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Antigen-specific CD8(+) T cell subset distribution in lymph nodes draining the site of herpes simplex virus infection


Cose, SC; Jones, CM; Wallace, ME; Heath, WR; Carbone, FR
1997-09
EUROPEAN JOURNAL OF IMMUNOLOGY
Journal Article
27
9
2310-2316
Inoculation with replicating virus leads to an increase in T cell numbers within lymph nodes that drain the site of infection. This increase has been associated with a nonspecific proliferation of bystander cells, with only a minority thought to be directed to the infectious agent. Such an assumption is largely based on precursor cytotoxic T lymphocyte (CTL) estimations using limiting dilution analysis. Recently, studies using more advanced molecular approaches have suggested that such functionally derived precursor frequencies considerably underestimate the proportion of T cells specific for the antigen under investigation. We have defined T cell receptor sequences characteristic of CTL populations directed to a dominant determinant of the herpes simplex virus (HSV) glycoprotein B (gB). In this investigation, we used this receptor signature as a probe to directly monitor changes occurring within lymph nodes draining the sites of active infection with HSV. We found that although lymph node CD8(+) T cell numbers increase as a consequence of HSV infection, the majority of these cells are small resting cells that are not enriched for gB-specific receptors. In contrast, a significant proportion of activated T cells are highly enriched for CTL bearing gB-specific receptors. Our results are therefore consistent with a nonspecific migration of CTL precursors into the lymph nodes draining the site of infection, followed by the activation and proliferation of the antigen-specific subset that normally makes up a small proportion of the naive T cell repertoire.
VCH PUBLISHERS INC
IN-VIVO; IMMUNE-RESPONSE; MEMORY; LYMPHOCYTES; RECEPTOR; ACTIVATION; DIVERSITY; PROLIFERATION; REPERTOIRES; INVIVO
10.1002/eji.1830270927
Refer to copyright notice on published article.

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Creation Date 1997-09-01 12:00:00