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D Iványi

Publications and source records attributed to D Iványi.

At least 19 recordsLinked to original sources

One (H-2D2b) of the three Db region-controlled molecules (H-2D1b, H-2D2b, H-2Lb) is not detected in bm13 mutant.

Analysis of the antigenic heterogeneity of Db region products by the technique of antibody-induced redistribution of cell surface antigens (capping) revealed the existence of two types of H-2 molecules reactive with the monoclonal anti-Db antibody, B22-249R 1 (H-2.m2). The relationship of the two H-2.2-positive molecules described here is similar to that of H-2D and H-2M detected in the products of the Dd region; they differ in the repertoire of the H-2 public specificities, although they share the private specificity. We designate them, in accordance to recently proposed nomenclature, H-2D1b and H-2D2b. Both types of molecule have been detected on T lymphocytes of C57BL/6 (H-2b), C3H.B10(H-2b), and B10.A(2R) (H-2h2, KkDb) strains. In mutant strain B6.C-H-2bm13, however, only one type of H-2.2-positive molecule, H-2D1b, could be detected. This finding resembles the situation in the d haplotype, in which mutant strain B10.D2 (M504) (H-2dm1) had only one molecule (H-2Dd), of the two H-2.4-positive molecules H-2Dd and H-2Md that could be detected. A third Db region molecule, H-2Lb, does not carry the Db private specificity H-2.2, and it is detectable by some of the antibodies against the H-2.28 family of specificities; it is distinct from the Qa-2 molecule. The H-2Lb molecule was detected in all strains tested in this experiment, including the bm13 mutant.

Animals↗

Molecular heterogeneity of D-end products detected by anti-H-2.28 sera. II. B10.D2(M504) (H-2dm1) mutant fails to express one of the two H-2.4-, 28 + Dd region molecules.

By the technique of antibody-induced redistribution of cell surface antigens (capping), two serologically distinct molecules that do not react with anti-D-private sera were detected in the products of Dd and Dq regions. One of them is H2L, H-2Ld and H-2Lq. The other molecule is different from H-2L as well as from any known Qa molecule and it is either an H-2-like or Qa-like molecule. We designate it provisionally L2d and L2q, respectively. All these molecules carry the specificity H-2.28. Nevertheless, one antiserum against a H-2.28-like specificity, D29 (s X k anti-m) shows differences between these molecules. This antiserum reacted with H-2Ld and H-2Lq but not with L2d and Leq molecules. The same antiserum reacted, however, only with the H-2.4 positive (H-2D) molecule in mutant B10.D2 (M504) (H-2dml) cells. No antipublic serum was found that was able to distinguish different H-2.4 negative molecules in dml haplotype. The serological characterization of H-2.4 negative molecule in dml mutant indicated that this molecule is similar to the L2d molecule detected in the parental H-2d haplotype. Thus, dml mutant fails to express the H-2Ld molecule but does express H-2.4 negative, H-2.28 positive molecule, analogical to L2d. Together with our recent data demonstrating previously unknown molecules in the products of Dd and Kd regions, six serologically distinct molecules other than Qa-2 controlled by H-2d haplotype could be detected -- H-2K1d, H-2K2d, H-2Dd, H-2Md, H-2Ld, and L2d. BALB/c-H-2dm2 mutant fails to express H-2Ld and L2d molecules, while B10.D2(M504) (H-2dm1) mutant fails to express H-2Md and H-2Ld molecules.

Animals↗

Molecular heterogeneity of D-end products detected by anti-H-2.28 sera. III. Reactivity of certain anti-H-2.28 alloantisera with Qa-2 antigen.

In capping experiments with peripheral T lymphocytes, two anti-H-2.28 sera (AKR anti-AKR.L, anti-Kb, and C3H anti-C3H.B10, k anti-b) that do not contain any Qa-2-specific antibodies are able to redistribute not only the H-2.28-positive H-2 molecules, but also Qa-2 molecules. This is due to the capacity of these sera to react with Qa-2 molecules because on cells where all known molecules of the H-2d haplotype were capped (K1d, K2d, Dd, Md, Ld, L2d), both antisera still reacted when the cells came from a Qa-2 positive Dd strain (B10.A) but not when the cells were of Qa-2 negative strain (BALB/cByA). The reaction with Ia and non-H-2 antigens was excluded in these experiments. These data show that Qa-2 and H-2 antigens share some specificities of the H-2.28 family. Other anti-private and anti-public anti-H-2 sera failed to react with the Qa-2 molecules.

Animals↗

Further molecular complexities of H-2 K- and D-region antigens.

The K and D regions of the H-2 gene complex are highly polymorphic and control cell-surface structures involved in the H-2 restriction of cytotoxic T lymphocytes. Originally it was assumed that each of these regions controlled only one type of antigenic molecule, H-2K and H-2D, respectively. The finding that the D region controls H-2L and H-2M, as well as H-2D, molecules suggests that the system of H-2 antigens is more complicated. We demonstrate here previously unknown H-2 molecules detected by anti-K- and D-region alloantisera in co-capping experiments. Three different types of molecule, distinct from Ia and Qa antigens, are distinguished in the products of the Ddx region, and two in the products of the Dk and Kd regions. Analysis of the antigenic heterogeneity of K- and D-region products may further understanding of the function of these regions in cell-mediated immunity.

Animals↗

Serological characterization of previously unknown H-2 molecules identified in the products of the Kd and Dk region.

The molecular relationship between H-2 private and some public specificities was studied in C3H.OH (H-202) mice using surface-antigen re-distribution methods. Besides the Kd- and Dk-region antigens, which can be capped by antisera against the private and public specificities characteristic for a given allele, a previously unknown type of molecule was found in the products of both the Kd and Dk regions. These can be capped by the respective anti-private serum but not by antisera against some public specificities. The two Kd-region molecules are provisionally named H-2K1d and H-2K2d. We detected them on H-202 (Kd, Id, Sd, Dk) and also on H-2dx (Kd, If, Sf, Ddx) T lymphocytes. Similarly, the two types of molecules detected on the products of the Dk region are provisionally named H-dD1k and H-2D2k. The serological characteristics of these molecules are described. When compared with the products of the Dd region, in which we previously described three different molecules (H-2Dd, H-2Md, and H-2Ld), the mutual relationship between H-2K1d and H-2K2d as well as between H-2D1k and H-2D2k appears to be similar to that between H-2Dd and H-2Md. In the absence of relevant recombinants or informative biochemical data, it is, however, difficult to establish homology between molecules produced by different K- and D-region alleles.

Absorption↗

Qualitative and quantitative aspects of anti-H-2Ld sera.

Two anti-H-2Ld sera were analyzed, BALB/c-H-2dm2 anti-BALB/cBy and (C3H X BALB/c-H-2dm2)F1 anti-BALB/cHe, the latter also containing anti-Qa antibodies. Their reaction patterns were compared with an anti-Qa serum (C3H X BALB/cBy)F1 anti-BALB/cHe. Four H-2 specificities could be detected by the anti-H-2Ld sera, two already known (H-2.64, H-2.65) and two new specificities (H-2.81, H-2.82). According to their reaction pattern H-2.64, H-2.81, and H-2.82 can be regarded as members of the H-2.28 family of specificities. A quantitative difference in the expression of these H-2 specificities exists in different haplotypes. The cells of the strain against which the sera were made (BALB/cHe and BALB/cBy, respectively) did not give the highest titers with the antisera and had a relatively low absorbing capacity. The H-2dx haplotype carries two new specificities of the H-2.28 family, namely, H-2.81 and H-2.82. Lysostrip tests showed that the antibodies against those specificities cap the H-2.1-positive H-2Ddx molecules, suggesting that these molecules may react with both anti-H-2.1-like and anti-H-2.28-like antibodies. The H-2 specificities detected by the BALB/c-H-2dm2 anti-BALB/cBy serum were detected also in liver, kidney, spleen, heart, and lung tissue. New information on the strain distribution of Qa-2 was obtained from the experiments and a quantitative difference in Qa-2 antigens between H-2 congenic strains was observed as well. The H-2b strains react with these antibodies with higher titers than the strains carrying the H-2d haplotype.

Animals↗

Molecular heterogeneity of H-2 antigens.

Since the discovery of the H-2Ld molecule (Lemonnier et al. 1975) we have demonstrated that several K and D region alleles produce more than one type of H-2 molecules. Two of four different molecules were distinguished in the products of different alleles. Some of these molecules are products of different genes (H-2D, H-2L), in other instances the evidence for distinct genes is not available. Some of the different molecules produced by the same region might be modified products of the same gene. In the instances where no information implicating different genes is available, we use a neutral terminology which does not presume a genetic difference: H-2K1d and H-2K2d, H-2D1k, H-2D2k, H-2D1dx, H-2D2dx, H-2L1d, H-2L2d, etc. Immunoprecipitation experiments with some anti-H-2L and anti-Qa-2 sera revealed proteins with the apparent molecular weight of 41,000. We designate these antigens provisionally Lq and Qx, respectively. The Lq protein is polymorphic and it is at least partly under the control of H-2L-linked genes since it is absent from BALB/c-H-2dm2 cells. Since we have never seen the 41,000 proteins in precipitates of H-2K or H-2D antigens, it appears that whatever the origin of these molecules, they reveal some features common to products of L and Qa region. The basic relationship of H-2 K, D, L antigens is revealed also by the shared antigenic specificities between these H-2 molecules which we demonstrate using anti-H-2.28 sera. In summary, our results show that the class I antigens in each haplotype represent a family of several distinct but antigenically related molecules. The specificities of the H-2.28 family are the strongest allotype common to different H-2 K, D, and L molecules. Recent direct demonstration of several different genes in the Dd region (Steinmetz et al. 1981) provides evidence for the genetic complexity of H-2 genes which may be underlying basis of the molecular heterogeneity of H-2 antigens discussed here.

Animals↗

H-2L: demonstration of four new allelic products and independence of H-2D and H-2L molecules.

The H-2L molecules were detected for the first time in the Dd region products using antisera against the public specificity H-2.28. This specificity was analyzed because its presence in K as well as in D region products and its apparent allelism with another public specificity, H-2.1, indicated that these two specificities may have a special position may have a special position in the H-2 system. This was corroborated by subsequent identification of H-2L molecules in Dq and Dk products using anti-H-2.28 AND ANTI-H-2.1 sera, respectively, while none of the other previously known public or private specificities was detected on H-2L molecules. We tested the products of four D region alleles which had not been analyzed previously. In each of them we identified two distinct types of molecules: H-2D, which reacts with sera agains the D region private specificity, and H-2L, which does not react with these sera, but which is detectable either by anti-H-2.28 sera (H-2Lb, H-2Lf, H-2LS) or by anti-H-2.1 sera (H-2Ldx). This increases the number of identified H-2L alleles to seven (five H-2.8+, two H-2.1+). No association between H-2D and H-2D and H-2L molecules on the cell surface was detected in capping experiments.

Alleles↗

H-2.28, an alloantigenic marker allelic to H-2.1, is expressed on all three known types of H-2 molecules.

Each allele at the K or D region of the H-2 complex produces two kinds of "allelic" or mutually exclusive antigenic characteristics: its unique private specificity and a public specificity(ies) of either the H-2.28 or H-2.1 family. The private specificities of the K and D regions are expressed on H-2K and H-2D molecules, respectively. The D region produces another molecule, H-2L, which lacks the H-2K and H-2D private specificity but exhibits the H-2.28 or H-2.1 specificity. We analyzed the expression of the H-2.28 determinants on H-2K, H-2D, and H-2L molecules. When an antiserum against H-2.28 is used to sensitize cells where it can react with only H-2K molecules or H-2D molecules, by subsequent elution antibodies against H-2.28 are recovered that can also react with H-2L molecules. Hence, determinants reactive with antibodies against H-2.28 are present on H-2L as well as on H-2K and H-2D molecules. The expression of the H-2.28/H-2.1 polymorphism on all three known types of H-2 molecules, without some obvious relation to the private specificities, suggests that the antigenic determinants of these two kinds of allelic systems (private in contrast to H-2.28/H-2.1) may be controlled by separate genes, even when they are expressed on the same molecule.

Animals↗

HLA antigens as possible markers of heterogeneity in schizophrenia.

The distribution of HLA-A-, B- -and -C-locus antigens was tested in 200 male patients with final diagnosis of schizophrenia. A significant increase of HLA-A28 and HLA-Cw4 antigens and haplotype A10--B18 was found. Indications were obtained for the increase of HLA-A1 in hebephrenic patients. It was presumed that the increase of CW4 represents the common denominator of the diverse findings on paranoid schizophrenia. The increase of CW4 indicates that the paranoid schizophrenia disease susceptibility locus is either the C locus itself or another closely linked locus (or loci). This would stress the importance of the HLA 'central' regions for HLA and disease associations. A hypothesis is presented which points to the possibility that HLA antigens could be genetic markers of three ethiopathogenetic subgroups of schizophrenia. The possible tests of this hypothesis are also suggested.

Adult↗

HLA--Dw3 in Sjögren's syndrome.

The increased frequency of HLA-B8 in Sjögren's syndrome was recently reported independently by Gershwin et al. (1975) and Iványi et al. (1976). The association of HLA-B8 antigen with other diseases, characterized generally by impaired immunologic reactivity, has been shown (see Svejgaard et al. 1975, Dausset & Hors 1975), and in some of these diseases MLC typing has revealed the strong association also with the Dw3 determinant. The degree of association with each of the two, B8 and Dw3, varied between different diseases, in some of them having been reported to be higher for antigen B8 (Möller et al. 1976) and in the others for the determinant Dw3 (Thomsen et al. 1975, 1976). In some of the diseases, the association was found to be equally strong for both determinants (Solheim et al. 1976, Thorsby et al. 1975). In this communication, we describe the typing of HLA-Dw3 in 29 patients with Sjögren's syndrome (Ss). They represent part of the experimental group reported in a previous study (Iványi et al. 1976).

HLA Antigens↗

HLA--Cw4 in paranoid schizophrenia.

On a group of 40 paranoid schizophrenic patients HLA serotypes for HLA--A, B, C antigens a significant increase of Cw4 was observed. It is argued that this finding represents the common denominator for previous data reporting increased A9 and A28 antigen in SCH because these antigens are frequently present on haplotypes bearing Cw4. The possible role of the HLA "central" parts, i.e. the chromosomal segment between HLA--A and HLA--B locus in the pathogenesis of schizophrenia was stressed.

HLA Antigens↗

HLA antigens in systemic lupus erythematosus.

Forty-five patients suffering from systemic lupus erythematosus were studied in respect of their serologically defined HLA antigens. HLA-B8 antigen was found in 37-8% of patients as compared to 22% of controls. Individuals carrying the HLA-B8 antigen have a 2-15 times greater risk of developing systemic lupus erythematosus than those not carrying this antigen.

Adolescent↗