Journal
JOURNAL OF IMMUNOLOGY
Volume 165, Issue 11, Pages 6015-6019Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.165.11.6015
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Funding
- NCI NIH HHS [R01 CA52527] Funding Source: Medline
- NIAID NIH HHS [R01 AI40171] Funding Source: Medline
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STAT4 and STAT6 are essential for the development of CD4(+) Th1 and Th2 development, respectively, Tumor immunologists have hypothesized that Th1 cells are critical in tumor immunity because they facilitate differentiation of CD8(+) T cells, which are potent anti-tumor effectors. We have used STAT4(-/-) and STAT6(-/-) mice to test this hypothesis. BALB/c and knockout mice were challenged in the mammary gland with the highly malignant and spontaneously metastatic BALB/c-derived 4T1 mammary carcinoma. Primary tumor growth and metastatic disease are reduced in STAT6(-/-) mice relative to BALB/c and STAT4(-/-) mice. Ab depletions demonstrate that the effect is mediated by CD8(+) T cells, and immunized STAT6(-/-) mice have higher levels of 4T1-specific CTL than BALB/c or STAT4(-/-) mice. Surprisingly, Th1 or Th2 cells are not involved, because CD4 depletion does not diminish the anti-tumor effect. Therefore, deletion of the STAT6 gene facilitates development of potent anti-tumor immunity via a CD4(+)-independent pathway.
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