# MECHANISMS OF NONSTERILIZING IMMUNITY IN MALARIA

> **NIH NIH R01** · HAHNEMANN UNIVERSITY · 1987 · $196,161

## Abstract

Resistance to acute Plasmodium chabaudi adami malaria in mice is mediated
by non-antibody mechanisms of immunity.  Adoptive cell transfer studies
demonstrate that T cells are required for both the induction and expression
of this form of immunity.  The purpose of the proposed study is to
determine which Lyt subsets of splenic T cells are involved.  Lyt subsets
of spleen cells from euthymic mice prepared by selective killing with
anti-Lyt monoclonal antibody in the presence of complement or by panning
rat anti-mouse Lyt coated spleen cells on petri plates coated with anti-rat
Ig will be injected into histocopatible athymic nude mice prior to
challenge with P. chadaudi adami.  The resulting parasitemias will be
plotted against time in order to see which Lyt subset(s) suppress
infection.  Also, Lyt subsets of spleen cells prepared from the spleens of
P. chabaudi adami immune B-cell deficient mice as well as immunologically
intact mice will be tested for their ability to adoptively transfer
immunity to P chabaudi adami infection to irradiated homologous
recipients.  In order to define mechanisms of nonantibody immunity to P.
chabaudi adami T-cell clones and T-cell hybrids constructed with spleen
cells of immune mice will be tested for their capacity to protect nude mice
against challenge infection.  Similarly, soluble factors from protective
cell lines will be characterized and tested for their ability to mediate
protection in nude mice.

Two additional parameters will be investigated in order to determine
whether they can be correlated with protection achieved with Lyt fraction
T-cell clones and T-cell hybrids.  These are splenic macrophage activation
as determined by chemiluminescence and the activation of splenic reticular
cells.  Finally, P. chabaudi adami antigens will be fractionated and
characterized in terms of their ability to activate protecting cell
populations as well as to induce protection in mice by immunization.

This approach, which will attempt to correlate protection with cell
function, factor-production, and effector cell activation, may provide a
coherent physiologic picture of events which must transpire for the
expression of antibody-independent immunity.

## Key facts

- **NIH application ID:** 3125258
- **Project number:** 5R01AI012710-12
- **Recipient organization:** HAHNEMANN UNIVERSITY
- **Principal Investigator:** WILLIAM Paul WEIDANZ
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1987
- **Award amount:** $196,161
- **Award type:** 5
- **Project period:** 1975-06-01 → 1988-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3125258

## Citation

> US National Institutes of Health, RePORTER application 3125258, MECHANISMS OF NONSTERILIZING IMMUNITY IN MALARIA (5R01AI012710-12). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3125258. Licensed CC0.

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