# HOST DEFENSES IN SYSTEMIC LUPUS ERYTHEMATOSUS

> **NIH NIH R01** · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · 1989 · $141,426

## Abstract

Infection is a major cause of morbidity and mortality among patients with
systemic lupus erythematosus (SLE).  One objective of the proposed research
is to examine in detail the nature, source, and mechanism of action of a
cationic protein that we have found in serum from some patients with SLE
and that inhibits (in a uniquely specific and reversible fashion) the
chemotactic activity of complement (C5)-derived peptides.  The hypothesis
will be tested that the inhibitor is a fragment of a native serum (or
plasma) protein that is generated as a consequence of complement activation
(i.e., Bb fragment of factor B).

Another objective of the proposed research is to determine the mechanism of
action of an anionic polypeptide (cochemotaxin) that we have found in
normal human serum (and plasma), and that permits low concentrations of
human C5a des Arg to exhibit chemotactic activity for human
polymorphonuclear leukocytes (PMN).  We have found that C5a des Arg plus
its cochemotaxin probably accounts for most of the chemotactic activity
that is generated in human serum after complement activation.  We also have
found that the cochemotaxin forms a physical complex with C5a des Arg,
possibly by attaching to a sialic acid residue on the oligosaccharide
portion of the molecule.  Experiments will be performed to characterize the
cochemotaxin and to examine further its interactions with C5a des Arg,
desialated C5a des Arg, and deglycosylated C5a des Arg.

Our final objective is to demonstrate physical interactions between the
purified inhibitor and either the cochemotaxin or C5a des Arg.  The
hypothesis will be tested that the cochemotaxin (not C5a des Arg) is the
target of the inhibitor.

The studies outlined in this proposal should yield new information that may
explain (in part) why patients with SLE have an increased susceptibility to
severe bacterial infections.  On a more basic level, these studies should
provide information concerning structure-activity relationships and
mechanisms involved in regulating the biologic activities of
complement-derived peptides.

## Key facts

- **NIH application ID:** 3155677
- **Project number:** 2R01AR028566-10
- **Recipient organization:** UNIVERSITY OF CALIFORNIA, SAN FRANCISCO
- **SAM.gov UEI:** KMH5K9V7S518
- **Principal Investigator:** H D PEREZ
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1989
- **Award amount:** $141,426
- **Award type:** 2
- **Project period:** 1980-09-01 → 1992-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3155677

## Citation

> US National Institutes of Health, RePORTER application 3155677, HOST DEFENSES IN SYSTEMIC LUPUS ERYTHEMATOSUS (2R01AR028566-10). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3155677. Licensed CC0.

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