One of house dust mites, dermatophagoides farinae, was considered one of the most important allergen contained in house dust from the skin test, inhalation provocation test, P-K test and fractionation by Sephadex. This was further confirmed by neutralization test and RAST.
36 species of mites weres detected in house dust but D. farinae and D. pteronyssinuswere found the important allergens among them, although there were cross allergenicity in 7 species of house dust mites studied. Allergenic potency of house dust was largely determined by the number of mite contained. Four major allergens were found in D. farinae extract to react with IgE antibody by autoradiography and were named Me₁, Me₂, Me₃ and Me₄.
Titer of IgE antibodies against them differs in each patients and appears somewhat to relate with different atopic diseases. Co-culture of T and B cells from mite sensitive patients and normal subjects showed that the suppressor activity of T cell was impaired or helper activity was enhanced to produce IgE antibody against mite in atopic patients.
Further studies showed that IgE antibody was partly produced by radioresistant long lived B cell and this appeared the reason why IgE antibody lasts long although half life of IgE is about 3 days.

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In order to resolve the question whether interferon (IF)-induced augmentation of human ADCC activity is due to an increase of the number of effector cell (K-cell) or an activation of individual effector cell, the effect of interferon on the number and size of K-cell plaque was examined at a single cell level by plaque assay method using Cunningham's chamber.
In the absence of IF, the number of K-cell plaque was reached to the maximum at 8hr, whereas in the presence of IF it was more increased depending on the concentration of IF at the early time of culture (3-5hr). However, 8hr of incubation, the maximum number of K-cell plaque in the presence of IF was equal to that in the abscence of IF. Furthermore, the area of individual plaque of K-cell in the presence or abscence of IF was measured at 8hr of culture and compared with each others. It was revealed that the average area of K-cell plaque in the presence of IF was significantly larger than that in the abscence of IF.
We concluded that the treatment of human peripheral lymphocytes with IF resulted in the augmentation of activity of the individual K-cell, but not the increase of number of K-cell.

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The natural cell mediated cytotoxicities (NCMC) were measured in 4 patients with Sjögren's syndrome (SjS) without complication of connective tissue disease (CTD), 4 patients with SjS associated with CTD other than rheumatoid arthritis (RA), 11 patients with SjS associated with RA, and 29 patients with RA without SjS. All 19 patients with SjS showed significantly suppressed NCMC. In the patients with RA without SjS, NCMC of 21 female cases were rather enhanced when compared with controls, while 8 male patients did not differ from controls. The reduced NCMC in SjS did not seem to correlate with the presence of antilymphocyte antibody (ALA). It is of interest that more accelerated NCMC were demonstrated in the patients with RA receiving gold therapy.

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Anti-nuclear antibody (ANA) examined by indirect immunofluorescent technique, anti-single stranded (ss) DNA antibody assayed as ¹⁴C•ssDNA bindings using Farr's method, and antilymphocyte antibody (ALA) assayed by cytotoxic test were examined simultaneously in sera from personnel working in SLE clinic, non-SLE clinic, and sera from blood donors. Six out of 70 (8.6%) SLE clinic workers, 2 out of 30 (6.7%) non-SLE clinic workers, and none of blood donors were determined to have ANA. Eighteen out of 70 (25.7%) SLE clinic workers, 5 out of 30 (16.7%) non-SLE clinic workers and 4 out of 96 (4.2%) blood donors were revealed to have anti-ssDNA antibody. Ten percent of SLE clinic workers, none of non-SLE clinic workers, and 4.2% of blood donors were also determined positive for ALA. In a group of SLE clinic workers, significant anti-ssDNA antibody was evaluated comparing in titer to blood donors (P<0.005). On the other hand, there was no significant difference in ALA titer and appearance of ANA in these three groups of sera. These three autoantibodies showed independent appearance with each other, without indicating the effect of ALA to the induction of other autoantibodies. Although significant titer of anti-ssDNA antibody was demonstrated in a group of sera from SLE clinic workers, especially in women, it is impossible to make clear the transmission of serologic abnormalities from SLE patients to medical workers.

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Human peripheral blood T lymphocytes were separated into theophylline-sensitive T cells (T_sen) and theophylline-resistant T cells (T_res); T_sen cells which lost the capacity to bind sheep red blood cells in the presence of the drug; T_res cells which were unaffected by the drug. T_sen cells could stimulate allogeneic cells in mixed lymphocyte reaction, but could not stimulate autologous unseparated T cells (T_total). T_res cells did not have the ability to stimulate al'ogeneic and autologous cells.
When we placed T_sen cells and T_res cells as responding cells in autologous mixed lymphocyte culture, both of the responses were significantly lower than that obtained when we placed unseparated T cells. These results suggest that the decreased autologous MLR may reflect an imbalance of T_sen cells and T_res cells.

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Much interest has been shown in the relationship between vitamins and immunity sincemany reports on thymus atrophy in vitamin B₆ deficient animals, suggesting that vitamins greatly influence immunity, were published. We examined the immune system of vitamin B₆ deficient guinea pigs (VB₆ DG) and performed the recovery test by giving vitamin B₆ to clarify the action of vitamin B₆ on the immune system. We also investigated the influences of vitamin B₆ and anti-vitamin B₆ on the blast-transformated reaction of peripheral lymphocytes simulated with PHA. Atrophy was noted around the T cell-abundant region of thymus and peripheral lymphocyte count was decreased to about 25% of the control. The number of T cells was decreased remarkably. ADCC% and gamma-globulin in VB₆ DG were also reduced to one half of the control, but were recovered by vitamin B₆ to 80 to 90% of the control. The peripheral lymphocyte blast-transformation rate in guinea pigs was lowered by anti-vitamin B₆. We suggest that vitamin B₆ influences the immune system by acting on the thymus and peripheral lymphocytes simultaneously.

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Sera from patients with systemic lupus erythematosus (SLE) contain antibodies to a number of nucleic acids. Antibodies to double stranded DNA have been found in patients with SLE, and their titer are generally associated with the disease activity. In this study, the sera from patients with SLE and other rheumatic disorders were examined for antibodies to double-stranded RNA in the major immunoglobulin classes by solid-phase radioimmunoassay employing polystyrene tubes coated with poly-L-lysine. The technique provided high specificity for the antibody to double stranded RNA. The anti-RNA antibodies were found not only in the sera of patients with SLE, but also from patients with other related diseases though less frequently.

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Effect of vitamin B₁₂ on the complement system was investigated in vitro and in vivo. Vitamin B₁₂ was found to reduced both the classical and alternative pathway activity of the complement in vitro. And vitamin B₁₂ was also found to increase serum complement level in guinea pig, measured by hemolytic assay using sensitized sheep erythrocytes (EA) for the classical pathway activity and unsensitized rabbit erythrocytes (RaE) for the alternative pathway activity. And assay of complement components revealed a significant increase in C3 and C4.
These evidences suggested that vitamin B₁₂ might potentiate immune response of the host by elevating serum complement level, in additino to activate the complement system.

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New major proteins of amyloid fibril are recently determined successively and then new classification of amyloidosis of these major proteins have been undertaken. In this paper, we performed to identify amyloid proteins in formalin fixed, paraffin embedded tissue section by immunohistochemical methods. The usefulness of potassium permanganate reaction (Wright method), distinguishing indirectly amyloid protein AA from the other forms of amyloid proteins, was also done in this study. Indirect immunoperoxidase method anti-AA serum applied to 16 cases of secondary amyloidosis and 27 cases of amyloidosis with plasma cell dyscrasia (PCD) consisting of both primary amyloid 16 cases and myeloma-associated one 11 cases.
The most frequent underlying disease in secondary amyloidosis was found to be rheumatoid arthritis (69%). Regarding immunoperoxidase method, protein AA was positive in the secondary amyloidosis and negative in the amyloid with PCD. All cases of secondary amyloidosis were sensitive to potassium permanganate treatment. Therefore, we would like to emphasize that immunoperoxidase method using anti-AA serum is quite useful directly to identify protein AA without performing amino acid analysis of amyloid fibril protein.

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A polyclonal B cell mitogen, formaldehyde-fixed Staphylococcus aureus Cowan I (SpA CoI) bacteria, stimulated proliferative response of human B cells and induced large quantity of IgM, G and A production. Proliferative response and Ig production by SpA CoI bacteria was independent of the presence of T cells.
Various B cell subsets from tonsil and peripheral blood were separated regarding complement receptor (C3R), IgG-Fc receptor (FcR) or surface immunoglobulin (SIg) on their surface using various rosette formation techniques. Which of the B cell subsets were activated by the stimulant was investigated in detail. Marked increase in the SpA CoI-induced proliferative response and Ig production was observed in C3R⁺ cells but not in C3R^- cells. It was also shown that FcR^- cells responded to SpA CoI bacteria more strongly than FcR⁺ cells. While SIg^- cells failed to respond to SpA CoI bacteria, SIg⁺ B cells responded markedly to the stimulant. Among the SIg⁺ B cell subsets, in particular, IgM⁺ and IgG⁺ B cells showed a marked response to the stimulant and much less response was seen in IgA⁺ and IgD⁺ B cells.
These results indicate that B cell subsets responding to SpA CoI bacteria were characterized as C3R⁺, FcR^- and SIg⁺ (in particular IgM⁺ and IgG⁺) B cells, which belonged to immature or young B cells. SpA CoI bacteria was thus capable of differentiating these B cells into mature B cells and plasma cells and was proved to be a useful tool in the study of the maturational development and differentiation.

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We reported a 49-year-old woman with adult Still's disease. She had developed intermittent fever with chills, polyarthralgia and myalgia since Dec., 1978. Her symptoms could not be controlled by several antibiotic therapy under the suspicion of infectious disease, and investigations in other hospitals during two years failed to make a diagnosis of this case. Then, she refered to our hospital and admitted in Apr. 28, 1980. Polyarthritis on a few joints, and hepatosplenomegaly were demonstrated, and abnormal laboratory data were as follows; Marked leukocytosis (22, 900/cmm; neutrophils 91%), elevation of erythrocyte sedimentation rate (119mm/h), and hypochromic anemia (Hb 9.1g/dl). RA factor was detected in her serum by two methods (RA test 2+, RAHA x 1280). Her synovial fluid obtained from knee joint showed increase of leukocytes (49, 700/cmm; neutrophils 98%), low levels of glucose (10mg/dl) and complement (CH₅₀ 8.4u/ml). Infectious and other rheumatic diseases were ruled-out by detailed examinations including bacteriological and serological studies. Her symptoms except polyarthritis and splenomegaly, were well controlled by the treatment with indomethacin (100mg/day) and prednisolone (10mg/day).
The clinical features of adult Still's disease reported in the literatures were reviewed, and compared with those of this case.

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So-called hereditary angioneurotic edema (HANE) is an autosomal dominant hereditary disease accompanied by a decrease or defect of protein of C1-inactivator (C1-INA) and/or a fall in the C1-INA activity.
We have encountered a family line of HANE with a 9-year-old girl as the proband, and the details of which were reported.
Nine-year-old girl was referred to our clinic by general physician because of the swelling of right hand. As for the past history, she began to have vomiting with abdominal pain almost every month since her two years of age and was diagnosed to have cyclic vomiting. She began to have swollen face, hands and feet frequently at 3 years of age. Similar symptoms were reportedly observed in her mother while young and also in her maternal grandmother. Suspecting nephritis, patient was snbjected to the various examinations at our clinic. Because of a marked decrease in the complement, HANE was suspected and her family members (parents and three sisters) were subjected to examinations.
CH50 was decreased markedly in the patient, maternal grandmother, mother and the youngest sister, while C1_q, C1_s, C1-INA and C4 were also decreased prominently compared with the control. However, CH50 was quite normal in her father and the middle sister.
On the basis of results obtained, diagnosis was established as being a family line of HANE with a 9-year-old girl as the proband.

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