# MYCOPLASMA ARTHRITIDIS T CELL MITOGEN

> **NIH NIH R01** · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · 1992 · $180,229

## Abstract

The long term aims of this project are designed to elucidate how
microbial mitogens can influence host susceptibility to disease or to
participate in disease, and to apply this knowledge to the development of
immunoregulatory substances which might be of benefit in the treatment of
human disease based upon immunological dysfunction.

The immediate specific aims for the current grant period are: 1. to
determine the structural features of the M. arthritidis T cell mitogen
(MAM) that are important for interaction with I-E protein accessory cell
surface receptor and for biological activity in respect to: a)further
develop procedures for production of homogeneous MAM; b) determination of
the primary amino acid sequence of MAM; c) identification of active
moieties of MAM by means of; i) specific residue derivatization, and ii)
biologic and I-E binding activities of proteolytic or chemically derived
oligopeptides from MAM. 2. Mechanism (s) of MAM-induced inhibition of T
cell responses to mitogens in respect to: a) changes in cell populations
in vivo following injection of MAM; b) cytokine production in vivo in
response to MAM; c) MHC restriction of suppression; d) identification of
the effector cell responsible for inhibition (i.e. is, cytolytic or
natural killer cells or macrophages; e) role of soluble factors in
suppression; f) effectiveness and potential toxicity of multiple doses of
MAM on T cell function. 3. Effects of MAM on various parameters of immune
function in respect to: a) inhibition of T cell responses to foreign
antigens in vivo: b) inhibition of the in vitro response of node T cells
and T cell hybridomas to antigens; c) inhibition of humoral antibody
responses to T cell dependent and independent antigens; d) inhibition of
the mixed lymphocyte reaction to mixtures of disparate MHC or Mls
determinants: e) prolongation of allograft survival with a view to
practical use of MAM as a new immunomodulator.

## Key facts

- **NIH application ID:** 3154646
- **Project number:** 5R01AR002255-32
- **Recipient organization:** UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH
- **SAM.gov UEI:** LL8GLEVH6MG3
- **Principal Investigator:** BARRY C COLE
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1992
- **Award amount:** $180,229
- **Award type:** 5
- **Project period:** 1978-03-01 → 1994-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3154646

## Citation

> US National Institutes of Health, RePORTER application 3154646, MYCOPLASMA ARTHRITIDIS T CELL MITOGEN (5R01AR002255-32). Retrieved via MORVS 2026-10-24 from https://api.morvs.ai/grant/nih/3154646. Licensed CC0.

---

*[NIH grants dataset](/datasets/nih-grants) · CC0 1.0*