Reduction of Natural Killer Activity in Athymic Nude Mice by Transfer of T Cells

Author(s):  
M. Harada ◽  
M. Matsumoto ◽  
H. Yagi
1992 ◽  
Vol 175 (2) ◽  
pp. 527-536 ◽  
Author(s):  
G M Bell ◽  
W E Seaman ◽  
E C Niemi ◽  
J B Imboden

The MRC OX-44 molecule, which is expressed on all peripheral leukocytes, identifies the subset of thymocytes capable of proliferating in response to alloantigens and lectins (Paterson, D.J., J.R. Green, W.A. Jefferies, M. Puklavec, and A.F. Williams. 1987. J. Exp. Med. 165:1). When we isolated monoclonal antibodies (mAbs) on the basis of their ability to activate the phosphatidylinositol signaling pathway in RNK-16 cells (a rat leukemia line with natural killer activity), three of the resulting mAbs recognized the OX-44 molecule. Addition of these mAbs to RNK-16 elicits protein tyrosine phosphorylation, generates inositol phosphates, and increases the concentration of cytoplasmic free calcium. These responses require the addition of intact mAb and are not observed with F(ab')2 fragments. One of these mAbs (7D2) is mitogenic for freshly isolated rat splenic T cells and synergizes with a mAb to the T cell antigen receptor in this activation. A 50-60-kD glycoprotein coprecipitates with the OX-44 molecule from RNK-16 cells and rat splenic T cells. Peptide mapping and reprecipitation studies indicate that the coprecipitating molecule is CD2. Thus, the OX-44 molecule can couple to multiple signaling pathways and associates with CD2 on both RNK-16 and rat T cells.


1992 ◽  
Vol 5 (1) ◽  
pp. 23-30
Author(s):  
Maria Aranzazu Goicoa ◽  
I.J. Ballart ◽  
M. Fernanda Palacios ◽  
Susana A. De Miani ◽  
Maria E. Estevez ◽  
...  

To evaluate whether indomethacin (IM) and thymostimulin (TP-1) could revert the alterations of natural killer cytotoxicity (NKC) observed in patients and carriers of Thalassemia Major (TM), 14 TM patients, 10 TM carriers, 16 normal controls, and 4 polytransfused patients were studied. In vitro, IM induced an increase in NKC of normal controls and TM carriers (Δ CI: + 5.98±2.49 and + 9.77±6.82 respectively), but not in TM patients (-0.32±1.45) or other polytransfused recipients. The addition of IM to Concanavalin A (Con A) also resulted in an increase of NKC in normal controls and TM carriers, similar to that induced by each substance separately in normal controls, or by IM alone in TM carriers. Similarly, TP-1 (50 μg/ml) induced increases of NKC in normal subjects (+ 4.66±3.62), but not in TM patients (-1.1±2.43). The impairment in NKC observed in TM and polytransfused patients, and the absence of response to Con A in both, TM patients and carriers, do not seem to be mediated by an excessive production of prostaglandins. The lack of response not only to Con A, but also to TP-1 could indicate a quantitative or qualitative defect in T cells, that affects NKC regulation, or a deficient response of NK cells to modulators produced by T lymphocytes.


1986 ◽  
Vol 97 (1) ◽  
pp. 164-172 ◽  
Author(s):  
Thomas M. Folks ◽  
Thomas M. Chused ◽  
Diane Portnoy ◽  
Linette Edison ◽  
William Leiserson ◽  
...  

Cytometry ◽  
1998 ◽  
Vol 32 (4) ◽  
pp. 280-285 ◽  
Author(s):  
Loris Zamai ◽  
Adriana R. Mariani ◽  
Giorgio Zauli ◽  
Luigi Rodella ◽  
Rita Rezzani ◽  
...  

1989 ◽  
Vol 15 ◽  
pp. 194
Author(s):  
H.S. Wang ◽  
M. Kariya ◽  
H. Kanzaki ◽  
M. Yoshida ◽  
M. Tokushige ◽  
...  

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