Mediation of effector functions by antibodies: report of a workshop.
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Biomedical subjects
Publications and source records attributed to J F Jones.
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Immunosuppression was examined at 10 to 12 days following oral inoculation of 10,000 to 12,000 embryonated Ascaris suum eggs. Reduced antibody responses to sheep red cells (SRC) following systemic immunization were confirmed in CD-1 and C57Bl/6 mice. Infection alone induced antibody reactive with DNP equivalent to that observed after immunization with DNP--Ficoll. There was a decrease in thymus and spleen size by day 8 of infection, followed by a splenic proliferative response during the second week. In the second week, serum antibodies reactive with SRC, chicken erythrocytes, DNP and bacterial lipopolysaccharide were demonstrated, suggesting polyclonal B-cell stimulation. The cellular basis of immunosuppression was investigated by in vitro culture of splenocytes from C57Bl/6 mice. Differential leucocyte counts of splenocytes before culture demonstrated a relative increase in plasma cells, blastoid cells, complement receptor-bearing lymphocytes and eosinophils, with a relative decrease in small lymphocytes. The splenocytes had reduced responses to T-cell mitogens, as measured by thymidine incorporation in vitro, and reduced antibody responses to SRC and DNP--Ficoll. In vitro, cell mixing experiments did not demonstrate suppressor cells in the spleens of infected mice.
To determine whether steroids exert a direct inhibitory effect on neutrophil function, thus contraindicating their use to increase granulocyte yields for white-cell transfusions to infected neutropenic patients, we gave normal donors a single intravenous dose of dexamethasone (4 mg per square meter of body-surface area). Approximately two hours later the absolute neutrophil count increased from an initial value (mean +/- 1S.D.) of 3800 +/- 1400 to 5700 +/- 2400 per microliter. Granulocytes were then collected by discontinuous-flow centrifugation and tested. Viability (98.4 per cent), the percentage of neutrophils capable of phagocytosis (97.6), particle accumulation (12.3 candida per phagocyte), fungicidal activity (1.08 "ghost" yeast cells per phagocyte), the percentage of bacteria killed (97.7) and chemotaxis (119 per cent) did not significantly differ from observations in nontreated paired controls. The functional competence of neutrophils used for granulocyte transfusions was not altered after short-term exposure of these healthy donors to steroid medication.
The ultrastructure of the lymphocytes from three children with severe combined immunodeficiency disease (SCID) is described. Parallel tubular arrays (PTA) were found in a large percentage of circulating lymphocytes (53%, 41%, and 13%) in three SCID patients when compared to age-matched controls. The size of these inclusions was quite variable, with some attaining a length of 1.7 micrometer. They contained a tubular substructure with a diameter of 36--44 nm. The PTA were mostly located in the centriolar and Golgi regions of the cytoplasm, and were sometimes membrane bound. A centriolar origin of the inclusion was suggested. A second inclusion, the tubuloreticular structure, was found in only 1.4% of the circulating lymphocytes from one SCID patient. The origin of the PTA and its occurrence in severe combined immunodeficiency disease are discussed.
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The number of stippled erythrocytes in the blood of lead workers counted under dark ground microscopy show a marked fall when blood is taken into an anticoagulant. The significance of this finding is studied and alternative methods of screening workers are examined.
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Although patients with chronic fatigue syndrome (CFS) can be diagnosed by clinical criteria, the lack of specific laboratory criteria delays or prevents the diagnosis and contributes to the quasi-disease status of the syndrome. A resurgence of interest in the syndrome has followed reports suggesting that CFS may be associated with chronic active infection due to the Epstein-Barr virus. Analysis of reports to date shows that the mean titers of antibodies to viral capsid antigen and to early antigen are greater for patients with CFS than for healthy individuals; this is particularly evident in cases for which serial samples were tested. However, these differences do not prove the cause of CFS. Cell-mediated immune responses in patients with CFS vary from study to study, and the number and function of natural killer cells in those patients are the most variable factors. Rates of isolation of virus from saliva do not differ, but in one comparison study with a large number of subjects, more lymphocytes that contained virus were isolated from patients than from controls. Other viruses, such as the Coxsackie B virus, have been implicated as causes of CFS in studies from Great Britain. The use of a working definition of CFS and standardized tests to address abnormalities revealed by laboratory tests among homogeneous populations should allow determination of useful tests for the diagnosis of CFS and studies of its mechanisms.
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This study used a brief battery of neuropsychological measures to examine the performance of patients with chronic fatigue syndrome (CFS) (N = 16) and patients in a major depressive episode (N = 23). The overall neuropsychological performance of the CFS group was not significantly different from depressed patients, and both groups scored within normal limits on most measures. Variability of neuropsychologic performance was in general unrelated to level of depressive symptoms. The results are discussed in terms of the validity of the cognitive criterion for the CFS diagnosis. Subjective complaints of cognitive dysfunction by CFS patients in light of the lack of objective evidence for the same are considered in terms of a somatic vigilance hypothesis.
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