# REGULATION OF MACROPHAGE INFLAMMATORY FUNCTIONS BY CSF

> **NIH NIH R01** · UNIVERSITY OF TENNESSEE KNOXVILLE · 1987 · $91,688

## Abstract

Glycoprotein colony-stimulating factors (CSFs) have been considered, since
their discovery, to be growth factors promoting myelopoiesis.  However,
there have been isolated reports suggesting that various CSFs can elicit
alterations in the functional status of more mature cells.  This project
was initiated to determine if macrophage-active CSFs can influence effector
and accessory functions of monocytes and/or macrophages.  Results indicate
that macrophage-type CSF (CSF-1) is an important regulator of the
inflammatory and immunoregulatory functions of mononuclear phagocytes as
well as proliferative agent.  CSF-1 promotes production of Alpha/Beta
interferons (IFN), interleukin-1 (IL-1) and E series prostaglandins by
macrophages.  Additional evidence indicates that there is a differential
distribution of CSF-responsiveness within macrophage populations derived
from different anatomical sites which can be further defined by phenotypic
expression of class II MHC antigens (Ia).  In addition, CSF responsiveness
of macrophages has been found to be positively influenced by previous
exposure to IFNs and negatively regulated by iron-binding ferritins which
appear to specifically inhibit CSF-1 stimulation of Ia+ macrophages and
progenitor cells.  Extended investigations indicate that CSF-1 also
augments the capacity of macrophages to stimulate antigen-dependent T cell
activation and to kill yeast cells of Candida albicans in a manner that is
independent of receptors for IgG and does not involve enhanced production
of toxic oxygen metabolites.  Lastly, a CSF-1 responsive accessory cell has
been identified in marrow that appears to critically regulate not only the
production rate of new monocytes but also the differentiation state of the
newly derived progeny.  Experiments are proposed to identify this accessory
cell and define the nature of its regulatory functions.  Further
experiments are proposed to probe the apparent relationship between CSF-1
responsiveness, expression of Ia antigen and ferritin inhabitability and,
additionally, to determine if immune augmentation elicited by CSF-1 is
restricted to IL-1 production or may also include augmented processing
and/or presentation of antigen.  Enhanced killing of Candida albicans will
be further investigated with regard to endogenous intermediary signals and
to any effect of CSF-1 on the expression of receptors for yeast mannans.
Lastly, CSFs from EL-4 thymoma cells and P388D1 macrophage cells will be
compared with CSF-1 from fibroblasts (L929) for their relative efficiencies
in stimulating functional activities of macrophages.

## Key facts

- **NIH application ID:** 3128371
- **Project number:** 5R01AI018960-05
- **Recipient organization:** UNIVERSITY OF TENNESSEE KNOXVILLE
- **SAM.gov UEI:** FN2YCS2YAUW3
- **Principal Investigator:** ROBERT N MOORE
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1987
- **Award amount:** $91,688
- **Award type:** 5
- **Project period:** 1983-03-01 → 1991-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3128371

## Citation

> US National Institutes of Health, RePORTER application 3128371, REGULATION OF MACROPHAGE INFLAMMATORY FUNCTIONS BY CSF (5R01AI018960-05). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3128371. Licensed CC0.

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