Interplay of antibody and T cell responses in acute myocardial infarction

Citation
Aw. Elahi et al., Interplay of antibody and T cell responses in acute myocardial infarction, J LA CL MED, 138(2), 2001, pp. 112-118
Citations number
37
Categorie Soggetti
Research/Laboratory Medicine & Medical Tecnology","Medical Research General Topics
Journal title
JOURNAL OF LABORATORY AND CLINICAL MEDICINE
ISSN journal
00222143 → ACNP
Volume
138
Issue
2
Year of publication
2001
Pages
112 - 118
Database
ISI
SICI code
0022-2143(200108)138:2<112:IOAATC>2.0.ZU;2-R
Abstract
This study sought to investigate the interplay between antibody and T cell responses triggered by an acute myocardial infarction (MI) and their possib le role in the progress of this disease. Serum samples were collected from two groups of patients, group A (n = 26) within the first week of MI, and g roup B (n = 28) at 2 weeks and 2 months after Mi. Patients in group A were older and had higher prevalence of hypertension and previous attack of Mi t han patients in group B. The levels of antimyosin immunoglobulin M and immu noglobulin G antibodies in the serum samples from group A were significantl y higher than those in normal control subjects. In group B, the levels of b oth antibodies were lower than those in group A but remained significantly higher than those in normal control subjects at both 2 weeks and 2 months. The levels of intercellular adhesion molecule-1 (sICAM-1) and vascular cell adhesion molecule-1 (sVCAM-1) in the serum samples from group A patients w ere significantly higher than those in normal control subjects. At 2 weeks after Mi (group B), only the level of sVCAM-1, but not that of sICAM-1, was significantly higher than that in normal control subjects, and there were no significant changes in the levels of these two molecules from 2 weeks to 2 months after MI. We conclude that the higher levels of anti-myosin antib odies and adhesion molecules in group A patients as compared with group B p atients may be due to higher or more frequent exposures of their immune sys tems to heart antigens. Furthermore, the immunoglobulin M antibody response during the first week of Mi had an inverse relationship with the level of interleukin-2R (sIL-2R), which suggested a possible suppressive or regulato ry role of this antibody on the cellular immune response during this time.