bluuebunny/crossref_metadata_2025_split huggingface dataset:
THE ELY‐1 LOCUS CONTROLS A DI‐ALLELIC ALLOANTIGENIC SYSTEM ON EQUINE LYMPHOCYTES
Authors: Byrns G. , Crump A. L. , Lalonde G. , Bernoco D. , Antczak D. F. 
Published: April 2007

SUMMARYThe ELY‐I locus controls the expression of a polymorphic cell surface antigen of equine lymphocytes which was detected using antibodies generated by alloimmunization with peripheral blood lymphocytes. The ELY‐1 antigens were not detected on erythrocytes or platelets by absorption experiments. The two alleles, which have been designated ELY‐1.1 and ELY‐1.2, are expressed codominantly and appear to constitute a closed system at the population level. In family studies, the ELY‐1 antigens segregated as products of an autosomal locus not linked to the major histocompatibility complex (MHC) of the horse. In the complement mediated lymphocyte microcytotoxicity test, antisera to the ELY‐1 antigens selectively killed peripheral blood lymphocytes which did not express surface immunoglobulin. The ELY‐1 antigens may be useful markers for equine T cells when assayed in this fashion. Three alloantisera were used in immune precipitation of iodinated and solubilized cell surface proteins from peripheral blood lymphocytes. Electrophoresis of the precipitates in sodium dodecyl sulphate (SDS)‐polyacrylamide gels demonstrated strong bands in the Mr 180–190K range that were shared in the three different preparations. These results suggest that the ELY‐1 allospecificities are expressed on an equine equivalent of the murine T200 molecule.
SHORT CU MMUNICA TION: OCCURRENCE OF THE IMMUNOGLOBULIN HAPLOTYPES Gm1,17;23;21 AND Gm1,2,17;23;21 IN A SAMPLE OF AUSTRALIAN CAUCASIANS
Authors: Propert D. N. , Janardhana V. 
Published: April 2007

SUMMARYPhenotypes positive for G2m(23) but negative for Glm(3) and G3m(5,10,11,13,14) are generally very infrequent in Caucasian populations. We recently Gm typed 372 Australian blood donors, predominantly of European descent, and found two Gm(1;23) and five Gm(1,2;23) individuals among them. This finding suggests that the haplotypes Gm1,17:23;21 and Gm1,2,17,23,21 may occur, in some European populations, with a frequency considerably higher than has been generally assumed.
STRAIN DIFFERENCES IN THE EXPRESSION OF THE EPA‐1‐RESTRICTING ELEMENT
Authors: Hadley G. A. , Snider M. E. , Steinmuller D. 
Published: April 2007

SUMMARYEpa‐1‐specific cytotoxic T lymphocytes (CTL) lyse epidermal cells (EC) of different Epa‐1+H‐2k strains, such as AKR, CBA, C58, and RF, at different levels. We used an H‐2Kk‐specific monoclonal antibody (mAb) to test the hypothesis that this phenomenon is due to differences in the H‐2‐restricting element. Initially, we established the specificity of this mAb for the Epa‐1‐restricting element by demonstrating its capacity to inhibit the lysis of CBA EC by Epa‐1‐specific CTL. We then used it as the probe in a cellular radioimmunoassay to quantify the expression of the restricting element by EC of different H‐2k strains. We found that C58 and RF EC bound significantly less of the mAb than did CBA EC. Although AKR also bound less of the mAb than did CBA EC, the difference was not statistically significant. To examine the generality of this phenomenon, we quantified the expression of Kk antigens on spleen cells (SC) of the same four strains. We found that RF SC, but not AKR or C58 SC, bound significantly less of the Kk mAb than did CBA SC. Thus, the differential CTL lysis of Epa‐1+ EC of different strains probably reflects differences in expression of the H‐2‐restricting element rather than of the nominal antigen.
GENETIC STUDIES OF LOW‐ABUNDANCE HUMAN PLASMA PROTEINS: VII. HETEROGENEITY OF THE C1, SUBCOMPONENT OF THE FIRST COMPLEMENT COMPONENT
Authors: Kamboh M. I. , Ferrell R. E. 
Published: April 2007

SUMMARYCharge‐based structural variation has been observed in the C1, subcomponent of the first complement component C1 after isoelectric focusing and immunoblot‐ting. One common and two uncommon autosomal co‐dominantly expressed alleles, designated ClS*1, ClS*2 and ClS*3, have been recognized at the ClS structural locus. The frequency of these alleles was 0·979, 0·016 and 0·005, respectively, in a U.S. white population. No variation at the ClS locus was observed in a U.S. black sample (n = 95).
Mls DETERMINANTS RECOGNIZED BY T CELLS
Authors: Abe R. , Hodes R. J. 
Published: April 2007

SUMMARYThe relationship among different minor lymphocyte stimulatory locus (Mis) determinants, Mlsa, Mlsb, Mlsc and Mlsd, remains unclear. Because of the high degree of cross‐reactivity between Mlsa and Mlsd determinants, the weak stimulatory capacity of Mlsc, and the generally non‐stimulatory nature of Mlsb, some investigators have recently suggested that Mis is composed of only a single expressed allele originally defined as the a andd alleles. In order to clarify the nature of Mls determinants, T cell clones positively selected for reactivity to the three stimulatory Mls determinants, Mlsa Mlsc and Mlsd, were generated and their specificities defined by extensive genetic studies. The response pattern of these Mls‐specific clones as well as the results of primary mixed lymphocyte responses indicated that: (i) Mlsa and Mlsc determinants recognized by T cells are distinct, demonstrating that polymorphism does exist within the Mls system; and (ii) Mlsd is not an independent Mls type since Mlsd determinants are composed of Mlsa and Mlsc determinants and anti‐Mlsd T cell responses are, in fact, the sum of anti‐Mlsa and anti‐Mlsc responses.
EVIDENCE FOR A HISTOCOMPATIBILITY LOCUS PROBABLY LINKED TO BUT DISTINCT FROM Mls AND H‐25
Authors: Berumen L. , Halle‐Pannenko O. 
Published: April 2007

SUMMARY BALB/c (Mlsb) and BALB.D2‐Mlsa strains of mice, both H‐2d, are congenic and differ for the Mls locus (and linked genes) located on chromosome 1. The BALB.D2‐Mlsa strain was obtained by introducing the Mlsa allele of DBA/2 mice into BALB/c mice. In previous studies we showed that BALB.D2‐Mlsa recipients reject, relatively rapidly, all skin grafts from BALB/c donors. We and other groups have questioned whether the rejections observed were indeed due to the incompatibility for Mlsb products or for products of a histocompatibility (non‐H‐2) locus linked to, but distinct from, Mlsb. To answer this question, several hybrids carrying either Mlsa or Mlsb in various genetic contexts were grafted with skin from Mls‐compatible BALB/c or BALB.D2‐Mlsa donors; in the genetic combinations selected, any rejection which might occur would reflect the effects of a non‐Mls incompatibility between BALB/c and BALB.D2‐Mlsa strains. In certain of the donor‐recipient combinations studied, the skin grafts were tolerated for > 200 days, but a relatively rapid rejection of BALB/c skin grafts was observed in (B10.D2 × BALB.D2‐Mlsa)F1 and (B10.BR × BALB. D2‐Mlsa)F1 hybrid recipients. These results indicated that in addition to Mls, the BALB/c and BALB.D2‐Mlsa strains differ for at least one other non‐H‐2 histocompatibility locus. The possible involvement of H‐25 was then investigated. Indeed, disparity for H‐25, which maps on chromosome 1 close to Mls, can induce relatively rapid skin graft rejection. The H‐25 allele of the DBA/2 strain has not been defined: we considered, therefore, that BALB/c and DBA/2 could be disparate at the H‐25 locus, and that H‐25 (transmitted by DBA/2 to the BALB.D2‐Mlsa strain, together with the Mlsa allele) could be responsible for the skin graft rejection we observed. Our results showed, however, that DBA/2, BALB/c and BALB.D2‐Mlsa strains of mice all share the H‐25c allele; they therefore ruled out a role for H‐25 incompatibility in the skin graft rejections we observed, and indicated that these rejections are due to the effects of a yet undefined histocompatibility locus (locus ‘x’), probably linked to, but distinct from, the Mls locus. Further experiments showed that the histocompatibility effect of locus ‘x’ cumulates with that exhibited by Mlsb (or by a putative histocompatibility locus linked to Mlsb).
GENETIC RELATIONSHIPS OF Mlsa AMONG POLYMORPHIC LOCI ON DISTAL MOUSE CHROMOSOME 1
Authors: Seldin M. F. , Abe R. , Steinberg A. D. , Hodes R. J. , Morse H. C. 
Published: April 2007

SUMMARYThe segregation of Mlsa with respect to genes localized distally on mouse chromosome 1 was examined in two sets of recombinant inbred (RI) strains. In order to localize Mlsa, a linkage map based on analysis of both interspecific backcross mice and multiple sets of RI strains was utilized: (centromere) ‐ Ren‐1,2‐10 centimorgans (cM)‐At‐3‐8cM.‐Apo‐A2/Ly‐17‐2 cM‐Spna‐1‐4cM.‐Akp‐1‐(telomere). The Mlsa allele was mapped to a region that extended just centromeric of Ly‐17 (one crossover in 40 RI strains) to just telomeric of Spna‐1 (no crossover in 40 RI strains). The identification of multiple polymorphic loci in the region of Mlsa should allow precise gene localization and assist in efforts to clone this gene.
Mlsa DETERMINANTS: RELATIONSHIP TO Fcγ RECEPTOR AND TISSUE DISTRIBUTION
Authors: Molina I. J. , Huber B. T. 
Published: April 2007

SUMMARYWe have analysed the genetic relationship between Misa and FcγR in mice. Using the FcγR‐specific DNA probes, we were unable to detect a restriction fragment length polymorphism (RFLP) which is consistent in DNA derived from Mlsa strains and which differed from that of Mlsb strains, while we could see a polymorphism that distinguishes Ly17.1 from Ly17.2, alleles of the FcγR. These results strongly suggest that Mlsa is neither a product of the αFcγR nor of the βFcγR gene.Furthermore, we have re‐examined the tissue distribution of Mlsa determinants using a major histocompatibility complex (MHC) class II antigen‐positive T‐cell tumour as well as a pure population of bone marrow derived macrophages of Mlsa genotype. Both these cell types were recognized to varying degrees by alloreactive cells; however, none of them expressed functionally detectable Mlsa determinants. We conclude from our studies that Mlsa is a highly stimulatory self peptide that is exclusively expressed in B cells.
A COMMENT ON H‐2‐RESTRICTED T CELL RECOGNITION OF Mls DETERMINANTS: A QUESTION OF PERSPECTIVE
Authors: Peck A. B. 
Published: April 2007

SUMMARYData presented here address the question of whether T lymphocyte recognition of Mis determinants is MHC restricted. Using isolated T cell blasts from primary MLCs involving H‐2‐identical, Mls‐disparate strain combinations as responding cell populations in secondary MLCs, and measuring their responses against fresh stimulating cells from different strains, has permitted the study of reactions towards Mis determinants in the presence of MHC antigenic differences. Results strongly suggest that recognition of Mlsc (Mls‐2 locus) determinants is H‐2 restricted. In contrast, there is still little evidence that the recognition of Mlsa (Mls‐1 locus) determinants is H‐2 restricted. Furthermore, data are also presented which refute the notion that different H‐2 haplotypes possess different abilities to present Mlsa determinants to responding T cells.
Mls DETERMINANTS AND ANTI‐Mls RECEPTORS
Authors: Webb S. R. , Okamoto A. , Sprent J. 
Published: April 2007

SUMMARYWe review evidence from this laboratory that T cell recognition of Mlsa determinants is not controlled solely by the α‐β T cell receptor (TcR) molecule. We propose a model in which Mlsa recognition reflects a receptor‐ligand interaction between two sets of complementary accessory molecules, one molecule (Mlsa) being expressed on B cells and the other (the anti‐Mlsa receptor) on T cells; this interaction augments recognition of self class II molecules by the TcR. The biological role of Mls molecules might be to facilitate physiological T‐B interaction.
SYNERGY BETWEEN STIMULATOR CELLS IN THE INDUCTION OF THE ANTI‐Mlsa RESPONSE
Authors: DeKruyff R. H. , Laning J. , Dorf M. E. 
Published: April 2007

SUMMARYWe have identified two types of clones responsive to Mls determinants. One type responded vigorously to purified B cells from mice bearing Mlsa‐stimulatory determinants. The other type, including clone Lyl‐N5, responded vigorously to unfractionated spleen cells, but failed to respond to B cells alone or to spleenadherent cells (SAC) alone from the Mlsa‐bearing mice. Synergy between two stimulator cell types, B cells and SAC, was required to induce the Mls response of clone Lyl‐N5. The failure of clone Lyl‐N5 to respond to Mlsa‐bearing B cells was reversed by the addition of SAC taken from mice bearing the Mlsb allele or the non‐stimulatory Mlsb allele. B cells were required to provide the Mlsa determinant.The Mls response of clone Ly1‐N5 is restricted by class II determinants shared by the H‐2b, H‐2d and H‐2k haplotypes, but not the H‐2q haplotype. The optimal response of the clone was obtained by using B cells bearing both Mlsa and the permissive H‐2 alloantigen. However, complementation was also observed between B cells bearing Mlsa and the non‐permissive Iaq and SAC bearing the non‐stimulatory Mlsb, but a permissive la epitope, resulting in activation of the clone.Clone Ly1‐N5 responds to Mlsa‐bearing B cells only in the presence of SAC. The SAC provide an undefined signal required for the proliferation of certain clones such as clone Ly1‐N5, which is not provided by normal B cells. In this report, we show that the AKTB‐lb B‐cell tumour line stimulates the proliferation of clone Ly1‐N5, in the absence of SAC, suggesting that the tumour line has acquired the capacity to provide this signal.
MULTIDIRECTIONAL INTERACTIONS IN AN Mls‐DISPARATE RESPONSE
Authors: Goldbach J. , Kirchner H. , Kölsch E. 
Published: April 2007

SUMMARYThe murine T cell clone E11, isolated from a primary H‐2k‐histocompatible, one‐way mixed lymphocyte culture of B10.BR anti‐C3H/Tif spleen cells, has been used to analyse multidirectional interactions in Mil‐disparate responses. Several events can be observed. There is proliferation of T cells upon stimulation by macrophages or B cells of Mls‐disparate stimulator cells. In addition, one finds induction of differentiation of B cells of stimulator strains. E11 T cells inhibit spreading and differentiation of macrophages of stimulator strains and also prevent the production of a T cell growth‐supporting mediator by Mls‐disparate spleen cells. All these phenomena can be explained by Mlsa,d,c‐specific induction of gamma‐interferon (γ‐IFN) production in the responder B10.BR (Mlsb) E11 T cells. It is suggested that γ‐IFN, as a regulator of feedback mechanisms, plays an essential role in Mls‐disparate cell interactions.
AN EXTERNAL STIMULUS THAT MIMICS Mls LOCUS RESPONSES
Authors: Janeway C. A. , Chalupny J. , Conrad P. J. , Buxser S. 
Published: April 2007

SUMMARYThe response to a novel set of T cell mitogens has been analysed and compared to the response to Mls locus differences. These polyclonal T cell activators, staphylococcal enterotoxins A and B, stimulate T cells in a way that requires an antigen‐presenting cell bearing class II MHC products and involves the CD4:T cell receptor complex. However, the specificity of MHC recognition by the T cell receptor is lost in this response. Thus, these mitogens produce a response with characteristics similar to that induced by Mls locus differences. These mitogens can be used to analyse the immunobiology of this response, and may help in understanding and identifying the Mls locus product as well.
Mls AND THE HELPER T‐CELL REPERTOIRE: II. does theMlsgene product influence the formation of the T‐cell repertoire? studies withMlstolerance
Authors: Hoffmann M. K. , Chun M. , Dennig D. , Hämmerling U. 
Published: April 2007

SUMMARYIn the formation of a repertoire, T cells are selected through a window of autoreactivity which is defined by a low boundary representing the minimal autoreactivity required to enter the T‐cell compartment and a high boundary which determines the highest admissible autoreactivity. We propose that the Mls gene product down regulates autoreactivity and thus modifies the formation of the T‐cell repertoire. Given the polymorphism of Mls and the assumption that Mlsb is more inhibitory than Mlsd, it is conceivable that Mlsb (responder) mice admit into their T‐cell compartment T cells with higher autoreactivity than Mlsd mice. We suggest that it is this highly autoreactive fraction of Mlsb T cells which responds in the overt Mls response. We show that Mls tolerance eliminates T cells responding in the overt Mls response but not T cells responding in the latent Mls response. This is consistent with the finding that T cells responding in the latent Mls response occur in Mlsb as well as in Mlsd mice.
COMPLETE CODING REGION SEQUENCE OF Eβk cDNA CLONES: LACK OF POLYMORPHISM IN THE NH2‐TERMINUS BETWEEN Eβk AND Eβb MOLECULES
Authors: King L. B. , Sharma S. , Corley R. B. 
Published: April 2007

SUMMARYSequence analysis of two independently isolated Eβk cDNA clones revealed that the Eβk molecule is identical to the Eβb molecule at the NH2‐terminus. These data resolve a discrepancy between previously published amino acid and nucleotide sequences and indicate that the Eβ NH2‐terminus is not as polymorphic as was once believed.
ALPHA‐1‐ANTITRYPSIN (Pi) TYPES IN MULTIPLE SCLEROSIS AND LACK OF INTERACTION WITH IMMUNOGLOBULIN (GM) MARKERS
Authors: Francis D. A. , Klouda P. T. , Brazier D. M. , Batchelor J. R. , McDonald W. I. , Hern J. E. C. 
Published: April 2007

SUMMARYSusceptibility to multiple sclerosis is thought to involve several genetic loci apart from the HLA region on chromosome 6. No Pi allotype nor phenotype was associated with the disease in 125 unrelated patients from the Grampian region of northeast Scotland. Despite a previously reported Gm‐HLA association in this population there was no apparent interaction between Pi alleles and Gm type which influenced disease susceptibility.
A MONOCLONAL ANTIBODY, R1, AND A POLYCLONAL SERUM, S10, RECOGNIZE THE SAME MOLECULES: A NOVEL USE OF DNA TRANSFECTANTS
Authors: Banting G. , Mondello C. , Hope R. , Goodfellow P. 
Published: April 2007

SUMMARYThe monoclonal antibody R1 defines the product of the MIC5 locus which has been localized to the long arm of the human X chromosome in the same region as the fragile site FRAXA. DNA transfectants, selected by R1 on the fluorescence‐activated cell sorter (FACS), have been used to demonstrate that a previously described polyclonal antiserum, S10 (Buck & Bodmer, 1976), recognizes the same cell surface molecule as R1. Immunoprecipitation from metabolically and surface‐labelled cells has shown that this molecule is a Mr 200 K phosphoprotein which is synthesized as a Mr 180 K precursor and subsequently modified to a Mr 195 K extracellular form. A Mr 150 K molecule is coprecipitated with the Mr 200 K phosphoprotein, but is only detected in lysates of surface‐labelled cells, raising the possibility that the 200 K molecule is a cell surface receptor and the 150 K molecule a ligand.
ROLE OF MHC, Mls AND TCR IN IMMUNE TOLERANCE
Authors: Anderson G. , David C. 
Published: April 2007

SUMMARYMHC class II molecules and self antigens, such as Mls, influence T‐cell selection by clonal deletion of potentially self‐reactive T cells. In order to examine the role of various class II molecules in the T‐cell receptor‐self antigen interaction, class II transgenic and recombinant mice were analysed for TCR expression. Our studies indicate that the Aα and Eα chains can present Mls gene products for the clonal deletion of Vβ6‐bearing T cells, and that the Aαq chain is defective in this process. We have also shown that Eα Aβ heterodimer in transgenic and recombinant mice is expressed and functions to delete I‐E reactive Vβ11 T cells, demonstrating again the role of the Eα molecule.
Qa‐12—‐A NOVEL DETERMINANT OF ACTIVATED T AND B LYMPHOCYTES
Authors: Oudshoorn‐Snoek M. , Demant P. 
Published: April 2007

SUMMARYInvestigation of the antigenic phenotype of activated lymphocytes using the broadly cross‐reactive mAb 6.3.4 revealed two phenotypic alterations as compared with the resting lymphocytes. The Qa specificity Qa‐m208 disappears after lectin activation of Qa‐m208‐positive T lymphocytes. Analysis of Q7 and Q9 transfectants expressing the Qa‐2 polypeptides shows that Qa‐m208 is an epitope of the Qa‐2 antigen. Because the Qa‐2 antigens are still expressed on T lymphoblasts which have lost Qa‐m208, changes of the Qa‐2 molecules occur and result in the loss of certain epitopes.The second phenotypic change that we observed is the appearance of a novel specificity, Qa‐12. Its expression is induced by lymphocyte activation and it is expressed on lymphoblasts of both T and B cell origin. The presence of this novel non‐ubiquitous antigenic specificity is determined by the Tla region.
ORGANIZATION OF THE AKR Qa REGION: STRUCTURE OF A DIVERGENT CLASS I SEQUENCE, Q5k
Authors: Weiss E. H. , Bevec D. , Messer G. , Schwemmle S. , Großhaus C. , Steinmetz M. , Schmidt W. 
Published: April 2007

SUMMARYWe established the organization of the AKR Qa region and determined the sequence of the 44 and Q5 genes. Restriction mapping and genomic Southern blot analysis revealed that the AKR strain codes for only three H‐2K homologous genes in this region. The AKR Q5 gene is not homologous to the Q5 gene of the C57BL strain, but is presumably allelic to the Q5 gene isolated from Balb/c. The organization and structure of the AKR Qa family is virtually identical to the Qa genes of the C3H mouse. The AKR Q5 gene, in contrast to other H‐2K homologous Qa region genes, codes for a typical transmembrane region, and upon transfection into BHK cells, a 1.6 kb Q5 transcript is detected.
H‐2Kb TRANSFECTION OF B16 MELANOMA CELLS RESULTS IN REDUCED TUMOURIGENICITY AND METASTATIC COMPETENCE
Authors: Porgador A. , Feldman M. , Eisenbach L. 
Published: April 2007

SUMMARYThe metastatic B16 mouse melanoma shows a low cell surface expression of H‐2Kb and H‐2Db class I antigens on cells of both the high‐metastatic line B16‐F10 and the low‐metastatic line B16‐F1. Similarly, newly generated clones of these lines, having different metastatic properties, all express low levels of major histo‐compatibility antigens. One of these clones, the high‐metastatic F10.9, was transfected with H‐2Kb genes to generate H‐2Kb‐expressing transfectants. The resulting clones showed reduced tumourigenicity and a low metastatic phenotype. Unlike the parental cells, H‐2Kb‐positive transfectants are potent inducers and sensitive targets of H‐2Kb‐restricted syngeneic cytotoxic T cells. Immunization of mice with H‐2Kb‐positive transfectants conferred protection against a subsequent challenge with Kb‐positive transfectants but had only a small effect on growth and metastatic spread of parental cells.
NK SENSITIVITY, H‐2 EXPRESSION AND METASTATIC POTENTIAL: ANALYSIS OF H‐2Dk GENE TRANSFECTED FIBROSARCOMA CELLS
Authors: Gopas J. , Rager‐Zisman B. , Har‐Vardi I. , Hammerling G. J. , Bar‐Eli M. , Segal S. 
Published: April 2007

SUMMARYWe have used the 3‐Methylcholanthrene induced T‐10 fibrosarcoma tumour cell system (H‐2b xH‐2k)F1 to elucidate the possible correlation between metastatic potential, expression of individual H‐2 antigens and susceptibility to NK cells.Transfection of the non‐metastatic and NK sensitive IC9 cells (Db+, Dk‐, Kb‐, Kk‐) with the H‐2Dk gene, altered the metastatic phenotype of the parental cells, yet had no effect on the susceptibility of these tumour cells to lysis by NK and did not elicit a specific CTL response in syngeneic hosts. Variants of the metastatic and NK resistant IE7 clone (Db+, Dk+, Kb‐, Kk‐), lacking H‐2Dk, were selected by treatment with monoclonal anti H‐2Dk antibodies and complement. These variants were sensitive to NK and poorly or non metastatic. Retransfection of ‘Dk′loss’ variants with the H‐2Dk gene, resulted in the isolation of several clones expressing a wide range of metastatic phenotypes but maintained sensitivity to NK. These results indicate that the H‐2D region of the MHC and or closely linked genes may be involved in the complex interrelationship between target susceptibility to NK and metastasis.