ISSN:
1534-4681
Keywords:
Breast cancer
;
Tumor-infiltrating lymphocyte
;
Immunohistochemistry Interleukin-2
;
Interleukin-4
;
Tumor growth factor-beta 1
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Abstract Background: Human breast cancers progressively grow despite the presence of extensive lymphocytic infiltration and specific antitumor immune recognition, thereby calling into question the competency of breast tumor-infiltrating lymphocytes (TIL). The function of breast TILs in vivo and their possible role in the suppression of an antitumor immune response are largely unknown. Methods: The cytokines produced in situ by lymphocytes in 89 breast carcinomas and 14 benign breast lesions were assessed using immunohistochemistry. Results: The majority of tumor and benign breast samples contained T-cell infiltrates, which were disclosed using an anti-CD3 antibody stain. The percentage of tumor samples in which ⩾3% of the lymphocytes were producing cytokines was as follows: interleukin (IL)-2 45%, IL-4 36%, tumor necrosis factor-alpha (TNF-α) 28%, transforming growth factor-beta 1 (TGF-β1) 20%, IL-10 11%, interferon-gamma (IFN-γ) 4%, and granulocytemacrophage colony-stimulating factor (GM-CSF) 3%. Production of IL-2, IL-4, and TGF-β1 by TILs in breast cancers exceeded that detected in benign breast lesions (p〈0.005). Significantly more tumor samples contained lymphocytes producing IL-2, IL-4, TGF-β1, and TNF-α than IFN-γ and GM-CSF (p〈0.002 for each comparison). One or more of the potentially immunoinhibitory cytokines—IL-4, IL-10, or TGF-β1—were produced by lymphocytes in 44% of the specimens. No significant associations were seen between lymphocyte production of a particular cytokine and disease-free survival (median follow-up 43 months). Conclusions: Immunohistochemical techniques can be used to detect cytokine secretion by TILs in preserved tissue. The relative lack of secretion of IFN-γ and GM-CSF, rather than a deficiency of IL-2, may explain why the antitumor immune response to breast cancer is impaired.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF02305798
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