scholarly journals Parasite and immunodeficiency and immunologic abnormality.A role of antigen-presenting cell and suppressor cell.

1991 ◽  
Vol 14 (5) ◽  
pp. 482-484
Author(s):  
AKIHIKO YANO
2007 ◽  
Vol 37 (11) ◽  
pp. 3122-3130 ◽  
Author(s):  
Fabio Bergamin ◽  
Isabelle E. Vincent ◽  
Artur Summerfield ◽  
Kenneth C. McCullough

1996 ◽  
Vol 39 (4) ◽  
pp. 600-609 ◽  
Author(s):  
George C. Tsokos ◽  
Birgit Kovacs ◽  
Peter P. Sfikakis ◽  
Stamatis Theocharis ◽  
Scott Vogelgesang ◽  
...  

1984 ◽  
Vol 159 (4) ◽  
pp. 1238-1252 ◽  
Author(s):  
K L Rock ◽  
B Benacerraf

A large panel of alloreactive, interleukin 2 (IL-2)-producing T cell hybridomas was constructed from B10 alpha BALB/c primary mixed lymphocyte cultures (MLC). Functional hybrids had specificity for either I-Ad or I-Ed. These cells were used to probe determinants on Ia molecules in an attempt to detect molecular association between a nominal antigen and an Ia molecule on an antigen-presenting cell (APC). The response of a small number of these clones was significantly blocked by the addition of the Ir gene-controlled copolymer L-glutamic acid60-L-alanine30-L-tyrosine10 (GAT) to culture. A comparison of the inhibited and uninhibited hybrids revealed an identical dose response curve. Further, both types of hybrids were activated by the same stimulator cell and frequently recognized the identical Ia molecule on that cell. Nevertheless, the inhibitory effect of GAT was localized to the stimulator cell and not to the T cell hybrids. All of the hybrids whose stimulation was blocked had specificity for the I-A molecule, which is the gene product known to control and restrict responsiveness to GAT. Further, only GT, but not a number of other related antigens, was also specifically inhibitory, which correlates with the known associational specificity of these antigens on an APC. Finally, the same stimulator cell could be shown to coordinately lose an allostimulatory determinant(s), while it was gaining an I-Ad plus GAT determinant(s). The implications of these findings on the nature of antigen-Ia association and on the role of polymorphic Ia determinants are discussed.


Cancer Cell ◽  
2016 ◽  
Vol 30 (1) ◽  
pp. 120-135 ◽  
Author(s):  
Sunil Singhal ◽  
Pratik S. Bhojnagarwala ◽  
Shaun O'Brien ◽  
Edmund K. Moon ◽  
Alfred L. Garfall ◽  
...  

1983 ◽  
Vol 157 (1) ◽  
pp. 353-358 ◽  
Author(s):  
A Lowy ◽  
A Tominaga ◽  
J A Drebin ◽  
M Takaoki ◽  
B Benacerraf ◽  
...  

We have found that an I-J+ I-A- antigen-presenting cell (APC) is required for Ts3 activation in vivo. Together with the I-J restriction previously reported for Ts3 induction (Takaoki, M., M.-S. Sy, A. Tominaga, A. Lowy, M. Tsurifiji, B. Benacerraf, R. Finberg, and M. I. Greene, 1982, J. Exp. Med., 156:1325), it appears that this I-J+ APC is responsible for I-J restriction in the triggering of Ts3. This restriction may be exerted via a pre-Ts3 associative recognition of antigen and I-J encoded determinants, analogous to the T helper recognition of antigen in the context of I-A and I-E determinants.


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