Kyoko Iida

Reaction Mechanisms of β1H Globulin

The reaction mechanisms of β 1H were studied. The generation of alternative pathway C3 and C5 convertases on the cell surface as well as in the fluid phase was inhibited by

Complement fixing abilities of IgA myeloma protiens and their fragments: The activation of complement through the classical pathway

Abstract Complement fixing abilities of IgA and its fragments chemically aggregated were tested. Both IgA1 and IgA2 myeloma proteins fixed considerable amount of human complement. IgA2 fixed complement more efficiently than IgA1 did. Fc and F(ab′) 2 of IgA1 were more active than undigestived IgA1, and their activities were comparable to that of Fc of IgG, whereas the activity of F(ab′) 2 of IgA2 was weak. Complement component profiles of human serum treated either IgA or its fragments revealed that the classical pathway of the complement system was activated.

A new method for the preparation of EAC14 cell with human or guinea-pig serum

Abstract By reacting EA with serum in the presence of triethylenetetramine-N,N,N′,N″,N‴,N‴-hexa-acetic acid (TTHA), active and stable cellular intermediate of immune hemolysis, EAC14, was successfully prepared. This method does not require isolated components of complement and is applicable to prepare EAC14hu.

A solid-phase anti-C3 assay for detection of immune complexes in six distinguished forms

A solid-phase anti-C3 assay detecting immune complexes associated with C3 fragments is described. Two monoclonal antibodies against C3 fragments are used; one recognizes an epitope expressed on C3b, C3c and C3i, the other recognizes an epitope expressed on C3dg and iC3b. Combining these monoclonal anti-C3s with antibodies against class-specific immunoglobulins in enzyme-linked immunosorbent assay (ELISA), immune complexes (ICs) are detected in six distinguished forms; C3b-IgG-IC, iC3b/C3dg-IgG-IC, C3b-IgA-IC, iC3b/C3dg-IgA-IC, C3b-IgM-IC and iC3b/C3dg-IgM-IC. About three-fourths of the plasma samples from patients with active SLE or IgA-nephritis were found positive in one or more types of ICs. IgA-type ICs were found very frequently in patients with autoimmune or renal diseases.

Abnormal expression of complement receptor (CR1) in IgA nephritis: increase in erythrocytes and loss on glomeruli in patients with impaired renal function.

The number of complement receptor for C3b (CR1) molecules in erythrocytes from patients with renal diseases was measured by an immunoradiometric assay using monoclonal antibodies against CR1. IgA nephritis patients with high serum creatinine value (Scr) showed markedly elevated levels of CR1, whereas patients with normal Scr had normal CR1 levels. A similar increase in CR1 number was observed in membranoproliferative glomerular nephritis with high Scr. CR1 of these patients functioned normally as a cofactor of C3b inactivator in cleaving immune complex-bound C3b. In contrast, a high frequency (5/6) of negative staining of glomerular CR1 was observed in IgA nephritis patients with high Scr by immunofluorescence study. We postulate that the disease-associated, acquired factors at least in part contribute to the abnormal expression of CR1: elevated levels in erythrocytes and defective expression on glomeruli.

Nomenclature for Factors of the HLA System – 1977

This article gives the decisions of the WHO nomenclature committee on leukocyte antigens, in particular concerning (a) the upgrading of certain HLA-A and HLA-B specificities to full HLA status, (b) the designation of new provisional specificities of the HLA-B, HLA-C, and HLA-D loci, and (c) the establishment of a nomenclature for the new specificities identified by serological techniques on B lymphocytes.