Area:
Neuroscience Biology, Immunology
We are testing a new system for linking grants to scientists.
The funding information displayed below comes from the
NIH Research Portfolio Online Reporting Tools and the
NSF Award Database.
The grant data on this page is limited to grants awarded in the United States and is thus partial. It can nonetheless be used to understand how funding patterns influence mentorship networks and vice-versa, which has deep implications on how research is done.
You can help! If you notice any innacuracies, please
sign in and mark grants as correct or incorrect matches.
Sign in to see low-probability grants and correct any errors in linkage between grants and researchers.
High-probability grants
According to our matching algorithm, Mark A. Agius is the likely recipient of the following grants.
| Years |
Recipients |
Code |
Title / Keywords |
Matching
score |
| 1990 — 1992 |
Agius, Mark A |
K08Activity Code Description:
To provide the opportunity for promising medical scientists with demonstrated aptitude to develop into independent investigators, or for faculty members to pursue research aspects of categorical areas applicable to the awarding unit, and aid in filling the academic faculty gap in these shortage areas within health profession's institutions of the country. |
Immune Network in Myasthenia
The immune idiotype:anti-idiotype (Id:anti-Id) network is important in immunoregulation and tolerance. Its analysis in experimental autoimmune myasthenia gravis (EAMG) should provide insight into the abnormal immunoregulation in a defined antibody-mediated autoimmune disease, We have produced isogeneic monoclonal anti-Id antibodies directed against EAMG-inducing anti-acetylcholine receptor (AChR) monoclonal antibodies (mAbs) to be used as tools to analyze the immune network in EAMG. We have purified and characterized five anti-Id mAbs directed against two of these anti-AChR mAbs. Immunochemical analysis reveals that these anti-Ids are noncompetitive inhibitors of antigen (Ag) (i.e., ACHR) binding to the anti-AChR mabs. The Ids defined by the anti-Ids are moderately crossreactive with other anti-AChR mabs and with EAMG sera without being present in dominant levels. We have, nonetheless, suppressed the total serum anti-AChR antibody levels and prevented the development of EAMG by pretreating animals, prior to immunization with AChR, with physiologic doses of individual anti-Id mAb. These anti-Id thus play a major immunoregulatory role in EAMG. In our present proposal, the aim is to analyze the mechanism(s) involved in this observed suppression of the total anti-AChR response induced by manipulating an Id that is moderately crossreactive but not dominant in EAMG sera. Experiments are proposed to: a) further analyze the parameters important to the development of suppression (animal age, Ag dose, adjuvants used, and dose and timing of anti-Id) in order to characterize this biological system and to maximize the suppression; b) analyze the structural and cellular mechanisms involved in the observed suppression. To analyze structural mechanisms at a molecular level, we will clone and sequence the variable regions of the anti-AChR mAb 132A and the corresponding anti-Id-mAb HC-4A. To analyze cellular mechanisms, altered B cell secretions of Ab by anti-Id, and the role of specific B cell populations (Id + and anti-Id +) will be determined. This analysis of the immune network in EAMG should have implications for the understanding and treatment of human MG and other autoimmune diseases.
|
1 |