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CD44v10 expression in the mouse and functional activity in delayed type hypersensitivity
1Department of Tumour Progression and Immune Defence, German Cancer Research Centre, Heidelberg, Germany.
Journal of Cellular Physiology
|June 1, 1997
Summary
CD44 exon v10 (CD44v10) expression varies in cancer metastasis and is regulated in specific mouse tissues. Anti-CD44v10 antibodies inhibited immune responses like edema and granuloma formation, suggesting a role in cell migration.
Area of Science:
- Immunology
- Molecular Biology
- Cancer Research
Background:
- CD44 exon v10 (CD44v10) expression is altered during cancer metastasis.
- This variant isoform's specific functions and expression patterns require further investigation.
Purpose of the Study:
- To generate a CD44v10-specific monoclonal antibody for research.
- To define the expression pattern and functional role of CD44v10 in mice.
Main Methods:
- Monoclonal antibody generation against murine CD44v10.
- Analysis of CD44v10 expression in various mouse tissues and developmental stages.
- In vivo functional studies using anti-CD44v10, including wound healing and delayed type hypersensitivity (DTH) models.
- Investigation of lymphocyte-monocyte interactions and cell adhesion in transfected tumor lines.
Main Results:
- CD44v10 expression was found in specific epithelial layers, bone marrow, and activated lymphocytes in mice, with expression beginning late in gestation.
- Anti-CD44v10 treatment inhibited edema and granuloma formation in DTH responses but did not affect wound healing.
- Lymphocyte-monocyte interactions were inhibited by anti-CD44v10, and CD44v10-transfected tumor cells showed no distinct adhesion patterns.
- Data suggest CD44v10 involvement in cell migration, potentially as a receptor for cytokine/chemokine signaling.
Conclusions:
- CD44v10 plays a role in immune responses, specifically inhibiting edema and granuloma formation in DTH.
- CD44v10 may regulate cell migration by interacting with cytokine/chemokine signaling pathways.
- Further research is warranted to elucidate the precise mechanisms of CD44v10 in cell migration and immune modulation.