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PubMed1973

Allotype suppression in the rabbit. I. The ontogeny of cells bearing immunoglobulin of paternal allotype and the fate of these cells after treatment with antiallotype antisera.

The ability to distinguish immunoglobulin (Ig) of paternal allotype both on lymphocyte membranes and in the serum of neonatal b(4)b(5) heterozygous rabbits has allowed us to study the postnatal ontogeny of cells bearing endogenously synthesized Ig that could not have been derived from the mother. In normal b(4)b(5) rabbits, such endogenously synthesized Ig of paternal allotype is present on the membranes of bone marrow-derived (B) lymphocytes from birth, but does not appear as detectable circulating Ig until approximately 2 wk of age. In the neonate, cells bearing the paternal allotype are potential targets for the induction of chronic allotype suppression. Within 24 h of exposure to anti-allotype antisera in vivo, Ig of the suppressed paternal allotype is no longer detectable on the surface of neonatal lymphoid cells. Further, this lymphocyte membrane Ig is eliminated and not simply masked by the suppressing antibodies. Finally, cells bearing the suppressed allotype are deleted from all lymphoid organs for the duration of total allotype suppression, and reappear first in bone marrow and peripheral blood at the time of spontaneous escape from suppression.

Animals↗
PubMed1991

[Homology between the Lpm system of allotypes in the American mink and the Gp system of allotypes in the domestic pig].

The 5 alpha-macroglobulin allotypes alpha M1, alpha M2, alpha M3, alpha M4 and alpha M5 were identified in pig. The alpha M1 allotype was reported as a marker of pig alpha-macroglobulin, the latter being homologous to alpha 2-macroglobulins in human and in mink. The allotypes alpha M2-alpha M5 were specified as markers of the second isotypical variant of pig alpha-macroglobulins, which was homologous to mink Lpm macroglobulin (alpha 1M). As seen from data obtained by International Comparative Test ISABR 87-88, alpha M1 is a new allotype, while allotypes alpha M2--alpha M5 correspond to four allotypes in the Gp system (Janik et al.). Based on these data, a conclusion was made on the homology between the Lpm system in american mink and the Gp system in pig. Since the allotypes studied are the part of alpha-macroglobulins, a locus controlling them was designated the AM locus. We also find it more advantageous to apply the same name to the homologous locus in mink, instead of the Lpm used earlier. Genetic control of 5 allotypes was studied and the structure of the AM locus in pig analysed in detail. Comparative study of organization of the above locus and the homologous locus in mink was carried out.

Animals↗
PubMed1990

The immunoglobulin allotype contributed by peritoneal cavity B cells dominates in SCID mice reconstituted with allotype-disparate mixtures of splenic and peritoneal cavity B cells.

We have studied potential regulatory interactions between mature B lymphocyte populations by analysis of C.B-17 severe combined immunodeficient (SCID) mice reconstituted simultaneously with immunoglobulin allotype-congenic mixtures of spleen (SP) and peritoneal cavity (PerC) B cells. We have previously shown that the independent transfer of B cells from these sources leads to the long-term survival of donor B cells and reconstitution of immunoglobulin levels in SCID mice (Riggs, J.E., D.L. Robertson, R.S. Stowers, and D.E. Mosier, manuscript submitted for publication). SP and PerC B cells differ in numerous respects, with the PerC having higher proportions of large, activated B cells that express the IgM greater than IgD phenotype and greater numbers of CD5 B cells. The injection of equal numbers of B cells from SP and PerC into SCID recipients (e.g., BALB/c SP + C.B-17 Per C----SCID) has led to the following observations: (a) serum IgM allotypes in B cell chimeras revealed strict dominance by the allotype contributed by the PerC B cells; (b) this dominance was not due to regulatory T cells; (c) B cells of the unexpressed (i.e., SP) allotype were present in the chimera in the spleen but not the peritoneal cavity; and (d) immunization with TI and TD antigens failed to elicit the SP IgM allotype, whereas secondary TD antigen immunization elicited low levels of the SP IgG2a allotype. Additional experiments demonstrated concurrent expression of IgM allotypes derived from both SP and PerC B cells in recipients that: (a) received a 10-fold excess of SP B cells; (b) received SP B cells before PerC B cell transfer; or (c) received SP B cells intravenously and PerC B cells intraperitoneally. We conclude that the establishment of IgM synthesis by PerC B cells leads to a feedback inhibition of subsequent IgM synthesis by SP B cells, and that the frequency of B cells that can lead to this effect is substantially higher in peritoneal cavity than in spleen. These data provide further confirmation of regulatory interactions between B cells in the absence of T lymphocytes, but confound the interpretation of experiments supporting the existence of a separate CD5+ B cell lineage.

Animals↗
PubMed1978

Rabbit latent group a allotypes: characterization and relationship to nominal group a allotypic specificities.

Latent group a allotypes were detected with a sensitive radioimmune inhibition assay. Sera, IgG preparations, and antibody fractions containing these allotypes inhibited the binding of insolubilized allotypic antisera to various radiolabeled antigens including IgG pools, homogeneous antibodies, and, in the case of a3, a VH fragment from a3/b4 IgG. Several different group a antiallotypic sera were used in the assays and all gave similar results. Comparison of inhibition curves for nominal and latent allotypes indicated that the full spectrum of allotypic subspecificities may be expressed in latent allotypes. Hemagglutination studies carried out with five sera containing high levels of latent allotypes confirmed the results obtained with the radioimmunoassay and indicated that inhibition values did not, at least in four of the five samples studied, reflect the presence of antiallotype antibodies.

Animals↗
PubMed1985

The nature of antiidiotype molecules induced by antiallotype. Presence of both latent allotype and allotypic internal images.

Previously (9), I found that immunization of rabbits with antibody directed against variable region heavy chain VH polypeptides of a1 allotype induced the production of antiidiotype (anti-Id) molecules that appeared to bear images of the original a1 allotype. I now show that these anti-Id molecules can be fractionated into two populations: one population (a2a3- anti-Id) that lacks the nominal VH a2 or a3 allotype of the rabbit from which it was derived, and another population (a2a3+ anti-Id) that expresses these allotypes. Both anti-Id populations display epitopes that resemble a1 since: (a) they were capable of inhibiting 125I-a1 Ig binding to rabbit anti-a1, goat anti-a1, and mouse anti-a1 mAb; and (b) immunization of normal a2a3 rabbits with either anti-Id fraction led to the formation of specific anti-a1 antibody. Reductive cleavage of the anti-Id molecules showed that the a1 determinants in the a2a3- population were fully displayed on isolated H chains, consistent with the presence of latent a1 Ig. On the other hand, as expected for internal images encoded by the antigen-combining site, the a2a3+ anti-Id population required intact H and L chains for maximal a1 expression. The a1-like images within the a2a3+ anti-Id population do not appear to be identical to nominal or latent a1, however, since a2a3- anti-Id was invariably a more efficient inhibitor of a 1 Ig-anti-a1 binding than a a2a3+ anti-Id. These results indicate that immunization with antiallotype can result in the simultaneous production of both latent allotypes and allotypic internal images.

Animals↗
PubMed1980

Experimental erythrocyte autoimmunity. I. Mice congenic for immunoglobulin allotypes vary in production of autoantibodies but produce suppressor cells not restricted by allotypes.

Erythrocyte autoantibodies can be elicited in mnce by injections of rat RBC which are cross-reactive with mouse RBC. This report shows that induction of autoantibodies is dependent, in part, on gene(s) outside the H-2 complex. Using CBA mice congenic for Ig allotype and the F1 and F2 hybrids, a higher incidence of autoantibody production was observed in mice bearing the Ig allotype 1b (1b/b or 1a/b) in contrast to mice homozygous for the allotype Ig-1a. Serum haemagglutination titres against rat RBC were not reduced in the groups of mice with the lower incidence of autoantibody production. A probable explanation for these observations is that the change in Ig allotype is associated with some change in the variable region determining autoimmune specificity that is governed by VH genes linked to allotype genes. The transfer of 30 x 10(6) spleen cells from Coombs' positive mice to syngeneic recipients before starting the immunization regime with rat RBC suppressed autoantibody production and enhanced antibody production against rat RBC. These suppressor cells were effective in congenic mice and in F1 hybrids, which suggest that the Ig allotype is not a crucial site for the effector stage of suppression of this autoimmune response.

Animals↗
PubMed1978

Structural and genetic studies on chicken 7S immunoglobulin allotypes. IV. The presence of an unexpected chicken immunoglobulin heavy chain allotype: subclass or pseudoallele?

Low concentrations of allotypic specificity CS-1.1 were detected in the sera of two inbred chicken lines [University of California, Davis (UCD) 7 and Regional Poultry Research Laboratory 15I4] previously reported to lack this specificity. The CS-1.1 alloantigen in 15I4 chickens has the same specificity as the major allotype in a line of chickens (UCD 2) in which it was initially defined. In 15I4 chickens, CS-1.1 allotype is present on a population of molecules distinct from those which carry the major allotype; thus a second 7S Ig H chain locus, CS-2, is proposed. The concentration of CS-1.1-bearing molecules determined by two different methods was 7 microgram/ml and 230 microgram/ml in 15I4, whereas UCD 2 chickens had 4 mg/ml of CS-1.1 molecules. The levels of CS-1.1 inhibitory activity in 15I4 birds remained relatively constant over a 30-day period. The presence of two 7S Ig populations in 15I4 chickens may be interpreted as evidence either for 7S Ig subclasses with shared allotypes or for a pseudoallelic organization of genes controlling expression of 7S Ig H chains. The results were consistent with the presence of redundant C region genes, differing in allotypes, whose expression is under the control of an as yet undefined regulatory mechanism.

Alleles↗
PubMed1965

Studies on rabbit lymphocytes in vitro. II. Induction of blast transformation with antisera to six IgG allotypes and summation with mixtures of antisera to different allotypes.

Specific antisera directed against all six of the well characterised allotypic determinants of rabbit IgG (As1, 2, 3, 4, 5, and 6) are capable of inducing blast transformation and DNA synthesis when added to lymphocyte cultures obtained from donor rabbits having the appropriate IgG allotype. Mixtures of antisera directed against two different allotypic determinants induce a "summation" of transformation and DNA synthesis over and above the effect of mixtures of two antisera directed against the same allotypic determinant. This summation effect is observed regardless of whether the antisera which have been mixed are directed against allotypic determinants controlled by the same locus or by different loci. The finding that summation occurs with mixtures of two antisera directed against both the allotypic determinants of a double homozygote rabbit (As1, 6) suggests that lymphocytes from the peripheral blood may be primed to produce only one or the other of the two polypeptide chains of IgG, but not both.

Animals↗
PubMed1972

Active suppression of immunoglobulin allotype synthesis. I. Chronic suppression after perinatal exposure to maternal antibody to paternal allotype in (SJL x BALB-c)F 1 mice.

Long-term (chronic) allotype suppression, previously reported only in rabbits, is shown here to occur in at least one strain combination of mice as well. Close to 50% of the offspring of SJL (Ig(b)) males mated to BALB/c (Ig(a)) females immunized against the paternal allotype were found to be suppressed for Ig-1b (gammaG(2a)) at 6 months of age. These mice are called "chronically" suppressed. The percentage of offspring in this strain combination suppressed for the paternal allotype at 8 wk of age is the same as that seen in an earlier strain combination tested, [(C57 x BALB/c)F(1)], in which all mice recover from suppression by 10-12 wk. After 8 wk, two distinct patterns of long-term (chronic) suppression emerge in (SJL x BALB/c)F(1) mice: a small number of these mice never produce detectable amounts of Ig-1b throughout their lives, while the majority produce detectable Ig-1b sporadically, sometimes over a period of several weeks, the level of which eventually falls below detectability. Attempts to "cure" suppression by destroying the existent lymphoid population and forcing endogenous repopulation in chronically suppressed animals were unsuccessful. Furthermore, attempts to restore Ig-1b production by injection of cells from syngeneic Ig(a)/Ig(b) donors into irradiated, chronically suppressed recipients were also unsuccessful, although the same cell inocula, when injected into irradiated BALB/c (Ig(a)/Ig(a)) mice produced high levels of gamma globulin carrying the allotype. These results suggest that long-term allotype suppression resulting from perinatal exposure of offspring to specific anti-allotype antibody (anti-Ig-1b), is not due merely to an absence of Ig-1b-producing cells or their progenitors, but appears to be an active process, which dominates physiologically over normal production.

Animals↗
PubMed1990

Conversion of the C4d.2 serologic allotype of murine complement component C4 to the C4d.1 allotype by site-specific mutagenesis.

C4d.1 and C4d.2 are serologically defined allotypes of murine complement component C4. Previous studies in Shreffler's laboratory have shown that the structural difference between the two allotypes lies within a single tryptic peptide of the C4 alpha-chain and that the sequences of this fragment from the two allotypes (determined from nucleic acid sequences of genomic clones) differ only by the substitution of arginine in C4d.2 for glutamine in C4d.1. Hence this single amino acid change apparently is responsible for the rather striking serological difference between the two allotypes. To test this conclusion, we have used site-specific mutagenesis to alter the sequence of a full-length C4 cDNA that was derived from a mouse strain expressing the C4d.2 allotype. We substituted a glutamine codon for the arginine codon at the specified site and expressed both mutant and parent recombinant C4 proteins by transient transfection of COS cells. We found that an alloantiserum specific for C4d.1 reacts with the mutant protein but not the parent whereas an alloantiserum specific for C4d.2 reacts with the parent protein, as expected, but not the mutant. These results confirm that a single amino acid difference specifies the C4d.1 and C4d.2 allotypes.

Alleles↗
PubMed1977

Regulation of allotype expression in heterozygous rabbits. III. Concomitant modulation and concomitant suppression oa a2 and a3 allotypes on individual peripheral blood lymphocytes.

Sensitization of peripheral blood lymphocytes from heterozygous a2/a3 rabbits with purified, monospecific anti-a3 antibodies, raised in a1/a1 rabbits, resulted in the disappearance of surface a2 and a3 allotypes (concomitant modulation) after subsequent incubation at 37 degrees C, as determined by the mixed antiglobulin (rosette) test. Similar results were obtained when anti-a2 antibodies were used. The dose dependence of modulation and comodulation were also studied. Testing of mixtures of homozygous a2/a2 plus a3/a3 cells never led to comodulation. Blocking studies, performed to determine the surface contiguity of a2 and a3 determinants, indicated that both allotypes are situated close together in the membrane on cells exhibiting allotype inclusion. Overnight culture in serum-free medium revealed that cells which underwent extensive modulation and comodulation were often suppressed for both homologous and alternate allotypes (concomitant suppression). These and other data suggest that a single modulation event, in which extensive removal of cell membrane Ig occurred, could serve to inhibit the re-expression of Ig. This may, in part, reflect interactions with membrane receptors involved in the regulation of expression of VH gene products. Implications of VH allotype inclusion are discussed.

Animals↗
PubMed1981

Allotype suppression in the chicken. II. Suppression in homozygous chickens with antiallotype antibody and allotype-disparate B cells.

Injection of heterozygous (M-1a/M-1b, G1g/G-1i) B 14-line chickens with antisera directed against either IgM-1a or IgM-1b induced suppression of the relevant IgM-1 and genetically linked IgG-1 allotypes, whereas a mixture of anti-M-1a and anti-M-1b antibodies failed to produce allotype suppression. Injection of anti-M-1 antiserum into M-1 homozygous chickens induced only a transient delay of a few days in the appearance and rise of serum IgM-1 levels. However, suppression of host allotypes was induced by injecting M-1, G-1 homozygous neonatal or embryonal recipients with anti-M-1 antisera together with B locus- histocompatible allotype-disparate spleen, bone marrow or bursal cells. The active cell type were donor B cells, which established chimerism in the injected host, whereas peripheral blood T lymphocytes from agammaglobulinemic donors were ineffective. Allotype suppression was attributed to a homeostatic control mechanism which is exerted by normal B cells (but not T cells) over B cell recruitment in anti-M-1 antibody-treated, immature hosts.

Animals↗
PubMed1984

Allotype suppression in the chicken. V. Abnormal isotype ratios of chronically suppressed IgM and IgG allotypes.

Chronic allotype suppression was generated in M-1 (C mu), G-1 (C gamma) heterozygous B14 line chickens either by embryonal injection or by maternal transfer of anti-M-1b allotype antibodies. Using a sensitive radioimmunoassay to detect the suppressed IgM-1b, a striking disparity was observed between the degree of suppression of the IgM-1b allotype and that of the genetically linked IgG-1i allotype. The amount of suppressed IgM-1b ranged between 0.2 and 3% of total serum IgM in chronically suppressed birds. The levels of the genetically linked IgG-1i, however, comprised 5 to 25% of total serum IgG in such birds. The allotypes measured in suppressed chickens were qualitatively identical to those in normal, nonsuppressed birds by serological criteria. These results are discussed within the context of isotype regulation in the chicken.

Alleles↗
PubMed1984

Kappa-chain allotypes and isotypes in the rabbit: cDNA sequences of clones encoding b9 suggest an evolutionary pathway and possible role of the interdomain disulfide bond in quantitative allotype expression.

The constant regions of rabbit kappa light chains are unusual because the sequences of the allotypic forms can differ more from each other than do some variable regions with which they associate. We report the nucleic acid sequence of a full-length cDNA clone of b9 allotype and show comparisons to available sequences of the rabbit kappa allotypes b4, b5, and bas-N4. Our analyses suggest that the primordial rabbit kappa gene encoded a bas-like sequence. They also reveal a surprising difference in the position of the variable region cysteine that forms the interdomain disulfide bond that is unique to most rabbit kappa chains. One b9 cDNA sequence lacks the usual cysteine-80 and instead encodes cysteine-108, which in three-dimensional models appears capable of forming the interdomain disulfide bond with cysteine-171 in the constant region. A partial sequence of a second b9 clone encodes both cysteine-80 and cysteine-108; the translation product of this clone could have a free reactive sulfhydryl group that might lead to an unstable nonfunctional Ig molecule. The fact that pre-B cells with b9 kappa chains do not differentiate and expand into productive Ig-producing cells with frequencies comparable to the other allotypes may be explained if a substantial proportion of the gene products have a free sulfhydryl group. Our sequence results suggest that in cells differentiating to produce kappa light chains of b9 allotype the number and location of the cysteines influence immunoglobulin expression.

Animals↗