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Dominant Vβ8 gene usage in response to TNP: failure to use other Vβ chains following removal of Vβ8+ T cells by monoclonal antibody <em>in vivo</em>.

Authors :
Dieli, F.
Asherson, G. L.
Sireci, G.
Tantillo, G.
del Carpio, C.
Salerno, A.
Source :
Immunology. May94, Vol. 82 Issue 1, p99-105. 7p.
Publication Year :
1994

Abstract

This paper investigates the Vβ usage of lymph node cells from mice immunized with TNP and of cell lines made from them. In cell lines stimulated weekly with TNP in vitro for 1 month, about 87% of the cells were Vβ8+ and further analysis showed that these cells were actually Vβ.2+. This was also true for the cells that proliferated in lymph nodes in response to TNP 4 days after primary immunization, i.e. proliferation occurred mainly in the Vβ+, and in particular in the Vβ8.2+, population while much less proliferation occurred when the Vβ8- or Vβ8.2- T-cell populations are used. This was not due to non-specific damage during separation, as the response to concanavalin A and alloantigen was intact. In a separate series of experiments, mice were acutely depleted of Vβ8+ T cells by treatment with F23.1 or a control monoclonal antibody (mAb) in vivo given before immunization. Treatment with the relevant mAb virtually abolished the response to TNP. In contrast, SJL mice, which lack the gone segment coding for the Vβ8 family and several other Vβ chains, made a normal proliferative and delayed-type hypersensitivity (DTH) response to TNP. This poses the problem, which may he important in the study of the T-cell repertoire, of why acute removal of Vβ8+ T cells, which are dominantly used in the response to TNP, does not allow T cells using other chains to substitute in the response, while the absence of this population over a long period of time, because of a deletion in the genome, allows the use of T cells hearing other Vβ chains. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
00192805
Volume :
82
Issue :
1
Database :
Academic Search Index
Journal :
Immunology
Publication Type :
Academic Journal
Accession number :
13634636