Abstract
While recent evidence from several laboratories has shown that interleukin-4 (IL-4) can act on a number of cells in addition to B lymphocytes, these have thus far been limited to cells of the hematopoietic lineage. Here we report that murine IL-4 promotes DNA synthesis in both primary and immortalized fibroblasts. Marked stimulation of [3H]thymidine incorporation was observed for primary skin fibroblasts of Balb/c3T3 cells stimulated with HPLC- or immunoaffinity-purified as well as recombinant IL-4. Responses to immunoaffinity and recombinant IL-4 were completely blocked with anti-IL-4 antibody. Similar dose/response relationships were observed for recombinant IL-4 on skin fibroblasts and an IL-4 responsive murine T cell tumor, suggesting that the receptors for this lymphokine on these cells is simular. Together, these results show that IL-4 can cause DNA synthesis by murine fibroblasts presumably through ligand-receptor interactions at the cell surface. Implications of these findings to inflammation during an immune response is discussed.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 292-298 |
| Number of pages | 7 |
| Journal | Clinical Immunology and Immunopathology |
| Volume | 49 |
| Issue number | 2 |
| DOIs | |
| State | Published - 1988 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Immunology
- Immunology and Allergy
- Pathology and Forensic Medicine
Cite this
Lymphokine regulation of inflammatory processes : Interleukin-4 stimulates fibroblast proliferation. / Monroe, John G.; Haldar, Subrata; Prystowsky, Michael B.; Lammie, Patrick.
In: Clinical Immunology and Immunopathology, Vol. 49, No. 2, 1988, p. 292-298.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Lymphokine regulation of inflammatory processes
T2 - Interleukin-4 stimulates fibroblast proliferation
AU - Monroe, John G.
AU - Haldar, Subrata
AU - Prystowsky, Michael B.
AU - Lammie, Patrick
PY - 1988
Y1 - 1988
N2 - While recent evidence from several laboratories has shown that interleukin-4 (IL-4) can act on a number of cells in addition to B lymphocytes, these have thus far been limited to cells of the hematopoietic lineage. Here we report that murine IL-4 promotes DNA synthesis in both primary and immortalized fibroblasts. Marked stimulation of [3H]thymidine incorporation was observed for primary skin fibroblasts of Balb/c3T3 cells stimulated with HPLC- or immunoaffinity-purified as well as recombinant IL-4. Responses to immunoaffinity and recombinant IL-4 were completely blocked with anti-IL-4 antibody. Similar dose/response relationships were observed for recombinant IL-4 on skin fibroblasts and an IL-4 responsive murine T cell tumor, suggesting that the receptors for this lymphokine on these cells is simular. Together, these results show that IL-4 can cause DNA synthesis by murine fibroblasts presumably through ligand-receptor interactions at the cell surface. Implications of these findings to inflammation during an immune response is discussed.
AB - While recent evidence from several laboratories has shown that interleukin-4 (IL-4) can act on a number of cells in addition to B lymphocytes, these have thus far been limited to cells of the hematopoietic lineage. Here we report that murine IL-4 promotes DNA synthesis in both primary and immortalized fibroblasts. Marked stimulation of [3H]thymidine incorporation was observed for primary skin fibroblasts of Balb/c3T3 cells stimulated with HPLC- or immunoaffinity-purified as well as recombinant IL-4. Responses to immunoaffinity and recombinant IL-4 were completely blocked with anti-IL-4 antibody. Similar dose/response relationships were observed for recombinant IL-4 on skin fibroblasts and an IL-4 responsive murine T cell tumor, suggesting that the receptors for this lymphokine on these cells is simular. Together, these results show that IL-4 can cause DNA synthesis by murine fibroblasts presumably through ligand-receptor interactions at the cell surface. Implications of these findings to inflammation during an immune response is discussed.
UR - http://www.scopus.com/inward/record.url?scp=0023698689&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0023698689&partnerID=8YFLogxK
U2 - 10.1016/0090-1229(88)90119-5
DO - 10.1016/0090-1229(88)90119-5
M3 - Article
VL - 49
SP - 292
EP - 298
JO - Clinical Immunology
JF - Clinical Immunology
SN - 1521-6616
IS - 2
ER -