Deficient lymphokine production of newborn lymphocytes.

Lymphokine production by newborn lymphocytes was assessed by measuring migration inhibition factor (MIF) and leukocyte inhibition factor (LIF) of isolated mononuclear cells from cord blood, 1-7-days-old newborns, and adult controls. Ficoll-Hypaque separated mononuclear cells were stimulated with phytohemagglutinin (PHA) or allogeneic lymphocytes in a mixed leukocyte culture (MLC), and the supernatants were harvested at optimal times for lymphokine assays. Thymidine incorporation into DNA was also assayed to calculate a proliferative index. MIF was assessed by the inhibition of adult mononuclear phagocyte cell migration under agarose; LIF was assessed by polymorphonuclear cell migration under agarose. Although the proliferative responses of cord and newborn cells are equivalent or greater than those of adult controls, the PHA-induced MIF production in cord blood and newborn lymphocytes was only 46% and 12.5% respectively of mean adult levels; MLC-induced MIF production was 44% and 7%, respectively of mean adult levels. PHA-induced LIF production in cord blood was 27% of adult levels. These differences are only appreciated if dilutions of the supernatants are assayed. Simultaneous assay of MIF and LIF production in dilution of supernatants from adult lymphocytes showed higher LIF activity, whereas in cord lymphocytes MIF activity was greater than LIF activity. This further emphasizes the non-identity of MIF and LIF. These results indicate another abnormality of T cellular immunity in newborns not detected by T-cell enumeration or proliferative responses and parallels other defects in specialized T cell function such as cytotoxicity and immune interferon production.

Bactericidal activity and chemotaxis in pemphigus vulgaris and bullous pemphigoid.

Host defense mechanisms were studied in six patients with pemphigus vulgaris (PV) and six patients with bullous pemphigoid (BP). Polymorphonuclear (PMN) leukocyte killing of Staphylococcus organisms was evaluated, and chemotaxis of PMN and mononuclear (MN) leukocytes in patients was compared with that in twenty age- and sex-matched controls. All patients had extensive widespread disease with the clinical diagnosis confirmed by immunopathologic studies. No statistically significant differences were observed in the PMN leukocyte bactericidal activity between PV patients and controls. In BP patients, PMN leukocyte bactericidal activity was very slightly reduced when normal cells and patient serum were used, but activity was normal when patient cells and patient serum were used. PMN leukocyte chemotaxis was normal in PV and BP patients. MN leukocyte chemotaxis was normal in PV patients and increased in BP patients when compared with that in controls. This study indicated that in spite of very severe and extensive disease, patients with PV and BP have intact neutrophil and monocyte functions. Drugs that compromise the patient's ability to fight infections should be used cautiously and judiciously.

Monocyte chemotaxis under agarose: defects in atopic disease, aspirin therapy, and mucocutaneous candidiasis.

Using Ficoll-Hypaque-separated cells, monocyte chemotaxis was measured by an agarose technique in patients with increased susceptibility to infection, with atopic dermatitis, and in individuals taking aspirin. In vitro effects of aspirin, hydrocortisone, aminophylline, ephedrine, and diphenhydramine were also studied. Significantly decreased chemotaxis was found in one 9-year-boy with severe mucocutaneous candidiasis and three of 22 patients with atopic dermatitis. In the atopic group of patients greater than 10 years of age, mean monocyte chemotaxis was significantly decreased from the age-matched control group. This decrease did not correlate with serum IgE levels, absolute blood eosinophil counts, or clinical symptom scores. Following aspirin ingestion, mean monocyte chemotaxis significantly decreased whereas neutrophil chemotaxis was unaffected. Using therapeutic concentrations, drug levels of aspirin and aminophylline in vitro caused greater than 35% inhibition of monocyte movement.