scholarly journals CELLS INVOLVED IN THE IMMUNE RESPONSE

1969 ◽  
Vol 129 (6) ◽  
pp. 1261-1273 ◽  
Author(s):  
M. Richter ◽  
N. I. Abdou
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Cells ◽  
Plaque Formation ◽  
Lymphoid Cells ◽  
Spleen Cells ◽  
Normal Bone ◽  
Large Numbers ◽  
Recipient Animal ◽  
Rabbit Bone ◽  
Marrow Cells

Bone marrow cells obtained from rabbits of one allotype were injected into irradiated rabbits of a different allotype. The recipients were also injected with sheep red blood cells, and their spleen cells were tested for plaque-forming capacity 7 days later. Spleen cells of all recipients gave large numbers of plaques as did spleen cells incubated with antiserum, directed toward donor allotype. However, incubation of the recipient spleen cells with antiserum directed toward recipient allotype completely suppressed plaque formation. These results demonstrate that antibody-formation in irradiated recipients of transferred lymphoid cells is a property of the recipient animal and that the antibody-forming cell is relatively irradiation-resistant. It was also demonstrated that only viable normal bone marrow cells are capable of transferring antibody-forming capacity to irradiated recipient rabbits. Neither sonicates nor heat-killed preparations of normal rabbit bone marrow cells possessed this capacity.

Transfer of donor immunological reactivity to x-irradiated F1 hybrid mice by injected parental bone marrow

1958 ◽  
Vol 196 (1) ◽  
pp. 100-104
Author(s):  
L. J. Cole ◽  
R. M. Garver ◽  
M. E. Ellis
Keyword(s):  
Bone Marrow ◽  
Protective Effect ◽  
Bone Marrow Cells ◽  
Marrow Cell ◽  
Test System ◽  
Lymphoid Cells ◽  
X Rays ◽  
Spleen Cells ◽  
F1 Hybrid ◽  
Marrow Cells

Mice of the (LxA)F1 strain were exposed to an ld100 dose of x-rays (870 r), and injected with bone marrow cell suspensions from A-strain mice. Excellent protection against death was observed during the first 3 weeks, followed by secondary ‘homologous’ deaths during the ensuing weeks. When A-strain (parental strain) spleen cells were injected, together with A-strain bone marrow, the protective effect was annulled. When A-spleen cells were injected together with LAF1 bone marrow cells into irradiated LAF1 mice, again no protection was observed. However, injected LAF1 spleen cells did not influence adversely the course of protection of x-irradiated A-strain mice by injected A-bone marrow. The findings formed the basis for an experimental test system for detecting the presence of A-lymphoid cells in the tissues of irradiated LAF1 mice which had been injected with A-bone marrow. The data indicate that the spleen and thymus of LAF1 mice 21 days after irradiation and injection of A-marrow contain A-lymphoid cells which when injected, in turn, into irradiated LAF1 mice treated with LAF1 marrow, annuls the protective effect of the injected marrow. It is concluded that a reaction (of an immunological nature) of the injected bone marrow cells, or their progeny, against the host tissues, contributes to the phenomenon of the late deaths. The significance of these results with respect to the problem of ‘homologous disease’ in lethally x-irradiated mice treated with homologous bone marrow, has been discussed.

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.

Effects of imatinib mesylate on normal bone marrow cells from chronic myeloid leukemia patients in complete cytogenetic response

2009 ◽  
Vol 33 (1) ◽  
pp. 170-173 ◽  
Author(s):  
Fermin M. Sanchez-Guijo ◽  
Jesus M. Hernandez ◽  
Eva Lumbreras ◽  
Patricia Morais ◽  
Carlos Santamaría ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Chronic Myeloid Leukemia ◽  
Imatinib Mesylate ◽  
Myeloid Leukemia ◽  
Bone Marrow Cells ◽  
Cytogenetic Response ◽  
Normal Bone Marrow ◽  
Normal Bone ◽  
Complete Cytogenetic Response ◽  
Marrow Cells

Cancer-induced cytolysis of normal bone marrow cells

Nature ◽  
1977 ◽  
Vol 265 (5596) ◽  
pp. 736-737 ◽  
Author(s):  
STANLEY ZUCKER ◽  
RITA LYSIK
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Cells ◽  
Normal Bone Marrow ◽  
Normal Bone ◽  
Marrow Cells

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 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.

Biosynthesis of cholinesterase in rabbit bone marrow cells in culture

1974 ◽  
Vol 23 (15) ◽  
pp. 2155-2163 ◽  
Author(s):  
Larrel W. Harris ◽  
Vincent F. Garry ◽  
Robert D. Moore
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Cells ◽  
Cells In Culture ◽  
Rabbit Bone ◽  
Marrow Cells

in vitro studies with melphalan and pediatric neoplastic and normal bone marrow cells

1986 ◽  
Vol 37 (6) ◽  
pp. 819-823 ◽  
Author(s):  
Diana A. Worthington-White ◽  
John R. Graham-Pole ◽  
Susan A. Stout ◽  
Christopher M. Riley
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Cells ◽  
In Vitro Studies ◽  
Normal Bone Marrow ◽  
Normal Bone ◽  
Marrow Cells

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.

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