scholarly journals The CD154/CD40 Interaction Required for Retrovirus-Induced Murine Immunodeficiency Syndrome Is Not Mediated by Upregulation of the CD80/CD86 Costimulatory Molecules

2002 ◽  
Vol 76 (24) ◽  
pp. 13106-13110 ◽  
Author(s):  
Kathy A. Green ◽  
W. James Cook ◽  
Arlene H. Sharpe ◽  
William R. Green
Keyword(s):  
Monoclonal Antibody ◽  
B Cells ◽  
Molecular Interactions ◽  
T And B Cells ◽  
Antibody Treatment ◽  
Monoclonal Antibody Treatment ◽  
Murine Aids ◽  
Cd40 Expression ◽  
Immunodeficiency Syndrome

ABSTRACT C57BL/6 (B6) mice infected with LP-BM5 retroviruses develop disease, including an immunodeficiency similar to AIDS. This disease, murine AIDS (MAIDS), is inhibited by in vivo anti-CD154 monoclonal antibody treatment. The similar levels of insusceptibility of CD40−/− and CD154−/− B6 mice indicate that CD154/CD40 molecular interactions are required for MAIDS. CD4+ T and B cells, respectively, provide the CD154 and CD40 expression needed for MAIDS induction. Here, the required CD154/CD40 interaction is shown to be independent of CD80 and CD86 expression: CD80/CD86−/− B6 mice develop MAIDS after LP-BM5 infection.

An investigation of allogeneic pregnancy in multiparous mice subjected to in vivo depletion of CD8 (Ly2)-positive lymphocytes by monoclonal antibody treatment

1988 ◽  
Vol 14 (3) ◽  
pp. 235-245 ◽  
Author(s):  
Pirkko Sulila ◽  
Rikard Holmdahl ◽  
Inga Hansson ◽  
Folke Bernadotte ◽  
Anita Mattsson ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Antibody Treatment ◽  
Monoclonal Antibody Treatment

scholarly journals A monoclonal antibody recognizing CD43 (leukosialin) initiates apoptosis of human hematopoietic progenitor cells but not stem cells

Blood ◽  
1996 ◽  
Vol 87 (4) ◽  
pp. 1272-1281 ◽  
Author(s):  
V Bazil ◽  
J Brandt ◽  
S Chen ◽  
M Roeding ◽  
K Luens ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Progenitor Cells ◽  
Lymphoid Cells ◽  
Hematopoietic Progenitor Cells ◽  
Proliferative Potential ◽  
Hematopoietic Progenitor ◽  
Antibody Treatment ◽  
Hematopoietic Stem ◽  
Monoclonal Antibody Treatment

CD43 (the major sialoglycoprotein of leukocytes) is an adhesion molecule broadly expressed on hematopoietic cells. A monoclonal antibody recognizing this molecule induces apoptosis of lineage marker- negative bone marrow hematopoietic progenitor cells (HPCs) that express CD34 at a high density (CD34hiLIN-). However, not all cells within this population undergo apoptosis on stimulation via CD43. Dividing progenitor cells are most highly affected, whereas more primitive quiescent cells survive anti-CD43 monoclonal antibody treatment. These surviving cells (1) are enriched for cobblestone area-forming cells, (2) repopulate fragments for human fetal bone implanted into C.B-17 scid/scid mice, (3) have a potential to differentiate in vivo to myeloid and lymphoid cells, and (4) have a high proliferative potential in long-term stromal cell-free liquid culture. These data indicate that cells with hematopoietic stem cell characteristics are relatively resistant to CD43-mediated apoptosis as compared with HPCs. Thus, CD43 may be specifically involved in the regulation of HPC proliferation.

scholarly journals A novel type of cell death of lymphocytes induced by a monoclonal antibody without participation of complement.

1995 ◽  
Vol 181 (6) ◽  
pp. 2007-2015 ◽  
Author(s):  
S Matsuoka ◽  
Y Asano ◽  
K Sano ◽  
H Kishimoto ◽  
I Yamashita ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Cell Death ◽  
T Cell ◽  
B Cells ◽  
Interleukin 2 ◽  
Cytolytic Activity ◽  
Target Cells ◽  
T And B Cells ◽  
Fab Fragments ◽  
T Cell Clone

A monoclonal antibody, RE2, raised by immunizing a rat with cell lysate of a mouse T cell clone, was found to directly kill interleukin 2-dependent T cell clones without participation of serum complement. Fab fragments of RE2 had no cytolytic activity, while the cross-linking of Fab fragments with anti-rat immunoglobulin reconstituted the cytotoxicity. The cytotoxicity was temperature dependent: the antibody could kill target cells at 37 degrees C but not at 0 degrees C. Sodium azide, ethylenediaminetetraacetic acid, and forskolin did not affect the cytolytic activity of RE2, while the treatment of target cells with cytochalasin B and D completely blocked the activity. This suggested that the cell death involves a cytoskeleton-dependent active process. Giant holes on the cell membrane were formed within 5 minutes after the treatment with RE2, as observed by scanning electron microscopy. There was no indication of DNA fragmentation nor swelling of mitochondria during the cytolysis, suggesting that the cell death is neither apoptosis nor typical necrosis. The antibody also killed T cell lymphomas and T and B cell hybridomas only when these cells were preactivated with concanavalin A, lipopolysaccharide, or phorbol myristate acetate. Preactivated peripheral T and B cells were sensitive to the cytotoxicity of RE2, while resting T and B cells were insensitive. These results provide evidence for a novel pathway of cell death of activated lymphocytes by membrane excitation.

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