# IMMUNITY TO PARASITIC INFECTION

> **NIH NIH R01** · CORNELL UNIVERSITY · 1988 · $173,584

## Abstract

This proposal would carry forward studies of acquired resistance
to T. spiralis in a model system using rats.  The focus of the
inquiry would be on the resistance to T. spiralis that is
transferred passively from a specifically immunized mother to her
young.  The objectives are to evaluate the role(s) of different
subclasses of antibody in acquired resistance to infection; to
elucidate the mechanism by which invading muscle larvae become
entrapped in mucus; to characterize parasite antigens targeted in
the immune response; to ascertain the natural history and
regulation of protective, antibody secreting B cells; and to assess
the effect of weaning on the ability of antibody to passively
protect rats against T. spiralis.

Polyclonal antibodies and monoclonal antibodies of known subclass
and specificity would be further characterized in passive
protection experiments.  Hybridoma variants producing antibodies
with a protective combining site associated with alternative heavy
chains would be selected to determine the importance of isotype in
defining the antibody's protect function.  This question would be
further analyzed by enzymatically cleaving the antibody into
F(ab)'2 fragments.  Additional monoclonal antibodies would be
produced in order to confirm our observation that IgG2c antibodies
can be highly protective.

The interaction of protective antibodies with mucus would be
critically examined.  The role of mucus would be investigated to
determine whether mucin release is triggered by antigen in the
presence of antibody; whether it binds to antibody to form an
antigen specific trap or if mucus is entirely passive in action
and, in fact, not required for rapid expulsion.  We would evaluate
the potential of antibodies to induce the release of substances
which inhibit larval mobility in mucus or to inhibit such mobility
directly.

Protective monoclonal antibodies would be used to investigate the
distribution and function of their target antigen in muscle larvae.
The central question is whether the relevant parasite antigen is
targeted because it is expressed on the surfaces of larvae or
because it is functionally important to the parasite, particularly
to its capacity to invade the epithelium.  Epitope mapping with
protective and non-protective monoclonal antibodies would be
conducted to identify and active site(s) on the target antigen.

Another objective is to determine the natural history of protective
antibody producing cells.  Specific B cell reactivity to relevant
parasite antigens during infection would be compared in both
mucosal and non-mucosal lymphoid tissues.  The influence of helper
T cells from various tissues on B cell reactivity and isotype
expression would be examined.  These experiments would address the
question of how an antibody response that is dominated by a single
isotype develops during a complex infection.

Finally we would assess the effects of weaning on the expression
of rapid expulsion.  In particular we would evaluate...

## Key facts

- **NIH application ID:** 3125760
- **Project number:** 2R01AI014490-10A1
- **Recipient organization:** CORNELL UNIVERSITY
- **SAM.gov UEI:** G56PUALJ3KT5
- **Principal Investigator:** Judith A Appleton
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1988
- **Award amount:** $173,584
- **Award type:** 2
- **Project period:** 1978-07-01 → 1993-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3125760

## Citation

> US National Institutes of Health, RePORTER application 3125760, IMMUNITY TO PARASITIC INFECTION (2R01AI014490-10A1). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3125760. Licensed CC0.

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