Specific B lymphocytes can act as very efficient antigen-presenting cells. They bind antigen with high affinity via their immunoglobulin receptors, process it through the class II major histocompatibility complex (MHC) pathway, and present its fragments to class II-restricted T lymphocytes. In general, exogenous antigens and noninfectious viral particles enter the class II pathway and are selectively associated with class II MHC molecules. The presentation of an exogenous antigen in association with class I molecules has been reported for only a few antigens, including the hepatitis B envelope antigen (HBenvAg). Here we demonstrate that antigen-specific B cells can efficiently deliver HBenvAg to the class I pathway, presenting its fragments to class I-restricted cytotoxic T lymphocytes (CTLs) which kill the specific B cells. This could represent a mechanism of suppression of neutralizing anti-hepatitis B virus (HBV) antibody response, a phenomenon that accompanies the development of the chronic HBV-carrier state.

We analyzed whether normal human hepatocytes, which normally do not display Class II major histocompatibility complex antigens, can be induced to express them in vitro, and whether this induction has an in vivo counterpart in chronic liver diseases. While both alpha- and gamma-interferon induced expression of Class I antigens, only gamma-interferon induced expression of Class II antigens on hepatocytes in vitro. Recombinant interleukin 2 had no effect on major histocompatibility complex antigen expression. Both Class I and Class II antigens could be detected by indirect immunofluorescence on hepatocytes from patients with various forms of chronic liver disease, regardless of etiology. These findings suggest that gamma-interferon produced by T lymphocytes that infiltrate the liver during the course of chronic hepatitis induces Class II major histocompatibility complex antigen expression and may endow the hepatocytes with the capacity to perform accessory (antigen-presenting) cell functions.

We conducted a controlled multicenter trial with central randomization and evaluation of events under blind conditions involving 652 patients with unstable angina. Patients were treated either with conventional therapy alone (group C) (n =338) or with conventional therapy combined with an inhibitor of platelet aggregation, ticlopidine 250 mg b.i.d. (group C+T) (n=314). Patients were assigned randomly within 48 hours of admission and followed up for 6 months. With the "intention-to-treat" approach, the primary end points, vascular death and nonfatal myocardial infarction, were observed in 13.6% of the patients in group C and in 7.3% of the patients in group C+T, which is a reduction in risk of 46.3% (p=0.009). Vascular mortality was 4.7% in patients in group C and 2.5% in patients in group C+T, which is a reduction in risk of 46.8% (p=0.139). The risk of nonfatal myocardial infarction was reduced by 46.1% (p=0.039), with a frequency of 8.9o in patients in group C and 4.8% in patients in group C+T. New Q wave myocardial infarction occurred with a frequency of 6.8% in patients in group C and 3.8% in patients in group C+T, which is a reduction in risk of 44.1% (p=0.091). Fatal and nonfatal myocardial infarction was 10.91% in patients in group C and 5.1% in patients in group C+T, which is a reduction in risk of 53.2% (p=0.006). These findings confirm the importance of platelets in the pathogenesis of unstable angina and the usefulness of antiplatelet treatment for the prevention of cardiovascular events.

The frequency of myocardial infarction and sudden death is increased between 6 AM and noon. To determine whether the same is true for the onset of ischemic stroke, we studied 426 consecutive patients within 12 hours after the onset of their first hemispheric stroke. The frequency of onset of hemispheric stroke was significantly (p=0.0001) higher from 6:01 AM to noon (56.1%) than from 12:01 PM to 6 PM (20.2%), from 6:01 PM to midnight (92%), and from 12:01 AM to 6 AM (15.5%). The identification of periods of high risk for vascular events may have important therapeutic implications, such as matching drug effects with vulnerability. (Stroke 199(^21^87-389)