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The IgG subclass distribution of anti Rh antibodies (anti-D, "anti-Da'. anti-c, anti-E), anti-Kell and anti-Duffy (anti-Fya) antibodies was measured by two haemagglutination techniques on microtitre plates. The first technique involved rabbit subclass specific antisera which were used to agglutinate red cells previously reacted with the patients' antibodies at high concentration. The second, which was more sensitive, had an additional step by introducing sheep anti-rabbit antibodies (sandwich technique). By the sensitive sandwich technique we revealed, for anti-D antibodies: IgGl 8/19, IgG3 1/19, IgG1/IgG3 8/19, IgGl/lgG2/IgG3/lgG4 1/19, IgG 1/IgG4 1/19; for the Da-reactive anti-D antibodies: IgGl 1/8, IgG1/IgG3 1/8, IgGl/IgG3/IgG4 6/8; for the anti-E antibodies: lgG1/IgG2/ lgG4 2/3,IgGl/IgG2/IgG3/IgG4 1/3: for the anti-c antibodies: IgGl 2/5, IgG3 1/5, IgG 1/ lgG3 1/5: for the anti-Kell antibodies: IgGl 9/20, lgGI/IgG3 1/20, IgGl/IgG4 8/20, IgGl/IgG3/IgG4 2/20; and for anti-Duffy antibodies: IgGl 1/8, IgGl/IgG4 7/8. These results are partly at variance with previously published results. [ABSTRACT FROM AUTHOR]

During routine ante-natal testing during the period 1953-73 anti-c was found in the serum of 63 women. Twenty-four of them had received blood transfusion previously and of these 22 were multigravidae. In 39 women pregnancies alone were responsible for the immunization. The anti-c titres of the 42 women giving birth to c positive babies showed that the probability of developing haemolytic disease increases with higher titres. But low titres by no means exclude the existence of such disease. Among the 42 c positive babies 32 had a positive direct antiglobulin test. Some of the affected infants had a serious degree of haemolytic disease. [ABSTRACT FROM AUTHOR]

A female patient in her early sixties had for a period of at least 4 months a monoclonal IgG1κ protein in her serum and at the same time a very high level of anti-thyroglobulin antibodies. Different isolation procedures showed that the M component was responsible for the high anti-thyroglobulin activity. Anti-idiotypic antibodies raised in a rabbit against the monoclonal protein inhibited the M component's anti-thyroglobulin activity, and purified thyroglobulin blocked the reaction between the M component and the anti-idiotypic antiserum. After the M component had disappeared, no cross-idiotypic immunoglobulins could be detected in the patient's serum, nor could the anti-idiotypic antiserum inhibit the residual anti-thyroglobulin activity present in the serum at this time. No reaction could be detected between the antiserum and the anti-thyroglobulin antibodies of sera of other patients. Idiotypic autoantibodies against the M component, which might have caused its disappearance, could not be demonstrated. [ABSTRACT FROM AUTHOR]

Blood samples from 15,426 blood donors from 17 out of Norway's 19 counties were tested for the presence of Kell (k) antigen. The K+ frequency in the total series was 8.28%, ranging from 4.61% in East-Agder county to 10.36% in Sogn and Fjordane. A1A2BO grouping of the donors showed that the lowest frequencies of group O were found in southeastern Norway (the counties surrounding the Oslo Fjord), and the highest along the coast of western Norway and in Nordland county. The highest A2 blood group frequencies were found in the three counties of northern Norway, with a maximum value in Finnmark county. The ratio between the genes determining the A1 and A2 properties (the p1/p2 ratio) was highest in southern Norway where in most counties was above 3. All the counties along the coast from Sogn and Fjordane northwards to the northern end of the country gave p1/p2 ratio below 3 and, in Finnmark, it was slightly below 2.

Testing of Ls(a+) and Rl(a+) red cells with numerous antisera containing antibodies to low-incidence antigens indicated that these antigens are identical. This conclusion was confirmed by adsorption and elution tests, and supported by immunoblotting of Ls(a+) and Rl(a+) cells with antibodies to glycophorin C and glycophorin D.

Scanning immune electron microscopy using a monoclonal anti-A antibody which reacts with all type A oligosaccharide chains revealed A antigens on less than 5% of Am and Ael cells, some of which showed extremely strong labelling. This explains why Am and Ael cells can absorb significant amounts of anti-A without being agglutinated. A3 may be a heterogeneous subgroup, since A antigens were found on 82 and 58%, respectively, of the cells of 2 A3 individuals. A antigens were found on 75% or more of Ax cells. In many weak A individuals A-positive cells are apparently best detected if an anti-A is used which reacts strongly with other A oligosaccharide chains than type 2. From hyperimmune pregnancy sera Ax, Am and Ael erythrocytes absorbed antibodies which seemed to have other fine specificities than those absorbed by A2 cells. We conclude that weak subgroups of A may deviate from A2 both by number of erythrocytes expressing A antigens and the biochemical nature of the antigens.

Survivors from meningococcal disease (serogroups B and C) and a control series (blood donors) were examined for their ability to secrete ABH blood group substance. The examination was done indirectly by determining their Lewis phenotypes. There was no significant difference in the secretor status between the two groups.

The proposita was classified as B(el), B(y), or B(m), Le(b+) by routine blood grouping and by adsorption/elution studies using anti-A and -B hyperimmune pregnancy sera. Red cells from the proposita adsorbed as much anti-B from the hyperimmune sera as did red cells from normal B individuals, but adsorbed less anti-A,B (group O serum). Saliva contained H, but not B, soluble substance. Red cells from the proposita and a normal B donor were sensitized with monoclonal A and B blood group antibodies immunolabeled with colloidal gold particles, and examined in a scanning electron microscope. B antigens were found on more than 95 percent of normal B cells, but on only 2-3 percent of red cells from the proposita. However, when the same cells were sensitized with anti-A,B that reacted strongly with B oligosaccharides other than type 2 chains, half of the labeled red cells from the proposita were labeled more strongly than any normal B cells. Our results explain why red cells from the proposita adsorb significant amounts of anti-B and anti-A,B without being agglutinated by these antibodies. The results of both adsorption/elution and immunolabeling suggest that the B antigen on her cells differs biochemically from that on normal B cells.

A 'new rare blood group antigen R1a (Rosenlund) is reported. The antigen is present in about 1 in 900 Norwegians. Nine unrelated R1(a+) people were found. Studies of seven families, leading to the discovery of 20 additional R1(a+) people, indicated the antigen is inherited as a Mendelian dominant character. Independent segregation was demonstrated between Rla and the ABO, MNSs, Rh, Lutheran, Duffy and Kidd blood group systems, the ABH secretor genes, and sex. The R1a antigen is inactivated by papain treatment. The corresponding antibody, anti-R1a, has so far been found in three sera that also contain antibodies to other rare blood group antigens.

The effect of the post-partum Rh prophylaxis in Norway was studied. From a preprophylaxis incidence of 47.4 new cases of Rh(D) immunization per 10,000 pregnant women the incidence fell to 8.9 per 10,000 in 1982-83, and further to 7.1 per 10,000 in 1986. In the period 1980-83 58 per cent of the new antibodies within the Rh system were anti-D, while 42 per cent had other Rh specificities occurring in Rh(D) positive women. The incidence of new immunizations within the Kell and Duffy systems was also studied. Fifty per cent of the antibodies detected within the three blood group systems occurred in Rh positive gravidae. It is known from other studies that at least 30 per cent of pregnant women who develop blood group antibodies do so after the first assay is performed. Therefore the number of antibodies found in Rh positive women would increase significantly if they too were retested towards the end of pregnancy.

A female patient in her early sixties had for a period of at least 4 months a monoclonal IgG1 kappa protein in her serum and at the same time a very high level of anti-thyroglobulin antibodies. Different isolation procedures showed that the M component was responsible for the high anti-thyroglobulin activity. Anti-idiotypic antibodies raised in a rabbit against the monoclonal protein inhibited the M component's anti-thyroglobulin activity, and purified thyroglobulin blocked the reaction between the M component and the anti-idiotypic antiserum. After the M component had disappeared, no cross-idiotypic immunoglobulins could be detected in the patient's serum, nor could the anti-idiotypic antiserum inhibit the residual anti-thyroglobulin activity present in the serum at this time. No reaction could be detected between the antiserum and the anti-thyroglobulin antibodies of sera of other patients. Idiotypic autoantibodies against the M component, which might have caused its disappearance, could not be demonstrated.

The frequency of irregular blood group antibodies detected for the first time in pregnant women during the period 1975-80 has been examined. Whereas Rh(D)-negative gravidae in Norway are examined immuno-hematologically three times during pregnancy, Rh(D)-positive women are tested once only, usually early in pregnancy. Nevertheless, about one-third of the new cases of immunization within the Rh system were found in the Rh-positive women. In the latter, anti-E and anti-c were the Rh antibodies most frequently encountered. Among other irregular antibodies which can cause hemolytic disease of the newborn (HDN), those of the Kell and Duffy systems are the ones second in frequency and clinical significance to the Rh antibodies. In the present series about 40% of the new cases of immunization within the Rh, Kell and Duffy systems were found in Rh-positive women. This proportion would undoubtedly have been greater if also the Rh-positive women had been retested for the presence of irregular blood group antibodies towards the end of the gestation. Such a retesting of Rh-positive gravidae is desirable both for a better prediction and early diagnosis of HDN and to facilitate the procurement of compatible blood if the woman should need an emergency blood transfusion.

A significant fraction (30%) of the genetically determined variance in plasma concentration of the von Willebrand factor antigen (vWf:Ag) has been shown to be related to ABH determinants. Individuals with blood group O, who have the highest amounts of blood group H substance, have the lowest concentration of vWf:Ag. The Lewis substances, Le(a) and Le(b), are biochemically closely related to the ABH substances as both can be produced from the same precursor substance. We studied the effect of the presence of the Lewis antigens on the plasma concentration of vWf:Ag and factor VIII antigen (VIII:Ag) in 323 individuals of different ABO groups from a series of twins and in 58 blood donors of blood group O. Among persons belonging to blood group O, those with the Le(a) antigen had a higher concentration of both vWf:Ag and VIII:Ag than individuals lacking Le(a). Le(a+b-) people are nonsecretors and Le(a-b+) people are secretors of ABH substance. Thus, the lowest concentration of vWf:Ag and VIII:Ag was found in group O secretors. The effect is most likely due to an effect of the secretor locus. This finding may be of importance for the detection of carriers of hemophilia A and for the diagnosis of type I von Willebrand disease.

A "new' rare blood group antigen Rla (Rosenlund) is reported. The antigen is present in about 1 in 900 Norwegians. Nine unrelated Rl(a+) people were found. Studies of seven families, leading to the discovery of 20 additional Rl(a+) people, indicated the antigen is inherited as a Mendelian dominant character. Independent segregation was demonstrated between Rla and the ABO, MNSs, Rh, Lutheran, Duffy and Kidd blood group systems, the ABH secretor genes, and sex. The Rla antigen is inactivated by papain treatment. The corresponding antibody, anti-Rla, has so far been found in three sera that also contain antibodies to other rare blood group antigens.