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PubMed1992

Genetic polymorphism of IgG in the mink. IX. High proportion of allotype-producing lymphocytes in individuals with minor level of allotypes H3 and H4 in serum.

The levels of mink C gamma-allotypes (H3, H4, H6 and H8) were determined in sera, and the proportion of the corresponding allotype-synthesizing B cells was estimated in peripheral blood, spleen and mesenteric lymph nodes. Individual differences in H6 levels and, possibly, those in H8 were entirely dependent on the proliferation degree of the corresponding clone of B cells and also determined by the dosage of the structural gene. There was no correspondence between the great numbers of H3+, H4+ cells and low levels of H3 and H4 allotypes in the sera of the majority of minks with their minor expression. A possible cause of this discrepancy may be a blockade of the secretion of IgG by H3+, H4+ cells. There exists most likely a gene (or genes) controlling the blockade of IgG secretion. The regulation of C gamma-allotype expression is presumably effected in a manner specific to each of the allotypes.

Animals↗
PubMed1975

In vitro studies on allotype suppression. III. compounds of antiallyotype serum active in release from allotype suppression.

Spleen cells of b4b6 rabbits, shown to be deficient in their ability to produce b4Ig due to prenatal exposure to anti-b4, formed anti-T2 antibodies marked with the b4 determinant in response to solubilized T2 phage (S-T2) only when cultured in the presence of antibodies specific for the nonsuppressed type (b6), thus confirming and extending the previously reported observation of release from b4 suppression in cultured cells of b4-suppressed b4b5 rabbits treated with anti-b5 serum. Only antiallotype sera made in b4 rabbits were active in reversing b4 suppression. Anti-b5 or anti-b6 sera from rabbits of allotypes b6 or b5, respectively, when used in concentrations which completely or partially inhibited the formation of anti-T2 antibodies marked with the corresponding nonsuppressed allotype of the spleen donor, proved to be almost completely ineffective in causing release of suppression. Exceptions were noted when spleen cells of rabbits advanced in spontaneous escape from suppression were tested with such sera. The addition of normal b4 serum to non-b4 antiallotypic sera rendered them as effective in releasing b4 suppression in vitro as were antisera from b4 rabbits. Furthermore, the capacity of a b4 antiallotype serum to cause reversal of b4 suppression could be potentiated by the addition of normal b4 serum, indicating that nonantibody b4 Ig is a limiting factor in such a serum. Thus, the release from allotype suppression observed in cultures of spleen cells from b4-suppressed heterozygous rabbits is dependent upon the presence of two components: antibodies directed against the nonsuppressed allotype of the donor and normal b4Ig. These findings are interpreted in terms of alternate hypotheses involving (a) a mechanism of b4 derepression and (b) inactivation of a suppressor cell with recognition for a b4-labeled target.

Animals↗
PubMed1977

Allotype suppression in rabbits: the requirement for CH3 domain of anti-allotype antibody.

Facb fragments of rabbit anti-allotype antibody were prepared by plasmin digestion and isolated by gel chromatography. The antibody preparation was used in an attempt to induce allotype suppression in newborn rabbits. The Facb fragments were found to be ineffective in inducing the allotype suppression. Administration of Facb fragments caused a "burst" of immunoglobulin synthesis almost immediately after the administration of the antibody. It was concluded that the CH3 domain, which is responsible for the cytophilic activity of the antibody, is essential in induction of allotype suppression.

Animals↗
PubMed1983

Analyses of the splenic mRNA expressed by rabbits of different immunoglobulin kappa-light chain allotypes: conserved sequences in the 3' untranslated region and allotype-specific probes.

The allelism of the structural genes for the complex rabbit b allotypes of immunoglobulin kappa-light chains has been questioned because of observations of unexpected phenotypic expression of "latent" allotypes. We find that the coding sequences of the b4 and b5 "alleles" are only 80% homologous for the last 60 nucleotides but there is a high degree of homology (96%) in the 3' untranslated region (3'DT). The high conservation of 3' DT region sequences enabled us to detect kappa-light chain mRNAs from rabbits of different genetic types (b4, b5, b9 and bbas) on northern blots and dot blots. We can distinguish mRNA encoding b9 and b5 allotypes on dot blots with b5 fragment-probes of known sequence and detect mRNA produced by unstimulated cultured splenic lymphocytes. Analyses of mRNA from cultured cells manipulated to enhance mRNA synthesis and production of unexpected or "latent" b allotypes can now be conducted.

Animals↗
PubMed1981

Allotype suppression of the responsiveness of adoptively transferred adult spleen cells induced by affinity prepared anti-allotype antibody.

In an adoptive transfer assay it has been shown that a form of allotype suppression can be induced in adult spleen cells. Use of SPF congenic mice, and either anti-allotype serum freed of IgM rheumatoid factor or affinity prepared antibody, has helped to eliminate the possibility of a role for non-specific factors in allotype suppression. Both memory-cell development and a conventional primary response are more susceptible to suppression than memory expression in a secondary response. Non-specific suppressive effects on isotypes other than that of the target allotype (CH) are present but are much smaller than for specific suppression.

Animals↗
PubMed1976

Synchronous regulation of VH and CH allotypes among Ig molecules in multi-heterozygous rabbits suppressed with anti-VH allotype antibody: emergence of IgA from suppression prior to IgG and IgM.

Heterozygous rabbits of genotype a1n81f73g74/a2n82f71g75 were suppressed at birth for the VH region a1 allotype. At 8 weeks of age, quantitative analysis of serum IgG, IgM, and IgA molecules showed that the VHa1 specificity was effectively suppressed in the three classes of Ig and that the suppression was extended to the CH region n81 specificity on mu-chains as well as to the CH region f73 and g74 specificities on alphaf and alphag chains. At 26 weeks of age, analysis of serum IgG and IgM molecules showed that a1 was still suppressed to approximately the same extent in both Ig classes and the suppression was still extended to the CH region n81 specificity. However, at 26 weeks, the percentage of molecules with a1 specificity had doubled among serum and colostral IgA molecules and this increase was extended to the CH region f73 and g74 specificities. Thus, the suppressed allotypes reappeared first among IgA molecules. Our data are consistent with a regulatory mechanism which controls and synchronizes the expression of the VHa and the CH allotypes expressed on the same heavy chain. The order of the re-expression of the suppressed allotypes with respect to Ig class may allow further definition of selective regulatory mechanisms for the synthesis of Ig classes.

Animals↗
PubMed1978

Regulation of allotype expression in heterozygous rabbits. I. Concomitant modulation of cell surface allotypes on peripheral blood lymphocytes from b4b6 rabbits.

Treatment of b4b6 rabbit peripheral blood lymphocytes with b5b5 anti-b4 antibodies at 4 degrees resulted in the modulation (disappearance) ob b4 and b6 cell surface allotype after subsequent incubation in serum-free medium for 1 h at 37 degrees. A clear dose dependence on the sensitizing anti-b4 antibody was observed. Similarly, b5b5 anti-b6 treatment demonstrated a dose dependence for b6 modulation and a threshold dose effect for b4 comodulation. Cells which formed rosettes with anti-b4-coupled SRBC (anti-b4 direct antiglobulin (DAG) rosettes) also demonstrated concomitant modulation of b4 and b6 allotype when incubated at 37 degrees. When cells formed anti-b6 DAG rosettes, subsequent b6 modulation could also be demonstrated, but no b4 comodulation occurred. Concomitant modulation did not occur when cells were incubated with anti-allotype antibodies at 37 degrees. Blocking studies disclosed that the two allotypes are not contiguous in the membrane since uptake of one antiallotype antibody did not block the uptake of another at 4 degrees. We therefore propose that concomitant modulation might occur during a process similar to patch formation.

Animals↗
PubMed1974

Recombinant rabbit secretory immunoglobulin molecules: alpha chains with maternal (paternal) variable-region allotypes and paternal (maternal) constant-region allotypes.

A population of IgA molecules having heavy chains coded by two parental chromosomes in trans position has been identified in rabbits heterozygous at both the V(H)a locus, which controls allotypic specificities on the variable part of heavy chains, and the C(alpha)g locus, which controls allotypic specificities on the constant part of alpha chains. These recombinant molecules have alpha-chain allotypic specificities controlled by both the maternal V(H)a gene and the paternal C(alpha)g gene or conversely, the paternal V(H)a gene and the maternal C(alpha)g gene. These recombinant molecules were found in F(ab)(2alpha) fractions obtained after passage of F(ab)(2alpha) preparations through immunosorbent columns designed to remove one population of F(ab)(2alpha) molecules, i.e., g74- or g75-type molecules. The effluent F(ab)(2alpha) fractions were then examined by radioprecipitation methods for allotypic specificities controlled by the V(H)a and C(alpha)g loci. About 40% of the g75 F(ab)(2alpha) molecules from each of three rabbits with the a(1)g(74) and a(2)g(75) allogroups were alg75 recombinants. These alg75 recombinant molecules represented from 2.5-5.6% of the total unfractionated F(ab)(2alpha) sample. The F(ab)(2alpha) fractions from two rabbits with the a(1)g(75) and a(3)g(74) allogroups had from 1.8-8.2% recombinant molecules: some were alg74 recombinants and some were a3g75 recombinants. Somatic recombination as a mechanism responsible for the synthesis of polypeptide chains in which part of the information is obtained from one chromosome and part from the homologous chromosome is discussed.

Alleles↗
PubMed1980

Anti-allotype antibody response in mice: expression of a cross-reactive idiotype and its regulation by auto-anti-idiotypic antibodies in maternally allotype suppressed F1 hybrids.

Anti-IgGb2a allotype antibodies produced by various responder strains of mice expressed a cross-reactive idiotype. This cross-reactive idiotype was evidenced with BAB. 14 and CXBI anti-idiotypic sera raised following immunization with affinity chromatography purified BALB/c anti-CBPC 101 (IgGb2a) antibodies originating from a single BALB/c mouse. F1 hybrids of BALB/c X C.B20 parents, which have been maternally suppressed for IgGb2a allotype as a result of immunization with CBPC 101, produced anti-allotype antibodies lacking cross-reactive idiotype. Furthermore, these mice produced auto-antibodies directed at the IdX of anti-IgGb2a allotypic antibodies.

Animals↗
PubMed1986

Mouse monoclonal antibodies induced by anti-allotype antibody display internal images of the rabbit VHa1 allotype: direct visualization by immunoelectron microscopy.

We have previously shown that injection of adult rabbits with anti-immunoglobulin (Ig) antibody (Ab) induces the expression of genetically unexpected Ig markers, i.e., a1 allotypic determinants. We now show that these rabbit Ig markers can also be induced in mice by a similar treatment; in the latter case the a1 determinants are located in the antigen-combining site and thus represent "internal images". Two monoclonal antibodies (mAb) were developed from mice treated with anti-allotype Ab. These mAb were reactive with all homologous and heterologous anti-a1 Ab but not normal Ig; efficiently inhibited the binding of rabbit a1 Ig to anti-a1 Ab; and elicited the production of anti-allotype Ab when injected into normal mice. To determine whether the a1-like determinants on these mAb were located in the antigen-combining site, immunoelectron microscopy was utilized to directly visualize Ab complexes. Complexes composed of intact Ab and anti-a1 Fab fragments yielded uniform binding patterns which were identical to those produced by anti-idiotypic reactions. In each case, an identical tip-to-tip binding configuration was observed with a single Fab fragment attached at an approximate 180 degree angle to the V region terminus of each Ab arm. In contrast, rabbit a1 Ig bound as many as two anti-a1 fragments per Ig arm; these fragments were attached laterally and at right angles to the intact molecule. These mAb thus provide the first direct evidence that Ab2 beta determinants are located in, or near, the antigen-combining site.

Animals↗
PubMed1995

Linkage of IgA deficiency to Gm allotypes; the influence of Gm allotypes on IgA-IgG subclass deficiency.

IgA deficiency (IgAD) is the most common immunodeficiency, characterized by an arrest in B cell differentiation. It has a sporadic occurrence or variable inheritance pattern, and is also linked to the HLA genes. IgA deficiency is sometimes associated with IgG subclass deficiency. In this study the Gm allotypes, as genetic characteristics of the IgG1, IgG2 and IgG3, were analysed in 83 Caucasian IgAD individuals. Half of the patients presented with IgG4 < 0.01 g/l compared with 5% (P < 0.001) in a healthy population. Three of the 83 had significantly low IgG2 and four had significantly low IgG3 levels. Gm allotype frequencies in IgAD deviated compared with a normal population. Of the 83 patients, 44 (53%) showed homozygous G2 m(",") expression on the IgG2 locus (33% in controls, P < 0.01). In IgAD the Gm(a,",g) haplotype was more frequent (43%) compared with controls (31%, P < 0.01). The Gm homozygous phenotype Gm(a,",g/a,",g) was most common, found in 20 of 83 patients (24%, P < 0.05) compared with controls (14%). On the other hand the Gm(f,n,b) haplotype of IgAD was rare (28%) compared with controls (45%, P < 0.001). The low IgG4, < 0.01 g/l, found in 50% of the patients, was even more frequent (56-69%) among the G2 m(",") phenotypes. IgG subclass levels were given for different Gm phenotypes of the IgAD group and compared with controls. Significantly low IgG4 was revealed in the Gm(a,",g/a,",g) phenotype (P < 0.01) and significantly low IgG2 in the Gm(a,",g/f,",b) phenotype (P < 0.01). The Gm(a,",g/f,",b) phenotype contained the three patients found with IgG2 levels < -2 s.d., and the four patients with IgG3 levels < -2 s.d. were present among those with the homozygous Gm(a,",g/a,",g) phenotype; both phenotypes with G2 m(",") on the IgG2 locus. The 'compensatory' increase of IgG was significant for both IgG1 and IgG3 in all Gm phenotypes, but in the Gm(a,",g/f,",b). Thus, the susceptibility of IgAD with the additional IgG antibody deficiencies, down-regulated IgG4 and IgG2/IgG3, is associated with Gm allotypes, especially the homozygous G2 m(",") expression on the IgG2 locus.

Hemagglutination Inhibition Tests↗
PubMed1977

Population genetics of Aa and Ab immunoglobulin allotypes in wild rabbits of south-eastern Australia. I. Allotype frequencies.

Aa and Ab allotype frequencies have been investigated in wild rabbit populations throughout Victoria and South-east South Australia. The overall mean allele frequencies for thirty-three populations are 0-53:0-12:0-36 for a1:a2:a3 and 0-72:0-22:0-05 for b4:b5:b9. The b6 allele was not found anywhere. The a1 frequency has been found to increase in proportion to increases in mean annual rainfall. While considerable variations exist in allotype and allele frequencies from area to area, the relationships a1 greater than a3 greater than a2 and b4 greater than b5 greater than b9 are almost always observed. The results are discussed in terms of the historical origins of Australian wild rabbits and possible genetic mechanisms to explain the maintenance of allotype 'hierarchies' in large populations breeding at random.

Alleles↗
PubMedDate not supplied

IgA2 allotypes determined by restriction fragment length polymorphism in IgA deficiency. Re-expression of the silent A2m(2) allotype in the children of IgA-deficient patients.

IgA2 allotyping was performed on DNA from 60 IgA-deficient Caucasian individuals. The frequency of A2m(2) was not statistically different from that of normal controls. Two informative families were selected for further studies. In both families, the A2m(2) allotype (derived from the IgA-deficient parent) was inherited by some of the children, as determined by Southern blotting experiments. In all cases the 'silent' IgA2m2 gene was re-expressed, as judged by conventional serological allotyping of serum proteins. These data strongly argue against structural gene deletions or mutations as a cause of IgA deficiency.

Alleles↗
PubMed1989

T cell-induced Ig allotypic suppression in mice. II. Both CD4+ CD8- and CD4- CD8+ T cell subsets from sensitized Igha mice are required to induce suppression of Igh-1b allotype expression.

We established the phenotype of T splenocytes (Ts) from Igha/a BALB/c mice sensitized against B splenocytes from the Ighb/b CB20 congenic mice that induce Igh-1b (IgG2a of the Ighb haplotype) suppression. This was achieved by studying the action of anti-T cell subset mAb on the capacity of Ts to induce this chronic allotypic suppression in Igha/b (BALB/c x CB20)F1 mice. The Ts were treated with cytotoxic anti-mouse CD4 or anti-mouse CD8 rat mAb in vitro before their injection into the Igha/b newborns or in vivo after their injection into the Igha/b newborns. Exposure to either anti-CD8 or anti-CD4 mAb in vitro or in vivo leads to loss of the capacity of Ts to induce Igh-1b allotypic suppression. Mixing CD4+-cell-depleted Ts and CD8+-cell-depleted Ts preparations restored the capacity of the cells to induce Igh-1b suppression. Thus, both CD4+ CD8- Ts and CD4- CD8+ Ts are required for the induction of this allotypic suppression. Bone marrow cells and B splenocytes from Igh-1b-suppressed adult Igha/b mice were shown to be able to durably express Igh-1b when transferred into irradiated Igha/a BALB/c hosts whereas whole spleen cells from such donors failed to do it. Abrogation of Igh-1b suppression by in vivo anti-CD8 mAb treatment was achieved in adult Igha/b heterozygotes but with a lower efficiency than in adult Ighb/b homozygotes, all being chronically Igh-1b suppressed. The CD4- CD8+ cell population essential for maintaining this suppression is resistant to in vivo 600 rad irradiation and seems to be slightly inhibited by in vivo administration of free Igh-1b.

Animals↗
PubMed1985

Autoanti-allotype antibodies and idiotypic network regulating allotype production in rabbits.

Anti-idiotype sera were prepared by immunization of inbred B/J as well as random-bred rabbits with anti-b4 antibodies from a syngeneic rabbit. These antisera inhibited the binding between b4 and anti-b4 from different animals to various degrees. Anti-anti-idiotype sera prepared in syngeneic rabbits also inhibited the binding between anti-b4 and anti-idiotype from different animals, and did not contain anti-b4 antibodies. These results suggest that at least some anti-b4 and anti-idiotype antibodies could carry the same or similar idiotypes, respectively. Treatment of b4b5 F1(B/J X Chbb:HM) hybrids at birth with these anti-idiotype sera from B/J rabbits resulted in a modulated production of the allelic allotypes in the serum. Anti-idiotype serum against anti-b4 induced an elevated production of b4 with little effect on the production of b5 in the same serum. In F1 hybrids born from a doe immunized with anti-idiotype antibodies against anti-b4, there was a decreased production of b4, followed by a gradual recovery to normal levels. Serum b5 levels in F1 offspring of one particular Chbb:HM doe were extremely low, as compared with those in other F1 hybrids and the b4/b5 ratio in the serum was unusually high. Such low b5 levels were no longer observed when offspring of this doe were given normal b5 serum at birth. Anti-b5 activity was not detected in the serum of this doe. These observations strongly suggest the presence in normal rabbits of the autoanti-allotype antibody and of the idiotypic network involving this antibody and regulating allotype production.

Animals↗
PubMed1984

Allotype suppression in an adoptive transfer system in adult mice: the specificity and feedback effects of a monoclonal IgG3 anti-(Igh-1b) allotype antibody.

Using an adoptive transfer system in mice, an allotype-specific suppression has been induced by a monoclonal IgG3 anti-Igh-1b (Hyb 5.7) reagent. Suppression was specific for IgG2a (Igh-1b) and led to a compensatory increase of the Igh-1a response in irradiated mice reconstituted with allotype heterozygous (Igha/b) spleen cells. Suppression, which was not antigen-specific, lasted for at least 1 month after anti-allotype treatment.

Animals↗
PubMed1983

T cell allotypic determinants encoded by genes linked to the immunoglobulin heavy chain locus. I. Establishment of monoclonal antibodies against allotypic determinants.

Monoclonal alloantibodies for T cell allotypic determinants were obtained by hybridizing SP-2 tumor cells with BALB/c (H-2d, Igh-1a) spleen cells, which had been repeatedly immunized with Con A-stimulated CB-20 (H-2d, Igh-1b) spleen cells. It was found that these monoclonal anti-CB-20 antibodies detect the new allotypic determinants (distinct from the B cell Igh-C region determinant) expressed only on the augmenting or suppressor T cells. Genetic analysis of these antigenic determinants revealed these antibodies react with the gene products located on the telomeric side chromosome of the Igh variable region gene (Igh-V) cluster. These antibodies when given in vivo caused a modification of antibody production. The antibody activity was absorbed by Con A-stimulated B10.BR (H-2b, Igh-1b), C57BL/6 (H-2b, Igh-1b), CWB (H-2b, Igh-1b), CB-20 (H-2d, Igh-1b), and BAB-14 (H-2d, Igh-1b) spleen cells, but not by Con A-stimulated C3H.SW (H-2b, Igh-1j), BALB/c (H-2d, Igh-1a), A/Sn (H-2a, Igh-1e), and C.AL-20 (H-2d, Igh-1d) spleen cells. In addition, in vivo these monoclonal antibodies modified anti-SRBC antibody production only in Igh-1b allotype-bearing mice. One monoclonal antibody reacted with 4-hydroxy-3-nitrophenyl acetyl- (NP) hapten-specific augmenting T cells, and the other two batches of monoclonal antibodies reacted with NP-specific suppressor T cells of NP-mediated cutaneous responses. A mapping study with these recombinants limits the gene coding for the T cell-specific determinants to a gene within the variable region to the telomeric side of NP-VH and to the centromeric side of prealbumin. This segment is inclusive of all immunoglobulin genes, the region Owen named IgT-C, and a histocompatibility gene (H-Ig).

Animals↗
PubMed1977

Structural and genetic studies on chicken 7S immunoglobulin allotypes. II. Distribution of allotypes on the 7S immunoglobulin of homozygous and heterozygous chickens.

We have previously reported that chicken 7S immunoglobulin (Ig) heavy (H) chain allotypes (CS-1 locus) segregate as phenogroups in F2 progeny. Specificity CS-1.1 formed a phenogroup with CS-1.4 in inbred chicken line UCD 2, and a second phenogroup with CS-1.3 in line UCD 3. To determine whether these phenogroups were formed by combinations of specificities on the same, or on separate subclasses of 7S Ig, their distribution on the 7S Ig molecules of birds homozygous for 7S Ig allotypes was analyzed by radioimmunoassay. Anti-CS-1.1 and anti-CS-1.3 alloantisera each bound more than 94% of line UCD 3 1252-7S Ig. Similar results were obtained with alloantisera to CS-1.1 and CS-1.4 WITH 125 I-7S Ig from line UCD 2. These results indicate that both phenogroups were formed by combinations of specificities present on the same H chain. Thus, each phenogroup described, probably is the product of a single structural gene which is responsible for more than 94% of the 7S Ig H chain constant regions. In F hybrids with the genotype CS-1.3, 1.3/CS-1.2, two populations of serum 7S Ig molecules were detected by direct and sequential binding analysis with specific alloantisera. One population of 7S Ig contained specificities CS-1.1 AND CS-1.3, but not CS-1.2; while the second population was exclusively the product of one parental allele. Consistent with a genetic regulatory mechanism involving allelic exclusion, no MS Ig containing allotypes produced by both alleles was detected.

Animals↗