PMID- 7790775
OWN - NLM
STAT- MEDLINE
DCOM- 19950721
LR  - 20190516
IS  - 0741-5400 (Print)
IS  - 0741-5400 (Linking)
VI  - 57
IP  - 6
DP  - 1995 Jun
TI  - Induction of macrophage suppressor activity by fibrosarcoma-derived transforming 
      growth factor-beta 1: contrasting effects on resting and activated macrophages.
PG  - 919-28
AB  - Tumor-derived transforming growth factor-beta 1 (TGF-beta 1) suppresses several 
      immune responses. Because tumor growth induces macrophage (m phi) suppressor 
      activity, we determined whether murine fibrosarcoma-derived TGF-beta 1 
      contributed to m phi-mediated suppression of autoantigen- and 
      alloantigen-stimulated T cell proliferation. The murine fibrosarcoma Meth-KDE 
      cell line constitutively produced TGF-beta 1. Meth-KDE tumor-bearing host (TBH) 
      syngeneic splenic m phi s suppressed autoantigen- and alloantigen-stimulated 
      normal host (NH) CD4+ T cell proliferation. Pretreatment with Meth-KDE 
      supernatants induced NH m phi s to suppress T cell proliferation as much as TBH m 
      phi s. Anti-TGF-beta 1 antibody treatment reversed Meth-KDE-induced NH m 
      phi-mediated suppression. Recombinant TGF-beta 1-induced m phi-mediated 
      suppression was not blocked during inhibition of prostaglandin E2 (PGE2), nitric 
      oxide (NO), or TGF-beta 1 production. However, Meth-KDE-induced m phi-mediated 
      suppression was partly reduced when PGE2 production was inhibited. Pretreatment 
      with tumor cell-derived TGF-beta 1, but not recombinant TGF-beta 1, increased 
      activated m phi PGE2 production. These results show that additional tumor-derived 
      molecules aid in TGF-beta 1-enhanced PGE2 production. Also, TGF-beta 1 alone 
      up-regulates m phi synthesis of suppressor molecules that are different from 
      PGE2, NO, and TGF-beta 1. Although TGF-beta 1 has direct suppressor activity on 
      lymphocytes, these results show that release of tumor cell TGF-beta 1 also 
      induces m phi suppressor activity.
FAU - Alleva, D G
AU  - Alleva DG
AD  - Department of Biology, Virginia Polytechnic Institute and State University, 
      Blacksburg 24061-0406, USA.
FAU - Walker, T M
AU  - Walker TM
FAU - Elgert, K D
AU  - Elgert KD
LA  - eng
PT  - Journal Article
PL  - England
TA  - J Leukoc Biol
JT  - Journal of leukocyte biology
JID - 8405628
RN  - 0 (Recombinant Proteins)
RN  - 0 (Suppressor Factors, Immunologic)
RN  - 0 (Transforming Growth Factor beta)
RN  - K7Q1JQR04M (Dinoprostone)
SB  - IM
MH  - Animals
MH  - Dinoprostone/physiology
MH  - Fibrosarcoma/*immunology/metabolism
MH  - Lymphocyte Activation
MH  - Macrophage Activation/*drug effects
MH  - Macrophages/*drug effects/physiology
MH  - Male
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Inbred C3H
MH  - Recombinant Proteins/pharmacology
MH  - Suppressor Factors, Immunologic/*biosynthesis
MH  - Transforming Growth Factor beta/biosynthesis/*pharmacology
EDAT- 1995/06/01 00:00
MHDA- 1995/06/01 00:01
CRDT- 1995/06/01 00:00
PHST- 1995/06/01 00:00 [pubmed]
PHST- 1995/06/01 00:01 [medline]
PHST- 1995/06/01 00:00 [entrez]
AID - 10.1002/jlb.57.6.919 [doi]
PST - ppublish
SO  - J Leukoc Biol. 1995 Jun;57(6):919-28. doi: 10.1002/jlb.57.6.919.