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Thirty-two adult patients with minimal change nephrotic syndrome (MCNS) were studied in order to clarify the characteristics of the immune system in MCNS and their relation to clinical activity. In the active phase (n = 17), serum immunoglobulin (Ig) M and E levels, B lymphocytes (surface Ig-positive cells) and their subsets, surface IgG, IgM and IgE positive cells; B gamma, B mu and B epsilon, were increased, whereas the serum IgG level and OKT3-reactive cells, peripheral T lymphocytes; T3, were decreased. In the remitted phase maintained by steroid therapy (n = 17), serum Igs and B lymphocyte subsets tended to return to normal levels concomitant with decreases in T3 and T4, and an increase in T8 in consequence of a marked decrease in T4/T8 (helper/suppressor) ratio. In stable remission continuing with no steroid therapy (n = 14), the above abnormalities returned to normal ranges, except for serum IgM which remained at a high level and re-elevated serum IgE. These results suggest that immunological abnormalities in MCNS are characterized by acceleration of the IgE and IgM producing systems and impaired maturation of the IgG producing system despite normal differentiation from the IgM producing to IgG producing system, possibly caused by T lymphocyte dysfunction.

Rare blood types are generally defined as those that occur at a frequency of 1 : 1000 or less. However, some rare blood types have much different frequencies in global regions or specific ethnic groups. This review explores rare blood types in the following categories: rare blood types that lack high-frequency antigens and where to find them, rare blood types that express low-frequency antigens, rare blood types with higher or lower frequencies in the Asia Pacific region and rare blood types that are difficult to find in the Asia Pacific region but are provided by the JRC. In addition, the study of rare blood types has revealed clinical correlations with disease states and resistance to infections. [ABSTRACT FROM AUTHOR]

The article presents the changes and updates made by the International Society of Blood Transfusion committee to the classification in Blood Terminology 2004 during its meeting in Macau Special Administrative Region, China. It states that a new blood group system was established and new antigens were added to Rh, Kell, and Dombrock systems. It also mentions that there are already a total number of 308 antigens recognized at present times.

Although flow cytometric (FCM) analysis is one of the most widely used approaches to screen the presence of leucocyte antibodies, it has several drawbacks. First, neutrophils and, especially, monocytes exhibit high background reactivity. Second, to determine antibody specificity, it is often necessary to examine not only neutrophils and monocytes but also other lineage cells including T cells, B cells and platelets. Therefore, we attempted to establish an FCM analysis system in which four lineages of leucocytes and platelets are simultaneously tested with low background. FCM analysis was performed using ethylene diamine tetraacetic acid-anticoagulated whole blood as cell sample without any cell preparation. Discrimination of five cell lineages was carried out based on the differences in forward vs. side scatter distribution and in the expression of CD4, CD20 and CD14. When anti-HNA (human neutrophil antigen) 1b antiserum was applied to HNA 1b-positive blood samples, only neutrophils were unambiguously positive. When anti-Naka (anti-CD36) antiserum was applied, only platelets and monocytes were positive. The background reactivity of neutrophils and monocytes was low enough. When anti-human leucocyte antigen (HLA) class II antiserum was tested, only B-lymphocytes and monocytes were positive. When anti-HLA class I antiserum was tested, all the five-lineage cells were positive. [ABSTRACT FROM AUTHOR]

It has been suggested that Proteus infection may be involved in the pathogenesis of rheumatoid arthritis (RA). Bacterial and peptide immune responses in patients with RA and other control subjects were investigated in two geographically different populations. Serum samples from Finnish patients with early (n=72) and advanced (n=27) RA and 30 Finnish healthy controls, as well as from Japanese RA patients from two different locations: Tokyo (n=30) and Otsu (n=30), 18 patients with systemic lupus erythematosus (SLE) and 23 Japanese healthy controls were all screened for the total, and class-specific (IgG, IgA and IgM) antibodies against Proteus mirabilis, Escherichia coli and Serratia marcescens by indirect immunofluorescence assay. These samples were also tested for the determination of levels of isotypic antibodies against the shared epitope involving 16-mer synthetic peptides containing the EQRRAA or ESSRAL sequences and compared to scrambled control peptide by using an enzyme-labeled immunosorbent assay method. Significantly elevated levels of IgG and IgM antibodies to P. mirabilis and antibodies against both EQRRAA and ESSRAL peptides were detected in sera of Finnish patients with early and advanced RA, and in Japanese patients from Otsu or Tokyo compared to their corresponding control groups. In contrast, no difference either in the total or in any of the isotypic antibodies were observed between these groups when serum samples were screened against each of E. coli and S. marcescens or against the control peptide. Furthermore, there was a significant correlation between the antibody levels against Proteus bacteria only and both EQRRAA and ESRRAL peptides. Our findings support the possibility for specific involvement of P. mirabilis in the etiopathogenesis of RA even in early cases. [ABSTRACT FROM AUTHOR]

The proportion of B lymphocyte subsets with surface immunoglobulin G (sIgG) was significantly increased in minimal change nephrotic syndrome (MCNS), membranous nephropathy, IgA nephropathy and mesangiocapillary glomerulonephritis (MCON) and with sIgA in IgA nephropathy and MCGN, and with sIgE in MCNS. Increased subsets in membranous nephropathy, IgA nephropathy and MCGN corresponded to the immunoglobulins deposited in the glomeruli, and the increased subset of sIgE in MCNS was correlated with the elevation of serum IgE. These results suggest that each disease studied has a characteristic subset pattern of B lymphocyte response. This may have an important rote in determining the histological type of idiopathic glomerulonephritis. [ABSTRACT FROM AUTHOR]

The extracellular antigens of Actinobacillus actinomycetemcomitans Y4 (serotype b) contain a 37-kDa protein which is a major target for IgGs from patients suffering from severe alveolar bone loss. Since the 37-kDa protein has not been studied sufficiently, our investigation focused on its characteristics, e.g., its localization, specificity, and whether it directly stimulates macrophages to produce cytokines. The 37-kDa protein was purified from the culture supematant of the Y4 strain by means of chromatofocusing and gel filtration. The 37-kDa protein is a unique glycoprotein which forms immune complexes with monoclonal antibodies against rhamnose-fucose polysaccharide. Patients with A. actinomycetemcomitans-associated periodontitis had higher antibody titers to the purified 37-kDa protein than healthy subjects (p < 0.001). Anti-37-kDa protein antibodies recognized a 37-kDa band in the cytosolic, ribosomal, and total membrane fractions from Y4 cells. Extracellular substances from other strains of A. actinomycetemcomitans (serotypes a and c) also reacted in the Western blots, but Haemophilus spp. or several periodontopathic bacteria did not. These results suggested that the 37-kDa protein is a cytosolic protein that is passed through the cell membrane, and its protein portion is specific for A. actinomycetemcomitans but common to serotypes. This protein induced IL-1β, IL-6, and TNF-α release from murine macrophages. The IL-6-inducing activity of the 37-kDa protein was higher than that of LPS. These findings suggested that the 37-kDa protein which is released from live cells plays a role in A. actinomycetemcomitans-associated periodontitis, as antigen inducing the release of inflammatory cytokines which are associated with alveolar bone loss. [ABSTRACT FROM AUTHOR]