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At least 19 recordsLinked to original sources

PubMed1990

Functional human T cell-B cell hybridomas established from fusion of normal T cells and an EBV-transformed B cell line.

Human T cell-B cell hybridomas containing 92 chromosomes were derived by fusing normal stimulated CD-depleted T cells with the EBV-transformed human B cell line 729-HF. These hybridomas coexpressed the T cell surface markers CD3, CD8, and CD2 and the B cell surface antigens CD19, CD20, CD23, DR, and DQ. They weakly and variably expressed surface IgM and TCR. Genomic analysis revealed the presence of rearranged Ig genes as well as beta-T cell receptor genes that could be ascribed to the B and T cell parent, respectively. Analysis of TCR rearrangement suggests that the T-B hybridomas are, in fact, subclones of a single dominant clone. Although the hybrids expressed CD8 and not CD4, following preincubation with PWM, some the of clones induced IgG synthesis from normal B cells while the parent B cell line failed to demonstrate this activity. Stimulation of the hybridomas with PMA down-regulated the T cell lineage-specific antigen display (CD3, CD8, and TCR) and increased IgM production from the hybrids without changing B cell surface antigen display. These hybridomas may be useful to dissect the steps involved in the ultimate commitment of a cell to the B or T cell lineages and will be made available to interested investigators.

Antigens, CD↗

PubMed1992

Expression and distribution of CD11a/CD18 and CD54 during human T cell-B cell interactions.

Interactions between intercellular adhesion molecule 1 (ICAM-1, CD54) and leukocyte function-associated antigen 1 (LFA-1, CD11a/CD18) play a critical role in T cell-B cell collaboration. The current experiments were carried out to determine the expression and distribution of these adhesion molecules on human peripheral T cells and B cells during T cell-B cell collaboration. Resting CD4+ T cells were largely ICAM-1 negative, whereas immobilized anti-CD3 monoclonal antibody (mAb) rapidly induced ICAM-1 expression. By contrast, most B cells expressed ICAM-1 before activation, and further increases in density were noted with stimulation. Both B cells and CD4+ T cells expressed LFA-1 before activation, although the density on CD4+ T cells was considerably greater. A double staining method for electron microscopic analysis was developed that permitted analysis of the expression and distribution of ICAM-1 to be assessed during T cell-B cell collaboration. Under the experimental conditions examined, B cells showed a uniform distribution of ICAM-1. In contrast, ICAM-1 was highly mobile on the surface of CD4+ T cells. If the T cells were not fixed, staining, even at 4 degrees C, caused rapid redistribution of ICAM-1 into aggregates. However, by fixing cells before the staining procedures, the distribution of ICAM-1 on CD4+ T cells could be accurately assessed. Most (85%) of the fixed activated CD4+ T cells showed a uniform distribution of ICAM-1. However, when activated CD4+ T cells were cocultured with B cells, redistribution of ICAM-1 on CD4+ T cells but not B cells occurred, such that the majority (85%) was found at or immediately adjacent to the point of attachment to the B cells. No redistribution of LFA-1 on either T cells or B cells was found. These findings suggest that rapid changes in density of ICAM-1 expression and the mobility of ICAM-1 on activated T cells may play a role in providing activation signals to B cells during T cell-B cell collaboration.

Antigens, CD↗

PubMed1990

Production of cytokines by mouse B cells: B lymphomas and normal B cells produce interleukin 10.

We have examined a panel of murine Ly-1+ B lymphomas and purified normal murine peritoneal B cells separated into subsets on the basis of expression of the Ly-1 surface antigen, for their ability to produce cytokines. Where possible, we have used a combination of cytokine detection methods in order to compensate for differences in sensitivity and specificity, and the possibility of inhibitors masking an activity. All the lymphomas tested were shown to constitutively express TGF-beta and CSIF/IL-10. In addition, varying levels of IL-6, TNF-alpha and TNF-beta, and G-CSF, were demonstrable in most of the lymphomas, and variants of one lymphoma (CH12) additionally produced varying levels of IL-3, IL-4, and GM-CSF. FACS purified normal Ly-1+ and Ly-1- peritoneal B cells, were also shown to express RNA encoding CSIF/IL-10, IL-6, TNF-alpha and TNF-beta, and very low levels of G-CSF, following stimulation with LPS. These data were supported by the detection of IL-6 and CSIF/IL-10 in supernatants from LPS-stimulated Ly-1+ and Ly-1- B cells using specific immunoassays. None of the lymphomas or B cell preparations produced IL-1 alpha, IL-2, IL-5, IL-7, or IFN-gamma. The purity of our normal B cell populations was assessed by phenotypic analysis on the FACS and also by the disappearance of certain mRNA transcripts after purification, e.g. CD4, c-fms, GM-CSF, and IFN-gamma, most of which could be detected in LPS-stimulated total peritoneal cell populations. This suggested that our B cell purification method had reduced, to a level undetectable in our assays, contaminating T cells (CD4), macrophages (c-fms, GM-CSF), and NK cells (IFN-gamma). Absence of IL-3, IL-4, IL-5, and GM-CSF expression by LPS-stimulated Ly-1+ and Ly-1- B cells reduced the concern that contaminating peritoneal mast cells could account for the observed cytokine production. We therefore believe our data provide strong support for production of a subset of cytokines by LPS-stimulated normal B cells. Both the Ly-1+ B lymphomas and normal Ly-1+ and Ly-1- B cells appear capable of expressing IL-6, TNF-alpha, TNF-beta, and CSIF/IL-10.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1988

The requirement for surface Ig signaling as a prerequisite for T cell:B cell interactions. A possible role for desialylation.

Models for T cell:B cell collaboration suggest that activated B cells process and present Ag to Th cells which subsequently induce B cell proliferation and differentiation. In contrast to activated B cells, resting B cells have generally been shown to be less efficient APC. If this model of T:B collaboration is physiologically correct, then resting B cells must undergo a phenotypic change that permits effective interaction with T cells. In this report, the requirement for rapid signaling through surface Ig on resting B cells for the induction of T:B interaction was investigated with an in vitro clustering assay. Resting splenic B cells were unable to form specific conjugates with T cell clones, unless the B cells were first treated with neuraminidase to remove sialic acid. In contrast, LPS-activated B cells were able to form conjugates without prior treatment. The ability of antibody against LFA-1 or L3T4 to inhibit cluster formation depended on the state of B cell activation in that anti-LFA-1 and anti-L3T4 mAb inhibited cluster formation by neuraminidase-treated resting B cells, but not by LPS-activated B cells. In addition, Ag-specific B cells which were isolated by their capacity to bind specific Ag were able to form clusters without any additional treatment. Moreover, treatment of resting splenic B cells with anti-mu-antibody induced clustering potential in B cells in as little as 10 min, suggesting that signaling through surface Ig was sufficient to induce this phenotypic change in B cells. Furthermore, activation of protein kinase C and Ca2+ mobilization were shown to be involved in that PMA and ionomycin treatment were also able to induce clustering potential in resting B cells. The rapid induction of clustering potential in resting B cells after signaling through surface Ig may represent a fundamental change in B cell physiology which occurs after recognition of specific Ag and may be required for effective cognate recognition between resting hapten-specific B cells and carrier-specific T cells. The potential role of desialylation for the induction of T:B interaction is discussed.

Animals↗

PubMed1990

Epstein-Barr virus (EBV) antigens processed and presented by B cells, B blasts, and macrophages trigger T-cell-mediated inhibition of EBV-induced B-cell transformation.

The ability of B cells, B blasts, and macrophages to present Epstein-Barr virion antigens to autologous T cells and trigger their capacity to inhibit Epstein-Barr virus-induced B-cell transformation was tested. Macrophages were as efficient as B cells and B blasts in presenting the virus to T lymphocytes. This function required antigen processing, because it was inhibited by chloroquine treatment and by fixation of the antigen-presenting cells immediately after viral exposure but not 18 h later. T cells exposed to the purified Epstein-Barr virus envelope antigen gp350 coupled to immunostimulating complexes also showed inhibitory function. These results suggest that recognition of processed virion antigens elicits the generation of T-cell-mediated inhibition of Epstein-Barr virus-induced B-cell transformation.

Antigens, Viral↗

PubMed1988

Function and behavior of surface immunoglobulin receptors in antigen-specific T cell-B cell interaction.

The expression and function of surface immunoglobulin (sIg) receptors was analyzed using antigen-specific monoclonal B cells and T cells. When B cells were incubated with antigen (hapten carrier), hapten-specific sIg receptor expression was greatly reduced. The specific antigen-presentation activity of the B cells was also markedly reduced. Following the removal of antigen, expression of the sIg receptors was restored to original levels within 3-4 hr. Specific antigen-presentation activity of these B cells was concomitantly restored. Reduction of sIg receptor expression and specific antigen presentation were inhibited by the addition of competing free hapten, suggesting that crosslinking of sIg receptors is required for the observed changes in sIg receptor expression and that specific antigen presentation is hapten specific. Using oligopeptide-specific Th cells, we could show the requirement for processing of antigen in the interaction between hapten-specific B cells and carrier-specific T cells. These results indicated that the expression of sIg receptors for a specific antigen and the ability to present the antigen are interrelated.

Animals↗

PubMed1985

Role of membrane immunoglobulin (Ig) crosslinking in membrane Ig-mediated, major histocompatibility-restricted T cell-B cell cooperation.

Resting murine B lymphocytes can present rabbit anti-Ig to T cell lines specific for normal rabbit globulin. The T cell-B cell interaction is major histocompatibility complex (MHC)-restricted, and leads to activation, proliferation, and differentiation of the resting B cell into an antibody-secreting cell. Efficient antigen presentation and B cell activation depends upon binding of rabbit globulin to (membrane) mIg. To investigate the role of mIg in this polyclonal model for a T cell-dependent primary antibody response, we determined whether crosslinking of mIg is required either for efficient antigen presentation, as measured by helper T cell activation, or for the B cell response to T cell help, since all the direct effects of anti-Ig on B cells require crosslinking of mIg. We found that monovalent Fab' fragments of anti-IgM or anti-IgD work as efficiently as their divalent counterparts. Therefore, a signal transduced through the antigen receptor seems not to be required when T cell help is provided by an MHC-restricted T helper cell recognizing antigen on the B cell surface. Moreover, rabbit globulin bound to class I MHC molecules in the form of anti-H-2K also results in efficient antigen presentation and T cell-dependent B cell activation. However, mIg still appears to be specialized for antigen presentation, since anti-Ig is presented about three- to fivefold more efficiently than anti-H-2K.

Animals↗

PubMed1987

An antigen-specific T8+ human clone of cells with a nonspecific augmenting function on the T4 cell-B cell helper interaction.

We isolated a T8+ T3+ Ia+ clone of cells from the peripheral blood mononuclear cells of a healthy subject. The clone was expanded and maintained with autologous feeder cells, interleukin 2, and a streptococcal antigen. The T8+ clone of cells responded specifically to the streptococcal antigen, in the absence of accessory cells, and released a soluble factor. Both the cloned cells and the corresponding soluble factor expressed augmenting helper but not suppressor activity. The augmenting helper activity for B cell antibody synthesis was demonstrable only in the presence of autologous T4 cells. Although stimulation of the T8+ cloned cells was antigen-specific, the resulting soluble factor elicited nonspecific antibody synthesis in the presence of T4 and B cells. The T8+ cloned cell-derived factor was adsorbed by B cells but not by T4 cells. Preliminary studies suggest that the factor has the properties of a B cell growth factor. We suggest that the T8+ population consists of functionally heterogeneous cell subsets, some that have suppressor function and others that augment the T4+ helper-inducer activity in B cell antibody synthesis.

Antigen-Presenting Cells↗

PubMed1990

Human hematopoietic precursors in long-term culture: single CD34+ cells that lack detectable T cell, B cell, and myeloid cell antigens produce multiple colony-forming cells when cultured with marrow stromal cells.

CD34+ human marrow cells not expressing T cell-, B cell-, and myeloid cell-associated antigens (TBM-) were cloned by two-color cell sorting into culture wells containing irradiated marrow stromal cells. After 4 wk of culture, 3.7 +/- 2.1% of these cells generated colony-forming cells (CFC), with each of these cells generating 6.3 +/- 5.3 CFC. This was not due to the 0.5 +/- 0.5% CFC present in the purified CD34+ TBM- cells, as less than 1% of CFC persist in these cultures. This is the first demonstration that single immature precursor cells in human long-term cultures generate multiple CFC progeny. The immature nature of these clonable CD34+ TBM- precursors suggests their candidate status as human hematopoietic stem cells.

Antibodies, Monoclonal↗

PubMed1988

Artificial T cell:B cell conjugation. A unique approach to analyze weak cell-cell interactions.

An antibody response against a thymic-dependent Ag requires cognate recognition of the Ag by B and T cells. Functional T-B cell (T-B) interaction involves binding of Ag by B cell surface Ig, internalization and processing of Ag, expression of an Ag fragment in the context of Ia, binding of Ag/Ia by the TCR and binding of T cell-derived lymphokines by B cell lymphokine receptors. It is becoming increasingly evident that B and T cell accessory molecules also are involved in T-B interactions. To determine the role of accessory molecules in T-B collaboration, we have designed a system in which T-B interaction was artificially induced in the absence of carrier protein. TNP-modified, turkey gamma-globulin-specific, Th cells were allowed to form conjugates with TNP-specific B cells in the absence of hapten-carrier complex. Both B and T cells were induced to proliferate and B cells partially differentiated into antibody-secreting cells when B cells were cultured with TNP-modified but not unmodified T cells. The activation of B cells by TNP-modified T cells was not MHC restricted but was blocked by anti-Ia antibodies, suggesting a role for Ia distinct from Ag presentation. Furthermore, B cell proliferation was also inhibited by antibodies to L3T4 and LFA-1, suggesting a functional accessory role for these molecules in induction of B cell proliferation/differentiation.

Animals↗

PubMed1979

Enumeration of T cells, B cells and monocytes in the peripheral blood of normal and lymphocytotic cattle.

The rosette-forming capacity of bovine peripheral blood lymphocytes (PBL) was determined with dextran and 2-aminoethylisothiouronium bromide (AET)-treated sheep erythrocytes (SRBC). Both dextran and AET-enhanced rosette formation; however, AET-treated SRBC detected a larger percentage of rosette-forming cells and thus was used in this study. The specificity of rosette formation by bovine thymus-derived (T) lymphocytes was shown by (1) demonstration of rosettes and surface-membrane immunoglobulins sIg) on different cells in PBL and nylon-wool fractionated lymphocyte populations and (2) rosette formation by a large percentage (83--90%) of thymocytes from three bovine foetuses and two 14-month-old heifers. A procedure was also developed to identify bovine monocytes by latex phagocytosis and 10--30% latex-ingesting cells were detected in PBL preparations isolated by Ficoll-Hypaque flotation. The frequency of sIg-bearing latex-ingesting, and sIg-bearing latex non-ingesting cells in bovine peripheral blood was also determined. These procedures were utilized to determine the distribution of T and bone-marrow derived (B) lymphocytes in peripheral blood of normal and lymphocytotic cattle. PBL from twenty normal cattle contained approximately 63% T and 11% B (sIg+ latex non-ingesting) lymphocytes. In peripheral blood of three cattle with persistent lymphocytosis, a prodromal stage of bovine leukaemia, the percentage of B cells was elevated approximately to 59% whereas T lymphocytes decreased to 35%, thus providing additional evidence that persistent lymphocytosis is a B-cell disease.

Animals↗

PubMed1985

[E-RFC (T cells) and Ig-positive cells (B cells) in the peripheral blood of patients with lymphogranulomatosis and possible immunocorrection with levamisole].

Forty patients with Hodgkin's disease were examined for cell-mediated immunity. Analysis of peripheral blood showed a decrease in the relative and absolute E-RFU counts depending on the disease stages. The changes in B-cells bearing surface immunoglobulins were negligible. E-RFC (T-cells) prevailed in the spleen of patients with Hodgkin's disease. However, some of the patients had a high enough count of B-cells in the spleen and peripheral blood. Multiple modality treatment for Hodgkin's disease, radiation therapy in particular, aggravated disorders of cell-mediated immunity. Thirty-one patients received levamisole at the definite stages of multiple modality treatment with a purpose of correcting cell-mediated immunity disorders. Two schemes of levamisole intake were tried. The drug was given in a dose of 150 mg for 21 days, the total dose amounting to 3, 150 mg, or in a dose of 150 mg for 4 days with a 10-day interval, the total dose being 2, 100 mg. Only two patients noted side effects one of them had a "gas taste" in the mouth, whereas the other one skin itch and urticaria that did not require any treatment. Application of levamisole increased the relative and absolute E-RFU counts, absolute lymphocyte count. Patients on levamisole noted the improvement of the well-being.

Adjuvants, Immunologic↗

PubMedDate not supplied

High affinity specific binding of vasoactive intestinal peptide to human circulating T cells, B cells and large granular lymphocytes.

We studied the specific binding of vasoactive intestinal peptide (VIP) to circulating lymphocytes (PBL) of normal subjects using the interaction of 125I-VIP with different PBL fractions and flow cytometry to detect the binding of VIP-coated polystyrene spheres to individual cells of the fractions. Enhanced binding of 125I-VIP was found with T-enriched compared to unseparated or T-depleted PBL preparations. Both CD4 and CD8 T cell-enriched suspensions showed high binding capacity, but the affinity of CD4-enriched preparation for VIP was higher. VIP-coated spheres also bound to individual T cells of PBL, but only a minority of CD4 T cells (32%) and CD8 T cells (23%) bound the spheres. 125I-VIP also specifically bound to fractions enriched for large granular lymphocytes (LGL) and B cells. A consistent proportion of CD16 marker-positive LGL bound VIP-coated spheres (24%, and approximately 15% of B cells also showed this ability. Thus there is marked heterogeneity in the ability of different phenotypes of normal human circulating lymphocytes to recognize this neuropeptide.

B-Lymphocytes↗

PubMed1988

Bovine T cells, B cells, and null cells are transformed by the protozoan parasite Theileria parva.

The target cells for infection and transformation by Theileria parva were investigated. Peripheral blood mononuclear cells were reacted with monoclonal antibodies specific for bovine leukocyte differentiation antigens, sorted into subpopulations with a fluorescence-activated cell sorter, and infected in vitro with T. parva sporozoites. Infected cells were cultured at limiting dilution, and transformed clones were screened with monoclonal antibodies. The results indicated that B cells, T cells (including BoT4+ and BoT8+ cells), and null cells but not monocytes or neutrophils were transformed in vitro after infection with T. parva. After transformation, peripheral blood T cells and T-cell clones retained expression of most or all of the T-cell differentiation antigens including the mature T-cell marker recognized by monoclonal antibody IL-A27, BoT2, and BoT4 or BoT8, and some cells acquired a low level of expression of BoT4, BoT8, or the null cell marker recognized by monoclonal antibody IL-A29. T. parva-transformed null cells retained expression of the IL-A29 determinant and acquired expression of BoT2 and BoT8 but not the IL-A27 determinant or BoT4. T. parva-transformed B cells in most instances lost expression of surface immunoglobulin and never acquired expression of the IL-A27 determinant, BoT2, BoT4, or BoT8, although some cells acquired a low level of expression of the null cell marker recognized by monoclonal antibody IL-A29. Further studies on cell lines and clones grown in vitro from populations isolated from T. parva-infected cattle suggested that the majority of the in vivo T. parva-transformed cells were of T-cell origin.

Animals↗

PubMed1977

Complement-dependent and -independent pathways of T cell-B cell cooperation.

BDF1 mice treated with CoV had markedly reduced levels (less than 20%) of native serum C3 32 hr later, whereas the frequency of splenic CR+ cells was normal. CoV treatment before immunization reduced the IgM PFC response to a T-dependent antigen (TNP-SRBC) by more than 60%. Inclusion of highly specific anti-C3 antibody had no effect on the T-dependent IgM response of CR- B cells. The residual PFC responses in cultures of unfractionated spleen cells treated with anti-C3 could be largely or completely accounted for by CR- B cells in the cultures. The effect of anti-C3 antibody was not due to cytotoxicity. These data collectively indicate that the effect of CoV on T-dependent antibody responses is due to decreased C3 in serum rather than to interaction of C receptors directly with CoV or with C3 cleavage products. They suggest the existence of at least two distinct pathways of T-B cooperation, one in which C3 is an obligatory participant and another in which it may be uninvolved.

Animals↗

PubMed1985

T cell-B cell regulation in the intestinal lamina propria in Crohn's disease.

Many patients with Crohn's disease have suppressor T cells circulating in the peripheral blood that are potent inhibitors of immunoglobulin synthesis in vitro. The purpose of this study was to examine the regulatory effects of T cells isolated from the lamina propria of patients with Crohn's disease or of patients with other diseases. Lamina propria cells were isolated from surgically resected intestine by sequential ethylenediaminetetraacetic acid and collagenase incubations. T cells were purified from lamina propria either by anti-F(ab)2' affinity columns or by a panning technique using monoclonal anti-T cell antibodies. Changes in the pokeweed mitogen-stimulated synthesis of immunoglobulin M, immunoglobulin G, and immunoglobulin A by normal peripheral blood indicator lymphocytes, as measured by sandwich enzyme-linked immunosorbent assay, was used as an index of help and suppression. Helper T-cell activity was sought by coculturing lamina propria T cells with normal peripheral blood cells plus pokeweed mitogen. Helper T-cell activity was found among lamina propria T-cell populations of patients and controls to a roughly comparable extent; help was provided for all isotypes. Suppressor T-cell activity was sought by coculturing lamina propria T-cells with normal B cells plus irradiated normal T cells plus pokeweed mitogen. No significant suppressor T-cell activity was observed in these cocultures, whether the cells were obtained from control intestine, the grossly uninvolved margin of Crohn's disease intestine, or actively inflamed Crohn's disease intestine. We conclude that suppressor T-cell activity of the sort found previously in the peripheral blood of patients with Crohn's disease is not demonstrable in the intestinal lesions of Crohn's disease. Helper T-cell activity is the predominant regulatory activity in both control and inflamed intestinal lamina propria.

Adolescent↗

PubMed1976

Differentiation of lymphoid cells: B cell as a direct target and T cell as a regulator in lipopolysaccharide-enhanced induction of immunoglobulin production.

The cells involved in the stimulatory effect of bacterial lipopolysaccharide (LPS) on the induction of immunoglobulin (Ig) production by rabbit spleen cells cultured in the absence of antigen has been analyzed. Addition of LPS caused a several-fold enhancement of both DNA synthesis and Ig production. These enhanced activities were not significantly affected by depletion of adherent cells in the spleen cell population. Although inactivation of splenic T cells by anti-thymocyte serum (ATS) treatment did not affect the enhancement of DNA synthesis due to LPS, such treatment did adversely affect the enhancement of Ig production by LPS. Furthermore, the enhancement of Ig production of ATS-treated spleen cells by LPS was found to be dependent on the number of thymocytes added. In addition, the prior incubation of ATS-treated spleen cells with LPS resulted in effective enhancement of Ig production when such ATS-treated spleen cells and thymocytes were combined after removal of LPS. An identical experiment, except that thymocytes instead of ATS-treated spleen cells received the prior incubation with LPS, did not result in enhancement of Ig production. Finally, the enhanced Ig production due to LPS was inhibited by hydroxyurea, a known inhibitor of cellular DNA synthesis. The relationship between the mitogenic activity of LPS on B cells, the regulatory function of T cells, and the enhancement of Ig production by LPS is discussed in relation to the contrasting reports concerning the cellular target of LPS.

Animals↗

PubMed1987

Auranofin increases the affinity of phorbol dibutyrate receptors in chronic lymphocytic leukemia cells (B cells).

Previous studies have shown that auranofin (AF), a lipophilic gold I complex, modulates metabolic events in leukocytes stimulated by phorbol esters, whose major cellular binding site is now known to be the Ca++/phospholipid-dependent protein kinase (protein kinase C). In these experiments we have investigated the effect of AF on the binding of phorbol dibutyrate (PDBu) to human chronic lymphocytic leukemia (CLL) B cells. AF enhanced binding of PDBu to its receptor in CLL cells by a) causing an increase in the affinity of PDBu receptors from Kd 20.3 nM to 7.3 nM, and b) enhancing translocation of PDBu receptors to the cell membrane. The increase in PDBu binding induced by AF in whole cells was only partially reversible by EGTA or the intracellular Ca++ antagonist TMB-8. Studies performed with quin-2-labeled cells showed that 100 microM AF caused a mean (+/- SD) rise in cytosolic Ca++ levels from 0.41 (0.12) to 0.85 (0.33) (n = 5). Thus the mechanism by which AF increases binding of PDBu to its receptor appears to be partially dependent on Ca++. These effects of AF occurred at cellular levels achieved in mononuclear cells during chrysotherapy of patients with rheumatoid arthritis.

Auranofin↗