Studies of Altered Response to Infection Induced by Severe Injury.
Abstract
The goals of this research are (1) to delineate the role of suppressor T cells and inhibitory monocytes (M0) in mediating the immunosuppression that follows severe injury, (2) to develop and improve assays for assessment of macrophage function, (3) to investigate the relationship between immunosuppression and post-trauma alterations in M0 subsets, and to investigate prophylactic modalities for reversing immunosuppression. We have demonstrated that trauma induced suppressor T cells (Ts) can depress monocyte function and that at least some of the Ts mediate immunosuppression by stimulating monocytes to produce elevated levels of prostaglandin E2 (PGE2). We have concentrated on trying to associate a change in M0 function with a change in M0 phenotype. We have shown that elevation of M0 PGE2 production appears to correlate with the shift toward a M0 subset that can be identified by its expression of a high affinity receptor for the crystalline fragment of Immunoglobulin G (i.e., Fc+). We have demonstrated that there is an increase in the numbers of the Fc+ M0 subset and that this increase correlates both to elevation of PGE2 production and poor clinical outcome.
Document Details
- Document Type
- Technical Report
- Publication Date
- Mar 01, 1987
- Accession Number
- ADA185914
Entities
People
- Carol L. Miller
Organizations
- University of Massachusetts Medical School