# LEISHMANIA AND HOST DEFENSE

> **NIH NIH R01** · WEILL MEDICAL COLL OF CORNELL UNIV · 1989 · $121,148

## Abstract

We have been interested in how intracellular organisms infect mononuclear
phagocytes and what determines their survival in these cells.  Our previous
work showed that Leishmania promastigotes fix complement to their surface
by activating the alternative complement pathway, and that the major class
of receptors with which they then interact on the macrophage is the
complement receptor type 3 (CR3).  We have also shown that the parasite
surface protease p63 can modify  the form of C3 on the surface of the
parasite and in this way change the receptor to which the parasite binds.
Finally, we have shown that the mechanism of promastigote binding is
crucial to the ultimate intracellular fate of the organism.  While we are
continuing to work on the promastigote form, we have also begun a major
effort to analyze the binding, uptake, and fate of the amastigote.  We have
already reported that amastigotes are also alternative pathway activators.
However, preliminary data suggest that they interact primarily with the
complement receptor type 1 (CR1), probably because their p63 lacks the
proteolytic activity to convert C3b (the CR1 ligand) to C3bi (the CR3
ligand).  Using new assays for the binding and intracellular fate of
amastigotes, and a number of new analytic techniques for studying the role
of complement in parasite-phagocyte interactions, we are now trying to
determine how the difference in receptor class between the promastigote and
amastigote forms may relate to the ultimate intracellular fate and
virulence of the two forms, and how changes in the physiology of cell
receptors in the activated macrophage may explain the ability of cell
mediated immunity to limit leishmanial infection in vivo.

## Key facts

- **NIH application ID:** 3129348
- **Project number:** 2R01AI019888-04A2
- **Recipient organization:** WEILL MEDICAL COLL OF CORNELL UNIV
- **SAM.gov UEI:** YNT8TCJH8FQ8
- **Principal Investigator:** PAUL J EDELSON
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1989
- **Award amount:** $121,148
- **Award type:** 2
- **Project period:** 1984-07-01 → 1991-11-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3129348

## Citation

> US National Institutes of Health, RePORTER application 3129348, LEISHMANIA AND HOST DEFENSE (2R01AI019888-04A2). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3129348. Licensed CC0.

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