-9 cells were inoculated with 1 X 10(7) syngeneic FTL-13 thymic lymphoma cells or T-9 cells. The rats rejected the T-9 cells, whereas the FTL-13 cells grew gradually until the host died, indicating that the n-butanol extract from T-9 cells contained T-9 cell-specific TATA. The n-butanol extract was characterized by chromatographic separation on a TSK gel G3000SW gel filtration column and a Mono Q anion exchange column with the fast protein liquid chromatography system (FPLC). The TATA of T-9 cells was found to have a molecular weight of approximately 40,000-70,000 and was eluted at 0.6-0.9M NaCl from the Mono Q column. The cellular mechanisms responsible for the rejection of T-9 cells in the rats treated with the n-butanol extract were also examined. Adoptive transfer and in vitro experiments demonstrated that helper T cells for the generation of cytotoxic T lymphocytes were generated in the rats treated with n-butanol extract.

Animals↗

PubMed1986

[Aneurysm of the anterior inferior cerebellar artery at the internal auditory meatus: report of two cases].

Aneurysm of the vertebrobasilar system is not a rare lesion but constituting 5-10% of all intracranial aneurysms. Aneurysm at the peripheral part of the anterior inferior cerebellar artery (AICA), however, is rare and only 20 cases have been reported previously. In this report, two cases of aneurysm arising at the junction between the AICA and internal auditory artery and extending into the internal auditory meatus are reported. The first patient was a 51-year-old male who was admitted because of sudden onset of dizziness, rt. tinnitus and deafness. Left vertebral angiograms demonstrated an AVM in the rt. cerebellar hemisphere and two aneurysms on the feeding arteries, one on the superior cerebellar artery and the other on the meatal loop of the rt. AICA. Removal of the AVM and neck clipping of the aneurysms, which were found unruptured, were performed through the rt. suboccipital approach. The second patient was a 42-year-old female who was admitted because of sudden onset of severe headache and vomiting followed by rt. tinnitus, deafness and double vision. CT scan showed subarachnoid clot mainly located in the rt. cerebellopontine angle. Repeated vertebral angiograms revealed an aneurysm at the meatal loop of the rt. AICA. Complete neck clipping was carried out. The clinical features of the aneurysms of this location can be divided into three subgroups according to the characters of onset: sudden onset with subarachnoid hemorrhage, insidious onset of the VII th, VIII th, nerve palsies by the mass effect of the aneurysm, intermittent episodes of the VIII th nerve disfunction due to the insufficiency of the internal auditory artery.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1986

[Pituitary abscess: report of two cases and a review].

Two cases of pituitary abscesses are reported. The first case was a 22-year-old female who was admitted with 14 months history of intermittent fever and headache followed by amenorrhea and polyuria. Plain craniograms showed no remarkable changes on the sella turcica. Direct coronal CT demonstrated a cystic lesion with a ring-like enhanced capsule in the pituitary complex with the apparent bulging of the pituitary top surface. On dynamic CT, the cystic lesion showed no remarkable increase in density. Transsphenoidal surgery was performed and a purulent materials was drained by cutting the underlying fibrous pituitary tissue. Pathological specimen revealed a marked inflammatory reaction around the degenerative pituitary gland. The second case was a 27-year-old female who underwent transsphenoidal excision of craniopharyngioma on May 12, 1983. Postoperatively she did well with the hormonal replacement therapy until 9 months after surgery when a follow up direct coronal CT revealed a cystic lesion with ring-like enhancement in the pituitary fossa. Purulent material was found at transsphenoidal surgery. Pathological specimen from the hard capsule was a chronic inflammatory fibrous tissue without tumorous component. Over seventy cases of pituitary abscesses have been reported previously, but the majority of them were secondary infections associated with systemic sepsis, chronic sphenoid sinusitis or pituitary tumors. Primary pituitary abscesses were rare and would be difficult to be diagnosed preoperatively without an aid of recent CT technology. Thirty cases in the literature since 1970 are reviewed and its clinical pictures and radiological findings are discussed.

Abscess↗

PubMed1986

[A case of pineal teratoma with intraventricular free fat seen in CT scan].

Detection of an intraventricular or intratumoral fat-fluid level on the plain craniograms has been known as a characteristic sign indicating the presence of intracranial teratomatous tumors. On CT scans, however, only thirteen cases have been previously reported to be found an intraventricular and/or subarachnoid free fat associated with spontaneous ruptures of these tumors. We reported a case of pineal teratoma with intraventricular free-fat seen on CT scans. A nine-year-old male with precocious puberty was admitted to our hospital complaining a moderate nonpulsatile headache. Neurological examinations were normal without signs of meningeal irritation. The serum and CSF titer of HCG were raised markedly. The laboratory data of the CSF were normal and there were no pathological cells in the CSF. The CT scans revealed a large heterogeneous mass containing multiple areas of negative density in the pineal region. There were negative density droplets in the bilateral frontal horn on the same CT scans indicating a presence of free fats. At surgery, an yellowish oily material was drained from the tumor, but there was no sign of meningitis over the cortical surface of the occipital lobe. An intraventricular free fat on CT scan have been reported in fourteen cases including ours following the first case described by Fawcitt in 1976. Although most of the cases presented headache, only two cases was diagnosed clinically as chemical meningitis. Pathological changes indicating granulomatous meningitis, however, were noted in five cases, all of them presenting seizure attacks.

Brain Neoplasms↗

PubMed1985

Construction of rat-mouse T-cell hybridomas that constitutively produce rat IL-2.

We have established rat-mouse T-cell hybridomas that constitutively produce rat Interleukin-2 (IL-2). T-cell hybridomas cannot be boosted to a higher level of IL-2 production by Con A stimulation. IL-2 prepared from T-cell hybridomas and from Con A activated rat spleen cells was partially purified using Ultrogel AcA 54 chromatography and ion exchange chromatography on Mono Q or chromatofocusing on Mono P. When analyzed on Mono P, IL-2 activity derived from IA2-B10 T-cell hybridoma eluted as a single peak with pH range 6.9-7.1, whereas IL-2 derived from Con A activated spleen cells resolved into four peaks within the following pH range: 7.1-7.2, 6.5-6.6, 6.1-6.2, and 5.6-5.7. Neuraminidase-treated IL-2 derived from Con A activated spleen cells resolved into single peaks appearing in the pH range 7.1-7.2. In contrast, neuraminidase treatment did not change the elution profile of IL-2 derived from the IA2-B10 hybridoma. IL-2 activity derived from the 3D6-B1 T-cell hybridoma also eluted as a single peak with the pH range 7.1-7.2. Neuraminidase treatment did not change the elution profile of IL-2. These data demonstrate that heterogeneity of IL-2 might be due to differences in the degree of glycosylation of IL-2 and differences in the sources of T-cells from which the IL-2 has derived.

Animals↗

PubMed1985

Presence of an antigen-specific T cell subset that forms IgE-suppressive factor and IgG-suppressive factor on antigenic stimulation.

B6D2F1 mice were given three i.v. injections of ovalbumin (OA), and antigen-specific T cell clones were established from their spleen cells. One of the FcR+ T cell clones formed IgE-binding factors on incubation with OA-pulsed syngeneic macrophages. Neither soluble antigen nor macrophages alone induced factor formation. T cell hybridomas were constructed by fusion of the antigen-specific T cell clone with BW 5147 cells. Among 11 T cell hybridomas established, six clones produced IgE-binding factors on incubation with OA-pulsed BDF1 macrophages. Mouse IgE also induced the same hybridoma to form IgE-binding factors. The majority of IgE-binding factors formed by two T hybridomas and by those produced by the parent T cell clone had affinity for peanut agglutinin but for neither lentil lectin nor Con A. These hybridomas and the original T cell clone spontaneously released glycosylation-inhibiting factor, which inhibits the assembly of N-linked oligosaccharide(s) on IgE-binding factors. On antigenic stimulation, the T cell hybridomas produced both IgE-binding factors and IgG-binding factors. The IgE-binding factors consisted of three species with m.w. of 60,000, 30,000, and 15,000. Both the 60K and 15K IgE-binding factors selectively suppressed the IgE response of DNP-OA-primed rat mesenteric lymph node cells, whereas IgG-binding factors selectively suppressed the IgG response. The results indicate that antigen-primed FcR+ T cells produced IgE-suppressive factors and IgG-suppressive factors on antigenic stimulation. However, the T cell hybridomas were not committed to suppressive activity. When the hybridomas were stimulated by antigen in the presence of glycosylation-enhancing factor (GEF), the 60K, 30K, and 15K IgE-binding factors formed by the cells selectively potentiated the IgE response. IgG-binding factors formed by the cells in the presence of GEF failed to suppress the IgG response. It appears that antigen-specific FcR+ T cells regulate the antibody response through the formation of Ig-binding factors, but that the function of the cells could be switched from suppression to enhancement, depending on the environment of the cells.

Animals↗

PubMed1985

A soluble factor distinct from interleukin 2 is involved in the generation and differentiation of cytotoxic T cells.

The involvement of cytotoxic cell-generating factor (CGF) in the generation of cytotoxic cells against syngeneic tumor (T-9) cells and in the rejection of the tumor cells has been investigated. It was found that Con A-sup (culture supernatant of concanavalin A-stimulated rat spleen cells) contained CGF, which was distinct from interleukin (IL) 2 and interferon. It should be noted that spleen cells produced CGF upon inoculation of syngeneic tumor cells into tumor-sensitized rats. Production of CGF preceded the appearance of cytotoxic cells against inoculated tumor cells. In these rats, the inoculated tumor was rejected. In contrast, spleen cells failed to produce CGF upon inoculation of tumor cells into normal rats; in these rats, cytotoxic cells were not detected and the inoculated tumor grew. These data suggested that CGF was produced as an in vivo response of the host immune system and was involved in the generation of cytotoxic T cells. CGF obtained from sensitized spleen cells was chromatographically separated from IL 1, IL 2, and colony-stimulating factor, and the chromatographically separated CGF did not contain IL 3 activity.

Animals↗

PubMed1985

Functional analysis of mononuclear cells infiltrating into tumors: differential cytotoxicity of mononuclear cells from tumors of immune and nonimmune rats.

A million syngeneic gliosarcoma (T-9) cells injected subcutaneously are sufficient to kill Fisher rats within 2 mo. Fisher rats became resistant to T-9 cells by surgical removal of the implanted tumor and repeated immunization with MMC-treated T-9 cells. Histopathologic studies revealed massive accumulation of mononuclear cells in tumor tissues of immune rats that were rejecting syngeneic T-9 tumors, whereas very few mononuclear cells were found in tumor tissues of nonimmune rats. Cell populations infiltrating into tumor tissues were identified by immunohistochemical techniques. Mononuclear cells found within the regressing tumors of immune rats were identified mostly to be T cells, and two-thirds of these T cells were OX-8 positive. In contrast, mononuclear cells found within the growing tumors of nonimmune rats were identified to be mixtures of macrophages and T cells, and very few OX-8 positive cells were found. Mononuclear cells were isolated from implanted T-9 tumors to determine whether mononuclear cells lysed T-9 cells specifically. Significant tumoricidal activity was seen when mononuclear cells from tumors of immune rats were used, whereas no detectable tumoricidal activity was observed with mononuclear cells from tumors of nonimmune rats. Winn assays confirmed in vitro 51Cr release assays by showing that tumors were rejected only when T-9 cells were implanted into normal Fisher rats along with mononuclear cells from tumors of immune rats.

Animals↗

PubMed1985

Establishment of rat-mouse T cell hybridomas that constitutively produce a soluble factor that is needed for the generation of cytotoxic cells: biochemical and functional characterization.

Spleen cells from Lewis rats were cultured with 4 micrograms/ml Con A. These cells were then fused with BW 5147 mouse T lymphoma cells. Two hybrid clones (6B2-B8 and 6B2-E6) obtained by fusion formed CGF effectively. It was found that hybrid cells can be boosted to produce higher levels of CGF upon stimulation with Con A. 6B2-B8 express rat T cell markers. CGF formed by 6B2-B8 had a m.w. of 23,000 and 40,000. CGF was eluted from a Mono Q anion-exchange column with an FPLC system at 0.4 to 0.6 M NaCl as a major peak and at 0.8 M NaCl as a minor peak. CGF was eluted as three peaks with pH 4.1, 4.8, and 5.2 from a Mono P chromatofocusing column. CGF from 6B2-B8 does not contain IL-1, IL-2, IL-3, or CSF.

Animals↗

PubMed1985

Functional analysis of mononuclear cells infiltrating into tumors. II. Differential ability of mononuclear cells obtained from various tissues to produce helper factors that are involved in the generation of cytotoxic cells.

The requirement of CGF in the generation of cytotoxic cells against syngeneic tumor cells (T-9) and in the rejection of transplanted T-9 cells has been investigated. Spleen cells obtained from sensitized rats showed strong cytotoxicity against 51Cr-labeled T-9 cells upon incubation with CGF for 48 hr. Human recombinant IL 2 and rat IFN failed to generate cytotoxic cells from spleen cells of sensitized rats. CGF are produced by spleen cells upon inoculation of T-9 cells into sensitized rats as a host in vivo immune response. Production of CGF preceded the appearance of cytotoxic cells in regional lymph node and tumor tissues. In those rats, inoculated tumor cells were eventually rejected. In contrast, spleen cells failed to produce CGF upon inoculation of T-9 cells in unsensitized rats. Cytotoxic cells were not detected in unsensitized rats, and inoculated tumor grew in those rats. Thus, CGF is likely to be involved in the generation of cytotoxic cells and in the rejection of inoculated syngeneic tumor cells. A Mono Q anion-exchange column with an FPLC system allowed the chromatographic separation of CGF from IL 1, IL 2, IL 3, and CSF.

Animals↗

PubMed1984

Presence of an antigenic determinant common to rat IgE-potentiating factor, IgE-suppressive factor, and Fc epsilon receptors on T and B lymphocytes.

Polyclonal antibodies against purified IgE-potentiating factor were prepared in guinea pigs, and mouse monoclonal antibodies were prepared against inactive IgE-binding factor from a T cell hybridoma. The polyclonal antibodies and two of the monoclonal antibodies bound the IgE-potentiating factor, the IgE suppressive factor, and the inactive IgE-binding factor. The results indicate that the three IgE-binding factor molecules share a common antigenic determinant. The polyclonal antibodies and the monoclonal antibody bound intracellular IgE-binding factors that did not have affinity for either lentil lectin or peanut agglutinin, which suggests that the antibodies were directed against the peptide portion of IgE-binding factors. Pretreatment of Fc epsilon R+ T hybridoma cells and Fc epsilon R+ B cells with either the monoclonal or the polyclonal anti-IgE-binding factor (anti-IgE-bF) antibody prevented rosette formation of the cells with IgE-coated erythrocytes, whereas the same treatment failed to affect rosette formation of Fc gamma R+ cells with IgG-coated erythrocytes. Specific binding of the guinea pig anti-IgE-bF antibodies to Fc epsilon R on both B and T cells was confirmed by immunofluorescence. The results indicate that Fc epsilon R on B and T cells share a common antigenic determinant with IgE-binding factors. The F(ab')2 fragments of the guinea pig anti-IgE-bF induced the expression of Fc epsilon R on Fc gamma R+ lymphocytes and the formation of IgE-binding factors. The capacities of not only IgE, but also anti-IgE-bF, to induce both Fc epsilon R expression and IgE-binding factor formation indicate that Fc epsilon R on lymphocytes, rather than IgE, transmit the signal for the formation of IgE-binding molecules.

Animals↗

PubMed1984

IgE-binding factors from mouse T lymphocytes. III. Role of antigen-specific suppressor T cells in the formation of IgE-suppressive factor.

BDF1 mice were given three i.v. injections of ovalbumin (OA) to induce antigen-specific suppressor T cells. Incubation of spleen cells of OA-treated mice with homologous antigen resulted in the formation of IgE-suppressive factor. This factor was not derived from antigen-specific suppressor T cells, but suppressor T cells were essential for determining the nature of IgE-binding factors formed. In the spleen cells of OA-treated mice, antigenic stimulation of antigen-primed Lyt-1+ (helper) T cells resulted in the formation of inducers of IgE-binding factor, whereas Lyt-2+, I-J+ T cells released glycosylation-inhibiting factor (GIF), and these two factors, in combination, induced unprimed Lyt-1+ T cells to form IgE-suppressive factor. The role of GIF is to inhibit the assembly of N-linked oligosaccharides on IgE-binding factors during their biosynthesis, and thereby provide them with a biologic activity: suppression of the IgE response. Under the experimental conditions employed, GIF was released spontaneously from antigen-specific suppressor T cells. However, antigenic stimulation of the cells enhanced the release of the factor. GIF from antigen-specific suppressor T cells has a m.w. of 25,000 to 30,000, as estimated by using gel filtration, binds to anti-I-J alloantibodies and to a monoclonal antibody specific for lipomodulin, and has affinity for specific antigen. The possible relationship between antigen-specific GIF and antigen-specific suppressor factors is discussed.

Animals↗

PubMed1984

[An autopsy case of extramedullary plasmacytoma with systemic dissemination 2 years after the onset of a localized tumor in the nasal cavity].

A 73-year-old male was admitted because of a localized tumor in the nasal cavity, which was suspected to be malignant lymphoma by biopsy specimens. Laboratory findings were within normal limits except for small amounts of M protein (IgG-lambda) in the serum. The patient was successfully treated by radiotherapy, with the disappearance of both the tumor and M protein. Two years after the onset, however, a solid tumor was observed in the soft tissue, followed by rapid systemic dissemination. An increase in M protein was obvious, and the biopsy specimens disclosed plasmacytoma. The patient died three months after admission, and post-mortem examinations revealed a diffuse infiltration of plasmacytes predominantly in the soft tissues.

Aged↗

PubMed1984

IgE-binding factors from mouse T lymphocytes. II. Strain differences in the nature of IgE-binding factor.

Normal spleen cells from high IgE responder, BDF1 mice, formed IgE-potentiating factor upon incubation with mouse IgE, whereas those from low IgE responder, SJL mice, formed IgE-suppressive factor. The majority of the factors from BDF1 spleen cells had affinity for lentil lectin; those from SJL mice lacked affinity for the lectin. BDF1 spleen cells could be switched, however, to form IgE-suppressive factor if the cells were incubated with IgE in the presence of lipomodulin , a phospholipase inhibitory protein. In contrast, SJL spleen cells could form IgE-potentiating factor in the presence of lysolecithin, which enhances the glycosylation of IgE-binding factors. When the two strains were primed with alum-absorbed ovalbumin and their spleen cells were stimulated with homologous antigen, IgE-binding factors were detected in culture filtrates. The factors formed by BDF1 spleen cells selectively potentiated the IgE response, however, whereas those formed by SJL spleen cells selectively suppressed the response. Analysis of the cellular mechanisms for the selective formation of IgE-potentiating factor by antigen-primed BDF1 spleen cells revealed that antigenic stimulation of Lyt-1+ T cells resulted in the formation of two T cell factors, i.e., an "inducer" of IgE-binding factor and a glycosylation-enhancing factor, and that these factors induced the selective formation of IgE-potentiating factor. In SJL spleen cells, antigenic stimulation of Lyt-1+ T cells resulted in the formation of an "inducer" and a glycosylation-inhibiting factor, and those factors in turn stimulated the formation of IgE-suppressive factor. An additional difference between the two strains was found in Fc gamma R+ Ly-1+ T cells that were the cell source of IgE-binding factors. Upon stimulation with IgE or "inducer", BDF1 Lyt 1+ cells formed IgE-potentiating factor, whereas the same subset of T cells from SJL mice formed IgE-suppressive factor. The results indicate that the genetic differences between the two strains with respect to the nature of IgE-binding factors appear to be expressed in the process of glycosylation of IgE-binding factors.

Animals↗