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The Journal of Immunology, Vol 150, Issue 12 5494-5500, Copyright © 1993 by American Association of Immunologists
ARTICLES |
S Hou and PC Doherty
Department of Immunology St. Jude Children's Research Hospital, Memphis, TN 38105.
Patterns of LECAM-1 and CD45RB expression have been analysed for mediastinal lymph node (MLN) and bronchoalveolar lavage (BAL) populations from C57BL/6J mice with primary Sendai virus pneumonia. The findings indicate that virus-specific CD8+ CTL precursors differentiate in the regional lymph node and become effector CTL after localization to the virus-infected respiratory tract. Relatively few of the MLN CD8+ T cells were LECAM-1-, and all were CD45RB-hi throughout the acute and recovery phases of this disease process. The CD8+ CD45RB-hi and LECAM- 1+ T cells characteristic of the MLN were more apparent in the BAL during the 1st wk after exposure to virus, with this shifting to a predominant CD8+ LECAM-1- CD45RB-lo phenotype from day 10 after infection. In contrast, the CD4+ set was generally CD45RB-lo LECAM-1- in the BAL, although CD4+ CD45RB-lo and LECAM-1- cells maintained at relatively high levels in the MLN. The virus-specific CD8+ effectors found in the BAL from day 8 after infection were uniformly LECAM-1-, but varied in the level of CD45RB expression. Evidence of CTL activity was minimal for the MLN, though virus-specific CTLp were present from day 5 after infection and reached maximum numbers within a further 2 days. The ratio of LECAM-1-:LECAM-1+ CTLp in the MLN ranged from 25:1 to > 200:1, with this pattern being maintained for memory spleen cells recovered 3 mo later. Lack of expression of LECAM-1 is thus characteristic of the great majority of Sendai-virus-specific CD8+ T cells, identified either as effector CTL or as precursors that can be stimulated in vitro under limiting dilution conditions. These lymphocyte populations cannot be discriminated on the basis of hi or lo CD45RB expression.
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