The immunophenotype and activation status of the lymphocytic infiltrate in human breast cancers, the role of the major histocompatibility complex in cell-mediated immune mechanisms, and their association with prognostic indicators
The aims of this study were to characterize, phenotypically, the immune infiltrate in human breast cancers, to assess the activation status of tumor-infiltrating lymphocytes (TIL), and to define the association of these findings with established prognostic indicators. Immunohistochemistry was perfor...
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Veröffentlicht in: | Surgery 2003-11, Vol.134 (5), p.827-834 |
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Sprache: | eng |
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Zusammenfassung: | The aims of this study were to characterize, phenotypically, the immune infiltrate in human breast cancers, to assess the activation status of tumor-infiltrating lymphocytes (TIL), and to define the association of these findings with established prognostic indicators.
Immunohistochemistry was performed on frozen sections of 60 primary breast cancers by use of monoclonal antibodies to T lymphocytes (CD3), T-helper cells (CD4), cytotoxic T-cells (CD8), natural killer cells (CD56), interleukin-2 receptors (IL-2R), and major histocompatibility (MHC) class I antigen (HLA-ABC) and MHC class II antigen (HLA-DR).
All tumors stained positive for CD3, CD4 and CD8, but with marked variation in the intensity of the infiltrate. In tumors with a moderate infiltrate of TIL, there was a trend toward a greater representation of T–helper cells. However, as the intensity of TIL increased, there was a decline in the proportion of T–helper cells and a concomitant rise in the relative proportion of cytotoxic T cells. There was a relative paucity of natural killer cells. A significant association was found between the intensity of TIL and the number of positive nodes (
P
=
.02) and the intensity of the infiltrate of both T–helper cells and cytotoxic T cells with ER expression (
P
=
.03 and .05, respectively). Most tumors stained positive for IL-2R. The expression of IL-2R was associated with the intensity of TIL (
P |
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ISSN: | 0039-6060 1532-7361 |
DOI: | 10.1016/S0039-6060(03)00292-7 |