M. Eichelberger et al., FUNCTIONAL-ANALYSIS OF THE TCR-ALPHA(-)BETA(-INFECTED TCR-ALPHA(-() CELLS THAT ACCUMULATE IN THE PNEUMONIC LUNG OF INFLUENZA VIRUS)-) MICE/, The Journal of immunology, 154(4), 1995, pp. 1569-1576
In mice homozygous (-/-) for a targeted TCR-alpha gene disruption, som
e thymocytes express a cell-surface TCR-beta chain on the cell surface
in the absence of a TCR-alpha chain, and a few CD4(+)CD8(-) TCR-alpha
(-)beta(+) cells accumulate in the peripheral lymphoid organs. We have
infected these mutant mice with an influenza A virus to show that lar
ge numbers of TCR-beta(+) cells (most of which are CD4(+)) can be retr
ieved from the pneumonic lung. Both freshly isolated TCR-alpha(-)beta(
+) cells and TCR-alpha(-)beta(+) hybridoma cell lines derived from inf
luenza virus-infected mutant mice respond appropriately to stimulation
with anti-CD3 epsilon or the Mls-1 superantigen. It thus seems that C
D4(+) TCR-alpha(-)beta(+) ells in the peripheral lymphoid organs of TC
R-alpha mutant mice can signal through their TCR surface complex. Howe
ver, there are no indications that CD4(+) TCR-alpha(-)beta(+) lymphocy
tes can either recognize a complex between MHC and influenza virus pep
tide or act as effector or Th cells. The existence and function of suc
h cells in wild-type mice remains to be established.