scholarly journals Clonal deletion of postthymic T cells: veto cells kill precursor cytotoxic T lymphocytes.

1992 ◽  
Vol 175 (3) ◽  
pp. 863-868 ◽  
Author(s):  
K Hiruma ◽  
H Nakamura ◽  
P A Henkart ◽  
R E Gress
Keyword(s):  
Bone Marrow ◽  
T Cell ◽  
Bone Marrow Cells ◽  
High Dose ◽  
Spleen Cells ◽  
Clonal Deletion ◽  
Veto Cells ◽  
Veto Cell ◽  
Marrow Cells ◽  
Ctl Responses

Veto cell-mediated suppression of cytotoxic T lymphocyte (CTL) responses has been proposed as one mechanism by which self-tolerance is maintained in mature T cell populations. We have previously reported that murine bone marrow cells cultured in the presence of high-dose interleukin 2 (IL-2) (activated bone marrow cells [ABM]) mediate strong veto suppressor function. To examine mechanisms by which ABM may suppress precursor CTL (p-CTL) responses, we used p-CTL generated from spleen cells of transgenic mice expressing a T cell receptor specific for H-2 Ld. It was demonstrated that the cytotoxic response by these p-CTL after stimulation with irradiated H-2d/k spleen cells was suppressed by DBA/2 (H-2d) ABM, but not by B10.BR (H-2k) ABM or dm1 (Dd, Ld mutant) ABM. Flow cytometry analysis with propidium iodide staining revealed that these p-CTL were specifically deleted by incubation with H-2d ABM, but not with H-2k ABM. These data indicate that ABM veto cells kill p-CTL with specificity for antigens expressed on the surface of the ABM, and that the mechanism for veto cell activity of ABM is clonal deletion of p-CTL.

scholarly journals Bisecting GlcNAc structure is implicated in suppression of stroma-dependent haemopoiesis in transgenic mice expressing N-acetylglucosaminyltransferase III

1998 ◽  
Vol 331 (3) ◽  
pp. 733-742 ◽  
Author(s):  
Masafumi YOSHIMURA ◽  
Yoshito IHARA ◽  
Tetsuo NISHIURA ◽  
Yu OKAJIMA ◽  
Megumu OGAWA ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Transgenic Mice ◽  
Stromal Cells ◽  
Bone Marrow Cells ◽  
Adherent Cell ◽  
Wild Type ◽  
Spleen Cells ◽  
Bisecting Glcnac ◽  
Marrow Cells

Several sugar structures have been reported to be necessary for haemopoiesis. We analysed the haematological phenotypes of transgenic mice expressing β-1,4 N-acetylglucosaminyltransferase III (GnT-III), which forms bisecting N-acetylglucosamine on asparagine-linked oligosaccharides. In the transgenic mice, the GnT-III activity was elevated in bone marrow, spleen and peripheral blood and in isolated mononuclear cells from these tissues, whereas no activity was found in these tissues of wild-type mice. Stromal cells after long-term cultures of transgenic-derived bone marrow and spleen cells also showed elevated GnT-III activity, compared with an undetectable activity in wild-type stromal cells. As judged by HPLC analysis, lectin blotting and lectin cytotoxicity assay, bisecting GlcNAc residues were increased on both blood cells and stromal cells from bone marrow and spleen in transgenic mice. The transgenic mice displayed spleen atrophy, hypocellular bone marrow and pancytopenia. Bone marrow cells and spleen cells from transgenic mice produced fewer haemopoietic colonies. After lethal irradiation followed by bone marrow transplantation, transgenic recipient mice showed pancytopenia compared with wild-type recipient mice. Bone marrow cells from transgenic donors gave haematological reconstitution at the same level as wild-type donor cells. In addition, non-adherent cell production was decreased in long-term bone marrow cell cultures of transgenic mice. Collectively these results indicate that the stroma-supported haemopoiesis is compromised in transgenic mice expressing GnT-III, providing the first demonstration that the N-glycans have some significant roles in stroma-dependent haemopoiesis.

scholarly journals Differential Effects of IL-2 and IL-6 on the Development of Three Distinct Precursor T-Cell Populations in the Thymus

1990 ◽  
Vol 1 (2) ◽  
pp. 77-84 ◽  
Author(s):  
Naoko Nakano ◽  
Hitoshi Kikutani ◽  
Tadamitsu Kishimoto
Keyword(s):  
Bone Marrow ◽  
T Cell ◽  
Bone Marrow Cells ◽  
Cell Populations ◽  
High Dose ◽  
Transfer System ◽  
Cell Sorter ◽  
Lineage Markers ◽  
Low Levels ◽  
Normal Differentiation

Three distinct T-cell precursors: bone marrow cells that express low levels of the Thy-1 antigen but no lineage markers (Thy-1-lo/BM); CD4-, CD8-, and CD3-thymocytes that express low levels of the Thy-1 antigen (Thy-1-lo/Thym); and CD4-, CD8-, and CD3-thymocytes that express high levels of the Thy-1 antigen and the IL-2 Rαchain (Thy-1+/ IL2R+) were isolated by fluorescence-activated cell sorter (FACS). These three populations expanded with different kinetics in the thymus of irradiated recipient mice after intrathymic transfer. When a high dose of human recombinant IL-2 (r-IL-2) or human recombinant IL-6 (r-IL-6) was administered, r-IL-6 accelerated donor Thy-1+/IL2R+to differentiate, whereas r-IL-2 blocked normal differentiation and expansion of donor Thy-1-lo/Thym, but did not show any significant effect on donor Thy-1+/IL2R+. Neither r-IL-2 nor r-IL-6 worked directly on donor Thy-1-lo/BM in this transfer system.

scholarly journals In vivo modulation of myelopoiesis by prostaglandin E2. III. Induction of suppressor cells in marrow and spleen capable of mediating inhibition of CFU-GM proliferation

Blood ◽  
1988 ◽  
Vol 71 (6) ◽  
pp. 1633-1640
Author(s):  
LM Pelus ◽  
PS Gentile
Keyword(s):  
Bone Marrow ◽  
Monoclonal Antibodies ◽  
Steady State ◽  
Prostaglandin E2 ◽  
Bone Marrow Cells ◽  
Suppressor Cells ◽  
Spleen Cells ◽  
Granulocytic Differentiation ◽  
Marrow Cells

Intravenous (IV) injection of 0.1 to 10 micrograms of authentic prostaglandin E2 (PGE2) in intact steady-state mice induces a population of bone marrow and spleen cells having the capacity to suppress CFU-GM proliferation when admixed with normal bone marrow cells. Equivalent suppression of CFU-GM committed to monocytic as well as granulocytic differentiation was observed using colony-stimulating factors (CSFs) differing in their lineage specificities and by direct morphological analysis of proliferating clones. Kinetic analysis indicates that suppressive bone marrow cells appear within 2 hours after PGE2 injection, are maximal at 6 hours, and are no longer observed by 24 hours postinjection. Positive and negative selection studies using monoclonal antibodies indicate that the PGE2-induced suppressor cells react positively with anti-GMA 1.2, MAC1, and F4/80 monoclonal antibodies, suggesting a myeloid/monocytic origin. As few as 1,000 positively selected bone marrow or spleen cells were able to inhibit maximally normal CFU-GM proliferation by 50,000 control bone marrow cells. Suppression of normal CFU-GM can be substituted for by 24- hour cell-free supernates from unseparated bone marrow cells or GMA 1.2 or F4/80 positively selected marrow or spleen cells from PGE2-treated but not control mice. These supernates also inhibited BFU-E proliferation. Injection of as few as 2 million bone marrow cells from PGE2-treated mice into steady-state mice or animals hematopoietically rebounding following a sublethal injection of cyclophosphamide significantly suppressed total CFU-GM proliferation in recipient mice within 6 hours. In summary, these studies describe the detection of a novel hematopoietic control network induced by PGE2 in intact mice.

scholarly journals Irradiation-Mediated Rescue of T Cell–Specific V(D)j Recombination and Thymocyte Differentiation in Severe Combined Immunodeficient Mice by Bone Marrow Cells

1999 ◽  
Vol 190 (9) ◽  
pp. 1257-1262 ◽  
Author(s):  
Chiyu Wang ◽  
Molly A. Bogue ◽  
Jonathan M. Levitt ◽  
David B. Roth
Keyword(s):  
Bone Marrow ◽  
T Cell ◽  
T Cell Receptor ◽  
T Lymphocyte ◽  
Bone Marrow Cells ◽  
Cell Lineage ◽  
Cell Receptor ◽  
Immunodeficient Mice ◽  
Thymocyte Differentiation ◽  
Marrow Cells

In SCID (severe combined immunodeficient) mice, proper assembly of immunoglobulin and T cell receptor (TCR) genes is blocked by defective V(D)J recombination so that B and T lymphocyte differentiation is arrested at an early precursor stage. Treating the mice with gamma irradiation rescues V(D)J rearrangement at multiple TCR loci, promotes limited thymocyte differentiation, and induces thymic lymphomas. These effects are not observed in the B cell lineage. Current models postulate that irradiation affects intrathymic T cell precursors. Surprisingly, we found that transfer of irradiated SCID bone marrow cells to unirradiated host animals rescues both TCR rearrangements and thymocyte differentiation. These data indicate that irradiation affects precursor cells at an earlier stage of differentiation than was previously thought and suggest new models for the mechanism of irradiation rescue.

scholarly journals In vivo modulation of myelopoiesis by prostaglandin E2. III. Induction of suppressor cells in marrow and spleen capable of mediating inhibition of CFU-GM proliferation

Blood ◽  
1988 ◽  
Vol 71 (6) ◽  
pp. 1633-1640 ◽  
Author(s):  
LM Pelus ◽  
PS Gentile
Keyword(s):  
Bone Marrow ◽  
Monoclonal Antibodies ◽  
Steady State ◽  
Prostaglandin E2 ◽  
Bone Marrow Cells ◽  
Suppressor Cells ◽  
Spleen Cells ◽  
Granulocytic Differentiation ◽  
Marrow Cells

Abstract Intravenous (IV) injection of 0.1 to 10 micrograms of authentic prostaglandin E2 (PGE2) in intact steady-state mice induces a population of bone marrow and spleen cells having the capacity to suppress CFU-GM proliferation when admixed with normal bone marrow cells. Equivalent suppression of CFU-GM committed to monocytic as well as granulocytic differentiation was observed using colony-stimulating factors (CSFs) differing in their lineage specificities and by direct morphological analysis of proliferating clones. Kinetic analysis indicates that suppressive bone marrow cells appear within 2 hours after PGE2 injection, are maximal at 6 hours, and are no longer observed by 24 hours postinjection. Positive and negative selection studies using monoclonal antibodies indicate that the PGE2-induced suppressor cells react positively with anti-GMA 1.2, MAC1, and F4/80 monoclonal antibodies, suggesting a myeloid/monocytic origin. As few as 1,000 positively selected bone marrow or spleen cells were able to inhibit maximally normal CFU-GM proliferation by 50,000 control bone marrow cells. Suppression of normal CFU-GM can be substituted for by 24- hour cell-free supernates from unseparated bone marrow cells or GMA 1.2 or F4/80 positively selected marrow or spleen cells from PGE2-treated but not control mice. These supernates also inhibited BFU-E proliferation. Injection of as few as 2 million bone marrow cells from PGE2-treated mice into steady-state mice or animals hematopoietically rebounding following a sublethal injection of cyclophosphamide significantly suppressed total CFU-GM proliferation in recipient mice within 6 hours. In summary, these studies describe the detection of a novel hematopoietic control network induced by PGE2 in intact mice.

scholarly journals Influence of Cell Treatment with PDGF-BB and Reperfusion on Cardiac Persistence of Mononuclear and Mesenchymal Bone Marrow Cells after Transplantation into Acute Myocardial Infarction in Rats

2009 ◽  
Vol 18 (8) ◽  
pp. 847-853 ◽  
Author(s):  
Benjamin Krausgrill ◽  
Marius Vantler ◽  
Volker Burst ◽  
Martin Raths ◽  
Marcel Halbach ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Bone Marrow ◽  
Bone Marrow Cells ◽  
Cell Loss ◽  
Border Zone ◽  
High Dose ◽  
Myocardial Repair ◽  
Intramyocardial Injection ◽  
Rat Hearts ◽  
Marrow Cells

Bone marrow cells are used for cell therapy after myocardial infarction (MI) with promising results. However, cardiac persistence of transplanted cells is rather low. Here, we investigated strategies to increase the survival and cardiac persistence of mononuclear (MNC) and mesenchymal (MSC) bone marrow cells transplanted into infarcted rat hearts. MNC and MSC (male Fischer 344 rats) were treated with different doses of PDGF-BB prior to intramyocardial injection into border zone of MI (syngeneic females, permanent LAD ligation) and hearts were harvested after 5 days and 3 weeks. In additional experiments, untreated MNC and MSC were injected immediately after permanent or temporary LAD ligation and hearts were harvested after 48 h, 5 days, 3 weeks, and 6 weeks. DNA of the hearts was isolated and the number of donor cells was determined by quantitative real-time PCR with Y chromosome-specific primers. There was a remarkable though not statistically significant ( p = 0.08) cell loss of ~46% between 5 days and 3 weeks in the control group, which was completely inhibited by treatment with high dose of PDGF-BB. Forty-eight hours after reperfusion only 10% of injected MSC or 1% for MNC were found in the heart, decreasing to 1% for MSC and 0.5% for MNC after 6 weeks. These numbers were lower than after permanent LAD ligation for both MNC and MSC at all time points studied. Treatment with PDGF-BB seems to prevent loss of transplanted bone marrow cells at later times presumably by inhibition of apoptosis, while reperfusion of the occluded artery enhances cell loss at early times putatively due to enhanced early wash-out. Further investigations are needed to substantially improve the persistence and survival of grafted bone marrow cells in infarcted rat hearts, in order to fully explore the therapeutic potential of this novel treatment modality for myocardial repair.

The Orphan Nuclear Receptor NR2F6 Is a Novel Negative Regulator of T-Cell Development.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 915-915
Author(s):  
Christine V. Ichim ◽  
Dzana Dervovic ◽  
Juan Carlo Zuniga-Pflucker ◽  
Richard A. Wells
Keyword(s):  
Bone Marrow ◽  
T Cells ◽  
T Cell ◽  
Progenitor Cells ◽  
Nuclear Receptor ◽  
Bone Marrow Cells ◽  
Orphan Nuclear Receptor ◽  
Over Expression ◽  
Competitive Disadvantage ◽  
Marrow Cells

Abstract Abstract 915 The orphan nuclear receptor NR2F6 is a mammalian homologue of the Drosophila seven-up gene that plays key roles in decisions of cell fate in neuroblast and retinal cells. We have previously described a novel role for NR2F6 in decisions of cell fate of mammalian haematopoietic cells of the myeloid cell lineage. We have shown that over-expression of NR2F6 in bone marrow cells impairs differentiation and extends the proliferative capacity of myeloid and early progenitor cells eventually leading to acute myeloid leukaemia (AML), while silencing of NR2F6 expression in AML cell lines causes terminal differentiation and apoptosis. A role of NR2F6 in lymphopoiesis has yet to be identified. Here we describe for the first time a role for NR2F6 in the specification of lymphoid cells. NR2F6 expression is heterogeneous throughout the haematopoietic hierarchy, with expression being highest in long-term repopulating HSCs and generally declining with the differentiation of progenitor cells. We report that over-expression of NR2F6 abrogates the developmental program necessary for T-cell lymphopoiesis. We assessed the effects of NR2F6 on lymphopoiesis in vivo by competitive bone marrow transplantation of NR2F6-IRES-GFP or GFP retrovirally transduced grafts (n=43). Competitive repopulation of lethally irradiated murine hosts with GFP transduced bone marrow cells resulted in successful engraftment and T-cell development, with GFP+ T-cells present in the thymus, and periphery at rates comparable to the percent marked cells in the original graft. However over-expression of NR2F6 placed developing T-cells at a dramatic competitive disadvantage. Six weeks post transplant the proportion of CD3+ cells derived from NR2F6 transduced bone marrow cells was greatly diminished relative to control (more than 10 fold), while at 12 weeks post-transplant we observed an abrogation of CD3+ cells derived from NR2F6 transduced T-cells (with the percentage of NR2F6 transduced CD3+ cells being comparable to staining with IgG control) in both the thymus and periphery. This stark competitive disadvantage was observed in all recipients of NR2F6 transduced grafts. We confirmed that this is not a phenomenon specific to the marker CD3 by analysing a portion of the animals for expression of CD4 and CD8, which again showed a lack of mature t-cells. In a second series of bone marrow transplants, cells transduced with NR2F6 or GFP were purified by fluorescence-activated cell sorting and grafts of 100% transduced cells were transferred by tail vein injection into lethally irradiated recipients. Animals transplanted with NR2F6 transduced bone marrow demonstrated a gross decrease in their thymic size and cellularity (∼10 fold decrease, n=17). Furthermore, the thymus of NR2F6 transduced animals contained a larger proportion of non-transduced, GFP negative residual haematopoietic cells than the vector control animals, corroborating the competitive disadvantage that NR2F6 transduced bone marrow cells face in the thymus. As observed in our previous experiments these animals demonstrated a gross reduction in the proportion of CD3+ cells in the thymus, spleen, lymph nodes and peripheral blood. To rule out the possibility that over-expression of NR2F6 is preventing the trafficking of progenitor cells to the thymus we differentiated NR2F6 or GFP transduced haematopoietic stem cells (lin-,c-kit+,sca-1+) into T-cells in vitro on OP9-DL1 cells. We observed a drastic reduction in the number of cells generated from NR2F6 transduced stem/progenitor cells (>50 fold at day 23), suggesting that expression of NR2F6 greatly impairs T-cell development. Mechanistically, others have shown that NR2F6 functions as a transcriptional repressor inhibiting the transactivating ability of genes such as Runx1. We conjecture that in lymphoid progenitors as well NR2F6 functions as a transcriptional repressor preventing the activation of pathways necessary for T-cell survival, proliferation and lymphopoiesis. Taken together, these data establish that the orphan nuclear receptor NR2F6 is a novel negative regulator of T-cell lymphopoiesis, and demonstrate that down-regulation of NR2F6 is important for the survival and proliferation of T-cell progenitors. Disclosures: No relevant conflicts of interest to declare.

Could Cobalamin Deficiency Mimic a Clonal Aberration Cytogenetic? a Case Report

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 4882-4882
Author(s):  
Marcelo Bellesso ◽  
Daniela Ferreira Dias ◽  
Renato Torrescasana Centrone ◽  
Laura Yolanda Chialanza Garcia ◽  
Annelise Correa Wengerkievicz Lopes ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Vitamin B12 ◽  
Cytogenetic Analysis ◽  
Bone Marrow Aspirate ◽  
Bone Marrow Cells ◽  
Megaloblastic Anemia ◽  
Cobalamin Deficiency ◽  
Normal Range ◽  
Clonal Deletion ◽  
Marrow Cells

Abstract A 32 years old female patient presented to our service complaining asthenia, apathy and loss of her power to work. It was observed, by laboratory test, pancytopenia (Hb: 6.0 g/dL; WBC: 2,100/mm³, platelets 95,000/mm³, Reticulocytes 0.8%) associated with marked elevation of LDH 1,800 U/L (normal range: 240 – 480U/L). Bone marrow aspirate demonstrated morphologic features of megaloblastic anemia. Moreover, low serum concentration of vitamin B12 < 150pg/mL (normal range: 200 – 95-pg/mL), Folic acid 15,9ng/mL (normal range: 3 – 17 ng/mL) confirmed Megaloblastic anemia by cobalamin deficiency. It was not evidenced gastritis. It was initiated the treatment with vitamin B12. However, in the next clinical attendance it was observed an unexpected cytogenetic result: 46,XX,del(9)(q13q22)[3]/76~78,XXX,+1,+3,+4,+9,+11,+12,+17,+20,+21[cp3]/46,XX[34]. It was interpreted that del(9)(q13q22)[3] could be a clonal cytogenetics aberration and the others data due to defects in synthesis of DNA by cobalamin deficiency. It was important, because in diagnosis of Megaloblastic anemia frequently it is not included cytogenetic analysis of bone marrow cells and a new cytogenetic analysis has become necessary due to this data. After two months, a complete hematological recovery was achieved and six months later, bone marrow aspirate and cytogenetic analisys were repeated. Normal morphologic bone marrow cells and normal cytogenetic: 46,XX[20] were evidenced. Therefore, it was really hard to conclude this case. First, cobalamin deficiency could promote this clonal deletion or, as a second hypothesis, a clonal cytogenetic with low proliferative rate was selected due to inefficient hematopoiesis, by vitamin B12 deficiency, and after the recovery of the hematopoiesis, this clonal was suppressed. Disclosures No relevant conflicts of interest to declare.

scholarly journals Dendritic Cells Retrovirally Transduced with a Model Antigen Gene Are Therapeutically Effective against Established Pulmonary Metastases

1997 ◽  
Vol 186 (8) ◽  
pp. 1213-1221 ◽  
Author(s):  
Jennifer M. Specht ◽  
Gang Wang ◽  
My T. Do ◽  
John S. Lam ◽  
Richard E. Royal ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Dendritic Cells ◽  
T Cell ◽  
Bone Marrow Cells ◽  
Lung Metastases ◽  
Interleukin 4 ◽  
Gene Encoding ◽  
Antigen Gene ◽  
Her 2 ◽  
Marrow Cells

Dendritic cells (DCs) are bone marrow–derived leukocytes that function as potent antigen presenting cells capable of initiating T cell–dependent responses from quiescent lymphocytes. DC pulsed with tumor-associated antigen (TAA) peptide or protein have recently been demonstrated to elicit antigen-specific protective antitumor immunity in a number of murine models. Transduction of DCs with TAA genes may allow stable, prolonged antigen expression as well as the potential for presentation of multiple, or unidentified, epitopes in association with major histocompatibility complex class I and/or class II molecules. To evaluate the potential efficacy of retrovirally transduced DCs, bone marrow cells harvested from BALB/c mice were transduced with either a model antigen gene encoding β-galactosidase (β-gal) or a control gene encoding rat HER-2/neu (Neu) by coculture with irradiated ecotropic retroviral producer lines. Bone marrow cells were differentiated into DC in vitro using granulocyte/macrophage colony-stimulating factor and interleukin-4. After 7 d in culture, cells were 45–78% double positive for DC phenotypic cell surface markers by FACS® analysis, and DC transduced with β-gal were 41–72% positive for β-gal expression by X-gal staining. In addition, coculture of β-gal transduced DC with a β-gal–specific T cell line (CTLx) resulted in the production of large amounts of interferon-γ, demonstrating that transduced DCs could process and present endogenously expressed β-gal. DC transduced with β-gal and control rat HER-2/neu were then used to treat 3-d lung metastases in mice bearing an experimental murine tumor CT26.CL25, expressing the model antigen, β-gal. Treatment with β-gal–transduced DC significantly reduced the number of pulmonary metastatic nodules compared with treatment with Hank's balanced salt solution or DCs transduced with rat HER-2/neu. In addition, immunization with β-gal–transduced DCs resulted in the generation of antigen-specific cytotoxic T lymphocytes (CTLs), which were significantly more reactive against relevant tumor targets than CTLs generated from mice immunized with DCs pulsed with the Ld-restricted β-gal peptide. The results observed in this rapidly lethal tumor model suggest that DCs transduced with TAA may be a useful treatment modality in tumor immunotherapy.

scholarly journals Terminal deoxynucleotidyl transferase is found in prothymocytes

1976 ◽  
Vol 144 (2) ◽  
pp. 543-548 ◽  
Author(s):  
AE Silverstone ◽  
H Cantor ◽  
G Goldstein ◽  
D Baltimore
Keyword(s):  
Bone Marrow ◽  
T Cell ◽  
Bone Marrow Cells ◽  
Marrow Cell ◽  
T Cell Differentiation ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Murine Bone Marrow ◽  
Terminal Transferase ◽  
Separate Pathway ◽  
Marrow Cells

Terminal deoxynucleotidyl transferase is an enzyme which has the unique property of polymerizing polydeoxynucleotides onto a primer in the absence of a template (1,2). This enzyme is found both in the thymus and the bone marrow of birds, rodents, and humans (3-7). Whether the marrow cells that contain terminal transferase are related to thymocytes, or are on a separate pathway of differentiation, is not yet known (7,8). To determine the lineage of the murine bone marrow cells that have terminal transferase, we have investigated whether these cells have the antigen Thy-1 induced on the cells by treatment with thymopoietin (9). Thymopoietin is known to induce a set of characteristic T-cell markers including the Thy-1 alloantigen on the surface of a subpopulation of bone marrow cells committed to T-cell differentiation (prothymocytes) (10). Destruction of Thy- 1-positive cells after exposure to thymopoietin allows elimination of a substantial fraction of those bone marrow cells that can repopulate an irradiated thymus (11). We find that such an elimination after induction with the thymic polypeptide removes a substantial amount of terminal transferase from the bone marrow cell population, suggesting that at least one-half of the marrow cells bearing this enzyme are related to those found in the thymus.

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