CURRENT LITERATURE 229

no effect. Measurement of complement activation within the plasma showed that the mechanism of IVIg's action was at least partially dependent on its anti-complemetuary activity. These results suggest that one of the mechanisms of action of IVIg in delaying hyperacute rejection is through complement inhibition.

Effects of Job Strain on Helper-Inducer (CD4+CD29+) and Suppressor-Inducer (CD4+CD45RA+) T Cells in Japanese Blue-Collar Workers. Kawakami N, Tanigawa T, Araki S, et al. Psychother Psychosom 66:192-198, 1997.

It is well known that infection with the human immunodefi- ciency virus modulates the number of CD4+ T helper-inducer lymphocytes, and such measurements are frequently used to evaluate severity of disease and response to therapy. It is thus important to recognize other factors that may affect these cell populations. Psychological stressors and distress have been linked to alterations in immune function, and short-term and chronic stress have been shown to decrease the number and percentage of CD4+ and CD8+ T cells. These authors used a standm'dized questionnaire to evaluate various perceived job stressors in 65 subjects. Job control significantly and positively correlated with the number and percent of T helper-inducer cells. Job demands, supervisor support, and coworker support, however, did not. A job strain index (ratio of job demands to job control) significantly negatively correlated with the percentage of T helper-inducer T cells. There were no significant correla- tions with suppressor-inducer T cell levels. Although further research is needed to clarify psychophysiological mechanisms of the association between job stressors and T cells, for example, considering stages of stress coping, a low T helper-inducer count may perhaps provide objective evidence to your boss that you are working too hard.

An Original Method to Study Autoantibody Specificity in Haemoglobin Stained Eluates by the Column Agglu- tination Techniques. Florin F, Cozzi MR, Pradella P, et al. Clin Lab Haemost 19:209-211, 1997.

Column agglutination techniques (CAT) have an increased sensitivity in detecting red cell autoantibodies compared with the conventional tube test. When studying autoantibody specific- ity by the indirect antiglobulin test with CAT, ether and xylene elution techniques result in hemoglobin-stained eluates; the red color prevents identification of positive reactions. The authors describe an original method that overcomes the interference attributable to hemoglobin and takes advantage of the sensitivity of the CAT. Xylene eluates were incubated with group O red cell panels at 37~ for 45 minutes in microtiter plate wells. After washing, the sensitized red cells were suspended in low ionic strength solution and applied onto the microtubes containing antiglobulin serum. Positive reactions were recorded after centrifugation. In eluates that failed to show reactivity by the conventional indirect antiglobulin technique, 20 of 23 eluates from human immunodeficiency virus (HIV)-infected patients, and 12 of 12 of eluates from patients with red cell autoimmunity secondary to lymphoproliferative disease gave a positive result by the described CAT indirect antiglobulin method. This al- lowed serological elucidation of the pathogenesis of hemolytic anemia in five patients who otherwise appeared to have autoim- mune hemolysis with a negative direct antiglobulin test. This

method may be a useful adjunct in the investigations of patients with autoantibodies in hemoglobin-stained elnates.

Intravenous Immunoglobulins and Transforming Growth Factor I~. Kekow J, Reinhold D, Pap T, et ah Lancet 351:184-185, 1998.

As the indications for the use of intravenous immunoglobulin (IV IgG) continue to increase, any form of single unifying mechanism for therapeutic action of IV IgG becomes seemingly more and more obscure. While the concept of blocking antibod- ies able to interrupt pathogenic antibodies is widely circulated, it is difficult to reconcile a "blocking antibody" mechanism with such a wide variety of immune-based disorders, including autoimmune thrombocytopenia, chronic inflammatory polyneu- ropathies of variable origins, acute Guillain-Barr6 syndrome, Kawasaki's disease, and the like. In addition, globulin appears to have some benefit in disorders considered to be more "cellular" than humoral in nature.

This intriguing brief report in the Lancet suggests a com- pletely different mechanism of action for the beneficial effects of IV IgG. The authors measured a variety of different IV IgG products for evidence of soluble cytokines, including interleukin (IL)-6, IL-10, tumor necrosis factor-a (TNFa), and transform- ing growth factor-f31 (TGF[31), TGF[32, and TGF[33. Although there was no evidence for Th-2-type cytokines IL-6 and IL-10, they did find relatively high levels (> 10 ng/mL) of TGF[31 and TGF[~2 in all 238 samples tested. No IV IgG preparation sample was free of TGF[31 or TFG[32. TGF[3 did not appeal to be bound to immunoglobulin, as a protein A column did not deplete IV IgG of TGF[3.

The authors went on to measure TGF[31 and TGF[32 levels in 15 patients who were transfused with IV IgG. There was a significant increase in circulating levels of TGF[~ after treatment with globulin. Does administration of IV IgG to patients really translate simply into infusion of TGF[3? The answer is not known. However, it is of some interest that recent studies by Groux et al (reviewed elsewhere in these pages) show a new subset of immanosuppressive CD4+ cells (Trl cells), which are characterized by release of TGF[3. All clinical transfusion specialists who watch the widening circle of indications for IV IgG use and wonder what mechanism could possibly underlie its effect will find this article of interest.

Platelet Glycoprotein Ilia Polymorphisms and Risk of Coronary Stent Thrombosis. Walter DH, Schachinger V, Elsner M, eta/. Lancet 350:1217-1219, 1997.

Just when you thought the debate had died down on whether individuals carrying the platelet antigen PL A2 were at increased risk for coronary syndromes, the conversation heats up again. We reviewed in these pages some months ago an article (Ridker et al. Lancet 349:385, 1997) that concluded definitively that platelet polymorphisms were not related to coronary syndromes. However, in the current study, 318 consecutive patients undergo- ing coronary stent insertion were followed-up for the first month after the procedure t ~ determine the incidence of stent-vessel occlusion. Occlusion of the stent vessel occurred in 2% of PL A1/A1 individuals and 10% of individuals with a PL A2 allele (odds ratio, 5.26 [95% CI 1.5-17.8]). On multivariate analysis considering classical risk factors (smoking, cholesterol, hyper-