Immunodeficiency with low expression of the T cell receptor/CD3 complex. Effect on T lymphocyte activation

1991 ◽  
Vol 21 (7) ◽  
pp. 1641-1647 ◽  
Author(s):  
Françoise Le Deist ◽  
Gabriela Thoenes ◽  
José Corado ◽  
Barbara Lisowska-Grospierre ◽  
Alain Fischer
1996 ◽  
Vol 26 (11) ◽  
pp. 2781-2789 ◽  
Author(s):  
Valter Redoglia ◽  
Umberto Dianzani ◽  
Josè M. Rojo ◽  
Pilàr Portolés ◽  
Manuela Bragardo ◽  
...  

2003 ◽  
Vol 278 (29) ◽  
pp. 26983-26991 ◽  
Author(s):  
Marie-Agnès Doucey ◽  
Daniel F. Legler ◽  
Mustapha Faroudi ◽  
Nicole Boucheron ◽  
Petra Baumgaertner ◽  
...  

Stroke ◽  
2021 ◽  
Author(s):  
Juliane Schulze ◽  
Juliane Gellrich ◽  
Michael Kirsch ◽  
Alexander Dressel ◽  
Antje Vogelgesang

Background and Purpose: T lymphocytes contribute to secondary brain damage after stroke. It has not been fully investigated whether this contribution is caused by antigen-specific or antigen-nonspecific activation of T lymphocytes. Lymphocytes from Nur77 GFP transgenic mice express a fluorescent protein upon activation via the TCR (T-cell receptor), allowing the differentiation of activation mode in a natural repertoire of immune cells and antigens. Methods: Middle cerebral artery occlusion or sham surgery was performed, and T-lymphocyte activation was analyzed by flow cytometry in the brain, spleen, and blood 16 hours, 2 days, 3 days, 4 days, and 7 days after surgery. Results: Ipsilateral hemispheric T-lymphocyte invasion peaked on day 4 poststroke. Here, we observed PD-1 (programmed cell death protein 1) expression on almost all invading T lymphocytes, while CD25 expression was low. CD25+, CD69+, or PD-1+ T lymphocytes predominantly displayed antigen-specific activation; the opposite was observed for T lymphocytes isolated from the blood. A mixed activation that favored antigen-specific activation was observed in the spleen. PD-1 was upregulated within the brain, whereas CD25 was not. Antigen-specific T lymphocytes home to the brain, while antigen- nonspecifically activated cells remain within the blood. Conclusions: Our data clearly demonstrate antigen-specific activation of T lymphocytes infiltrating ischemic brain lesions in stroke. The high expression of inhibitory PD-1 and low expression of CD25 on activated T lymphocytes in the brain most likely reflect immunosuppressive mechanisms.


1993 ◽  
Vol 3 (1) ◽  
pp. 26
Author(s):  
M. Sensi ◽  
S. Salvi ◽  
C. Castelli ◽  
G. Nicolini ◽  
A. Anichini ◽  
...  

1999 ◽  
Vol 190 (9) ◽  
pp. 1257-1262 ◽  
Author(s):  
Chiyu Wang ◽  
Molly A. Bogue ◽  
Jonathan M. Levitt ◽  
David B. Roth

In SCID (severe combined immunodeficient) mice, proper assembly of immunoglobulin and T cell receptor (TCR) genes is blocked by defective V(D)J recombination so that B and T lymphocyte differentiation is arrested at an early precursor stage. Treating the mice with gamma irradiation rescues V(D)J rearrangement at multiple TCR loci, promotes limited thymocyte differentiation, and induces thymic lymphomas. These effects are not observed in the B cell lineage. Current models postulate that irradiation affects intrathymic T cell precursors. Surprisingly, we found that transfer of irradiated SCID bone marrow cells to unirradiated host animals rescues both TCR rearrangements and thymocyte differentiation. These data indicate that irradiation affects precursor cells at an earlier stage of differentiation than was previously thought and suggest new models for the mechanism of irradiation rescue.


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