In vitro Proliferation of Murine Spleen Cells: Inhibition by Monoclonal Antibodies to L3T4 and Lyt-2 T Cell Markers or Intracellular Cyclic Adenosine Monophosphate

Pathobiology ◽  
1989 ◽  
Vol 57 (6) ◽  
pp. 346-357 ◽  
Author(s):  
P. Zhou ◽  
T. Gorzynski ◽  
W.K. Dowjat ◽  
R. Rabin ◽  
M.B. Zaleski
Keyword(s):  
Monoclonal Antibodies ◽  
T Cell ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Spleen Cells ◽  
In Vitro Proliferation ◽  
Cell Markers ◽  
Murine Spleen

scholarly journals Obligatory role of gamma interferon in T cell-replacing factor-dependent, antigen-specific murine B cell responses.

1985 ◽  
Vol 161 (5) ◽  
pp. 953-971 ◽  
Author(s):  
M Brunswick ◽  
P Lake
Keyword(s):  
T Cell ◽  
B Cell ◽  
Cell Activation ◽  
Human Peripheral Blood ◽  
Gamma Interferon ◽  
Spleen Cells ◽  
Ifn Gamma ◽  
Murine Spleen

The role of gamma interferon (IFN-gamma) in T cell-replacing factor (TRF) activity for antigen-specific plaque-forming cell (PFC) responses in vitro was studied using antibodies to murine IFN-gamma (Mu IFN-gamma). TRF activity was present in supernatants (Sn) of Con A- or mixed leukocyte reaction-stimulated murine spleen cells as well as in an IL-2-rich fraction of phytohemagglutinin-stimulated human peripheral blood lymphocyte Sn and in the Sn of the Gibbon T lymphoma MLA-144. The human TRF was highly active with cells from nu/nu mice and normal mice but not with cells from animals with the xid immunologic defect, similar to the activity of murine TRF. Antibodies to IFN-gamma consisted of hyper-immune rabbit antisera, IFN-gamma affinity-purified rabbit immunoglobulin and an interspecies hybridoma specific for Mu IFN-gamma. The results show that the activities of all preparations of TRF are markedly diminished or abrogated by antibody to Mu IFN-gamma but not by antibodies to human IFN-gamma (Hu IFN-gamma), nor by normal rabbit sera or purified rabbit Ig. The degree of inhibition was dose dependent and was quantitatively reversed by the addition to the cultures of recombinant-derived Mu IFN-gamma (Mu rIFN-gamma) but not Hu rIFN-gamma. This reversal was fully antigen specific and thus not attributable to polyclonal B cell activation by IFN-gamma, which is inactive alone in the TRF assay. Kinetic analysis shows that IFN-gamma must act by 24-48 h to produce PFC responses at 4 d. Together, the data demonstrate that IFN-gamma is a necessary mediator for TRF effects and that IFN-gamma is induced by TRF from T-depleted murine spleen cells in sufficient quantity to support large antibody responses. The source of this IFN-gamma may be the potent natural killer cells that are induced in cultures stimulated with TRF.

In Vitro Proliferation of Murine Spleen Cells: I. Strain Variation of Response to Medium from Cultures of EL-4 Cells

1989 ◽  
Vol 18 (8) ◽  
pp. 1007-1017 ◽  
Author(s):  
W. K. Dowjat ◽  
P. Zhou ◽  
L. J. Quackenbush ◽  
T. Gorzynski ◽  
M. B. Zoleski
Keyword(s):  
Strain Variation ◽  
Spleen Cells ◽  
In Vitro Proliferation ◽  
Murine Spleen

In vitro Proliferation of Murine Spleen Cells

1989 ◽  
Vol 90 (2) ◽  
pp. 162-168 ◽  
Author(s):  
P. Zhou ◽  
L.J. Quackenbush ◽  
M.B. Zaleski
Keyword(s):  
Spleen Cells ◽  
In Vitro Proliferation ◽  
Murine Spleen

scholarly journals SPONTANEOUS RELEASE OF T-CELL RECEPTORS FOR ALLOANTIGENS

1974 ◽  
Vol 140 (3) ◽  
pp. 603-618 ◽  
Author(s):  
Hansruedy Ramseier
Keyword(s):  
T Cell ◽  
T Cell Receptors ◽  
Bone Marrow Cells ◽  
Culture Conditions ◽  
In Vitro Cultivation ◽  
Spontaneous Release ◽  
Spleen Cells ◽  
Cell Receptors ◽  
Murine Spleen

In vitro cultivation of murine spleen cells resulted in a spontaneous release of receptors for alloantigens. This was revealed by the capacity of cell-free culture supernates to recognize alloantigens as measured in the PAR assay. Qualitatively, recognition responses obtained with these supernates reproduced faithfully those found with the corresponding cells. Large amounts of receptors were released by untreated spleen cells and by spleen cells treated with a rabbit antimouse immunoglobulin serum and complement, smaller amounts were released by bone marrow cells, and native thymus cells released none. Spleen cells from nude mice and spleen cells from normal mice treated with anti-θ serum and complement showed no release of receptors. It was concluded that receptors active in the PAR test were of T-cell origin. Release of T-cell receptors was found to be discontinuous and proceeded in waves. The amount of released receptors depended on the number of cells cultivated. Release occurred at 37°C but not at 4°C. Interaction with antigen, however, was temperature-independent. In contrast to T-cell receptors, a release of H-2 antigens could not be detected with the culture conditions employed.

scholarly journals Evidence for the interleukin-2 dependent expansion of leukemic cells in adult T cell leukemia

Blood ◽  
1987 ◽  
Vol 70 (5) ◽  
pp. 1407-1411 ◽  
Author(s):  
M Maeda ◽  
N Arima ◽  
Y Daitoku ◽  
M Kashihara ◽  
H Okamoto ◽  
...  
Keyword(s):  
T Cell ◽  
Receptor Gene ◽  
Interleukin 2 ◽  
Leukemic Cells ◽  
Type I ◽  
T Cell Leukemia ◽  
Cell Leukemia ◽  
In Vitro Proliferation ◽  
Adult T Cell Leukemia

Abstract Interleukin 2 (IL-2) receptor/Tac antigen is abnormally expressed on cells of patients with adult T cell leukemia (ATL) caused by infection with human T lymphotropic virus type I (HTLV-I). Twenty-five patients with ATL were examined to determine whether their leukemic cells continued to show IL-2-dependent proliferation. In 21 patients, the in vitro proliferation of HTLV-I-infected nonleukemic T cell clones was found to be dependent on IL-2. However, clonality analysis based on T cell receptor gene rearrangement profiles and the site of HTLV-I provirus integration revealed IL-2-dependent growth in leukemic cells in four patients with ATL. These results provide evidence for the IL-2- dependent proliferation of leukemic cells in some ATL patients.

Modulation of T-Cell Functions in KIR2DL3 (CD158b) Transgenic Mice

Blood ◽  
1999 ◽  
Vol 94 (7) ◽  
pp. 2396-2402 ◽  
Author(s):  
Anna Cambiaggi ◽  
Sylvie Darche ◽  
Sophie Guia ◽  
Philippe Kourilsky ◽  
Jean-Pierre Abastado ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Transgenic Mice ◽  
T Cell Activation ◽  
Cell Activation ◽  
Killer Cell ◽  
In Vitro Proliferation ◽  
Cell Functions ◽  
Double Transgenic Mice

In humans, a minor subset of T cells express killer cell Ig-like receptors (KIRs) at their surface. In vitro data obtained with KIR+ β and γδ T-cell clones showed that engagement of KIR molecules can extinguish T-cell activation signals induced via the CD3/T-cell receptor (TCR) complex. We analyzed the T-cell compartment in mice transgenic for KIR2DL3 (Tg-KIR2DL3), an inhibitory receptor for HLA-Cw3. As expected, mixed lymphocyte reaction and anti-CD3 monoclonal antibody (MoAb)-redirected cytotoxicity exerted by freshly isolated splenocytes can be inhibited by engagement of transgenic KIR2DL3 molecules. In contrast, antigen and anti-CD3 MoAb-induced cytotoxicity exerted by alloreactive cytotoxic T lymphocytes cannot be inhibited by KIR2DL3 engagement. In double transgenic mice, Tg-KIR2DL3 × Tg-HLA-Cw3, no alteration of thymic differentiation could be documented. Immunization of double transgenic mice with Hen egg white lysozime (HEL) or Pigeon Cytochrome-C (PCC) was indistinguishable from immunization of control mice, as judged by recall antigen-induced in vitro proliferation and TCR repertoire analysis. These results indicate that KIR effect on T cells varies upon cell activation stage and show unexpected complexity in the biological function of KIRs in vivo.

scholarly journals Cell-mediated lympholysis to H-2-matched target cells modified with a series of nitrophenyl compounds.

1976 ◽  
Vol 144 (4) ◽  
pp. 1134-1140 ◽  
Author(s):  
T G Rehn ◽  
J K Inman ◽  
G M Shearer
Keyword(s):  
T Cell ◽  
Target Cells ◽  
Cell Recognition ◽  
Receptor Model ◽  
Spleen Cells ◽  
Effector Cells ◽  
T Cell Recognition ◽  
Cytotoxic Effector

The specificity of C57BL/10 cytotoxic effector cells generated by in vitro sensitization with autologous spleen cells modified with a series of related nitrophenyl compounds was investigated. The failure of trinitrophenyl (TNP)-sensitized effector cells to lyse TNP-beta-alanylglycylglycyl(AGG)-modified target cells is presented as evidence contradicting the intimacy or dual receptor model or T-cell recognition in its simplest form. Data are also shown indicating that sensitization with N-(3-nitro-4-hydroxy-5-iodophenylacetyl)-AGG-modified stimulating cells generates noncross-reacting clones of cytotoxic effector cells.

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