Two cases of Hyper IgE syndrome were studied immunologically and the following results were obtained.
(1) The cellular immunity and NBT-dye reduction tests were revealed normal. One of the 2 cases showed normal phagocytosis-bacteriocidal activity of polymorphonuclear leukocytes (PMN) using clinically isolated staphylococcus aureus.
(2) Chemotaxis of PMN were depressed or normal inaccordant with the levels of the total serum IgE or the titers of anti-staphylococcal IgE antibody or the existence of skin pustules.
(3) H₂ sensitivity of PMN was frequently revealed to be low compared with normal controls. This H₂ hyposensitivity was suspected due to the tachyphylaxis of histamine because of the exposure of PMN to the histamine released in vivo.
(4) The titers of anti-staphylococcal IgE antibody were high and booster effect was suspected. Anti-staphylococcal agglutination titers were normal in the 2 cases.
These results suggested that the susceptibility of this syndrome to the infection of staphylococcus aureus could not be explained by only the depression of chemotaxis of PMN.
It was considered that the chemical mediators were released from the anti-staphylococcal IgE antibody bearing mast cells which reacted to the organisms. These chemical mediators included histamine but PMN of H₂ hyposensitivity could not be controlled by histamine and continued to release lysosomal enzymes.
Then the inflammation was prolonged and the infected tissues became fragile. After all, the infection of staphylococcus aureus was prolonged.
In other words, we could explain the susceptibility to the infection of staphylococcus aureus by so-called infectious allergy.

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Iron metabolism in patients with rheumatoid arthritis was evaluated. In 42 patients, anemia was seen in 57.1%, in which normochromic anemia was 63%, hypochromic 24% and hyperchromic 13%, respectively. Serum iron concentration was lower in 66% and total iron binding capacity (TIBC) was lower or normal in 82%. Serum ferritin level was not lower in 83%. Ferrokinetic studies in 15 patients with rheumatoid arthritis revealed rapid PID T_??_, lower PIT and RIT, which were compatible with lower serum iron concentration, less in vitro erythroid colonies (CFU-E) and hypocellular erythroid bone marrow. The release of reticuloendothelial iron was evaluated after intravenous injection of ⁵⁹Fe chondrotin ferrous sulfate (Radio-Colloid). Percent radioactivity 4 and 6 hours after the injection to the injected dose was 7.9% and 6.7%, respectively, in patients with rhematoid arthritis, which was significantly lower than normal. The amounts of released iron in 8 hours were also reduced. These findings might suggest a defect in the release of iron from the reticuloendothelial tissues to the plasma, resulting in hypoferremia and inadeguate supply of iron to bone marrow. On the other hand, hypocellular bone marrow in erythroid series and lower PIT would explain the primary genesis of the anemia.

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Fibronectin is a major adhesive and opsonic glycoprotein found in plasma and tissue. Because this molecule appears to mediate a number of interactions between cells and extracellular matrix, and because the natural killer (NK) cell-tumor cell interaction results in NK cell-mediated cytotoxicity, we evaluated fibronectin in the NK cell-target cell (K 562) interaction. Fibronectin promoted dosedependent inhibition of NK cell-mediated cytotoxicity by ⁵¹Cr release assays and single cell level assays in agar gel. This inhibitory effect was demonstrated in only fibronectin-treated target cells, and fibronectin did not inhibit the formation of NK cell-target cell conjugates. Thus, fibronection should bind to target cells, and augmented the insusceptibility of target cells to cytotoxic reaction of NK cells.

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We have completed the evaluation of the immune response as a function of interferon-α₂ in vitro and in Phase I study. in vitro natural killer (NK) activity of peripheral blood lymphocytes (PBL) from patients with cancer was, as compared in the mean value, almost equal to that of PBL from healthy donors, however enhancement of NK activity by IFN-α₂ in patient with cancer was less than that in healthy donors.
In phase I study immunological effects of IFN-α₂ had a complex response: although PBL response to phytohemagglutinin (PHA) was suppressed in all of the cases, both NK and K cell activities were enhanced in some cases and also suppressed in some others.
Sera from patients to whom IFN-α₂ was given in general enhanced NK activity of PBL from healthy donors, but markidly suppressed healthy donors' PBL response to PHA, however IFN-α₂ concentration of serum was not co-related with either the degree of enhancement of NK activity or that of suppression of healthy donors' PBL response to PHA.
These results suggest that in vivo some immunological suppressive factors may be induced by dose of IFN-α₂ and it may be important to give an appropriate dosage of IFN-α₂ not inducing an immunological suppressive factors.

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On human blood cell membranes there are several kinds of complement receptors which have important roles to initiate each cell's function. Recently, high incidence of defective reactivity as well as low number of complement receptors for C3b (CR1) on erythrocytes was found in patients with systemic lupus erythematosus (SLE), which is thought to be inherited.
The study was designed to investigate the incidence of defective reactivity of CR1 on erythrocytes in various diseases by immuneadherence hemagglutination (IAHA) using aggregated human IgG (AHG). In normal controls, 21 out of 312 (6%) revealed defective CR1 reactivity, and there was no difference in the incidence between female (11/157, 7%) and male (10/155, 6%). Among various diseases examined, significantly high prevalence of defective reactivity of CR1 on erythrocytes was seen in SLE (22/30, 73%) and malignancy of hematopoietic system, especially in acute myelogenous leukemia (AML) (6/11, 55%).

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Basophil reactivity to anti-IgE and house dust extract was examined in 69 patients with bronchial asthma by measuring the amount of histamine release.
1. Histamine release by anti-IgE varied widely in the cases with a RAST score from 0+ to 1+ and low serum IgE levels. Basophil reactivity to anti-IgE in the cases with a RAST score of 2+ tended to increase as serum IgE levels increased, although there was no significant correlation between them. The cases with a RAST score of 3+ generally showed a high reactivity to anti-IgE regardless of serum IgE levels.
2. There was no positive correlation between histamine release by house dust extract and serum IgE levels.
3. Histamine release by anti-IgE was similar to that by house dust extract in the cases with a RAST score of 2+ and 3+.

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Asparagine-linked sugar chains of plasma membrane glycoproteins from healthy and primary immunodeficient patients' B lymphoblastoid cell lines (LCL) were investigated. LCL were, respectively, prepared from healthy individuals and two patients with common variable immunodeficiency, using Epstein-Barr virus. Each LCL had complement receptors, OKIal antigen and OKB antigen on the membrane. Crude membrane fractions were prepared by the hypotonic shock and the centrifugation. Analysis of the asparagine-linked sugar chains of plasma membrane glycoproteins was carried out by the chromatography and the sequential exogycosidase digestion. In results, the main oligosaccarides in asparagine-linked sugar chains of plasma membrane glycoproteins from healthy LCL were biantennary sugar chains with bisect N-acetyl-glucosamine (Gal₂•GlcNAc₂•Man₃•GlcNAc•GlcNAc•Fuc•GIcNAc_OT) and those from patients' LCL were the same sugar chains with above. There was no difference on the main sugar chains between two patients' LCL. On the other hand, the main oligosaccarides in asparagine-linked sugar chains of plasma membrane glycoproteins from T lymphoblastoid cell lines were biantennary sugar chains without bisect N-acetyl-glucosamine, according to our other report.

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A 40-year old female was admitted to National Defense Medical College Hospital on March, 13, 1983 because of ascites of unknown cause.
The patient had had several episodes of polyarthralgia since 1979 and leucopenia was pointed out at the time of regular check-up. She suffered from common cold in December 1982. From this time she began to notice gradual distention of the abdomen. In February 1983, ascites was pointed out at a nearby hospital, but the cause of her ascites was unknown.
On the admission in March 1983, there was no laboratory findings to suggest the constrictivepericarditis, nephrotic syndrome or liver disease. Laboratory evaluation revealed hypergammaglobulinemia and hypocomplementemia with positive LE test, FANA and DNA-antibody (RIA). Renal biopsy demonstrated mesangial lupus nephritis. Culture of her ascites for fungi and bacteria was negative. The cytology was class II. At this time she was diagnosed as having lupus peritonitis.
Immune complex (Clq-IC) of the serum and the peritoneal fluid was 2.0μg/ml and 6.1μg/ml, respectively. The complement (CH50) content of the peritoneal fluid was lower than that of the serum. FANA titre of the serum and the peritoneal fluid was 1:320 and 1:80, respectively. Furthermore, analyzing T cell subsets of the peritoneal fluid by Cytofluorograf Flow Cytometer, OKT 8⁺ T cells were significantly elevated.
These immunological findings suggested immune complex mediated tissue injury, an evidence of local immune complex formation and the role of cytotoxic T cell in the development of lupus peritonitis.
Her ascites comletely resolved after a high dose prednisolone therapy.

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