scholarly journals H-2 mutation affecting immune response to Thy-1.1 antigen

1977 ◽  
Vol 145 (6) ◽  
pp. 1602-1606 ◽  
Author(s):  
M Zaleski ◽  
J Klein
Keyword(s):  
Immune Response ◽  
Inbred Mice ◽  
Serum Antibody ◽  
Inbred Strains ◽  
Antibody Responses ◽  
Chromosome 9 ◽  
Chromosome 17 ◽  
Target Cells ◽  
Histocompatibility Complex ◽  
The Right

Mouse thymus, thymus-derived lymphocytes, and brain share an antigen determined by gene at the Thy-1 locus in chromosome 9 (1). Two alleles have been identified at this locus: Thy-1(a), coding for antigen Thy-1.1 (or θ-AKR) present in AKR and seven other strains; and Thy-1(b), coding for antigen Thy-1.2 (or{teta}-C3H) and present in C3H and all the remaining inbred strains. Injection of AKR thymocytes into inbred mice carrying the Thy-1(b) allele results in an immune response that can be measured either serologically by determining the level of antibodies in the recipients serum (1) or by counting plaque- forming cells (PFC) detectable in spleens of the recipients by means of an assay, with AKR thymocytes as target cells(2). The magnitude of PFC and serum antibody responses after a single thymocyte injection depends on the genetic make-up of the recipient. Three genes controlling the PFC response to the Thy- 1.1 antigen have been identified: Ir-Thy-1A and Ir-Thy-1B, which are closely linked to the major histocompatibility complex (H-2) of the mouse (3-6), and Ir-5, which is located at a distance of 17 cm to the right of the H-2 complex on chromosome 17 (6). Previous genetic mapping with H-2 recombinant strains has indicated that the two Ir-Thy-1 loci are located to the left of the IC subregion (7). Further experiments strongly suggested that either one or both Ir-Thy-1 loci map to the K rather than the I region of the H-2 complex (8). In this report, the study of an H- 2 mutant, CBA-H-2(ka) (M523) (9), and its parental strain, CBA/LacStoY (CBA) provided further evidence that one of these loci apparently resides in the K region and might even be identical with the H-2K locus in that region.

scholarly journals Induction of a ragweed-specific allergic state in Ir-gene-restricted nonresponder mice.

1977 ◽  
Vol 146 (1) ◽  
pp. 302-307 ◽  
Author(s):  
N Chiorazzi ◽  
A S Tung ◽  
D H Katz
Keyword(s):  
Inbred Mice ◽  
Inbred Strains ◽  
Antibody Responses ◽  
Pollen Extract ◽  
Antibody Synthesis ◽  
Ige Antibody ◽  
Gene Concept ◽  
X Irradiation ◽  
Suppressive Mechanism ◽  
Ir Genes

Mice of the inbred strains, C57BL/6 and C57BL/10 (H-2b), are genetically incapable of developing IgE antibody responses to ragweed pollen extract (RE) or its dinitrophenylated derivative, DNP-RE. This nonresponsiveness has previously been thought to reflect the absence of a relevant H-2-linked Ir genes controlling responses of inbred mice to these antigens. However, pretreatment of H-2b mice with either low doses of ionizing X irradiation or cyclophosphamide abrogates the nonresponder status of such animals, apparently by removal of a suppressive mechanism normally inhibiting development of IgE responses to these antigens. The implications of these findings for mechanisms of genetic control of IgE antibody synthesis and the Ir-gene concept are discussed.

scholarly journals A genetic basis for atrophy: dominant non-responsiveness and helicobacter induced gastritis in F1 hybrid mice

Gut ◽  
1999 ◽  
Vol 45 (3) ◽  
pp. 335-340 ◽  
Author(s):  
P Sutton ◽  
J Wilson ◽  
R Genta ◽  
D Torrey ◽  
A Savinainen ◽  
...  
Keyword(s):  
Immune Response ◽  
Serum Antibody ◽  
Antibody Responses ◽  
Host Factors ◽  
Mouse Strains ◽  
F1 Hybrid ◽  
Helicobacter Felis ◽  
Humoral Immune ◽  
Antibody Levels ◽  
Hybrid Mice

BACKGROUNDThe importance of host factors in helicobacter induced gastritis has been shown in animal models. Infection of most mouse strains withHelicobacter felis results in a functional atrophic gastritis, while other strains remain gastritis free.AIMSTo investigate these host factors further by using genetic crosses of responder and non-responder mice.METHODSF1 hybrids of the non-responder CBA/Ca strain and three strains of mice known to develop H felis induced gastritis were infected for three months with H felis. Gastritis was assessed by histopathology and serum antibody responses by ELISA.RESULTSInfection of CBA/Ca mice and F1 hybrids induced little or no gastritis. Analyses of the antibody responses in these mice revealed virtually undetectable anti-helicobacter antibody levels despite colonisation with high numbers of H felis. In contrast, infection of H felis responsive strains induced gastritis and a significant humoral immune response.CONCLUSIONSThe non-responsiveness of CBA/Ca mice to H felis infection is dominantly inherited. The lack of gastritis in CBA mice and their offspring is probably due to active suppression of the immune response normally mounted against H felis. Investigation of these mechanisms will provide important insights relevant to induction of gastric atrophy and cancer in humans.

scholarly journals Genetic analysis of albuminuria in collaborative cross and multiple mouse intercross populations

2012 ◽  
Vol 303 (7) ◽  
pp. F972-F981 ◽  
Author(s):  
Jill Thaisz ◽  
Shirng-Wern Tsaih ◽  
Minjie Feng ◽  
Vivek M. Philip ◽  
Yunyu Zhang ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Genetic Basis ◽  
Inbred Mice ◽  
National Laboratory ◽  
Human Kidney ◽  
Inbred Strains ◽  
Collaborative Cross ◽  
Chromosome 17 ◽  
Oak Ridge ◽  
Highly Correlated

Albuminuria is an important marker of nephropathy that increases the risk of progressive renal and chronic cardiovascular diseases. The genetic basis of kidney disease is well-established in humans and rodent models, but the causal genes remain to be identified. We applied several genetic strategies to map and refine genetic loci affecting albuminuria in mice and translated the findings to human kidney disease. First, we measured albuminuria in mice from 33 inbred strains, used the data for haplotype association mapping (HAM), and detected 10 genomic regions associated with albuminuria. Second, we performed eight F2 intercrosses between genetically diverse strains to identify six loci underlying albuminuria, each of which was concordant to kidney disease loci in humans. Third, we used the Oak Ridge National Laboratory incipient Collaborative Cross subpopulation to detect an additional novel quantitative trait loci (QTL) underlying albuminuria. We also performed a ninth intercross, between genetically similar strains, that substantially narrowed an albuminuria QTL on Chromosome 17 to a region containing four known genes. Finally, we measured renal gene expression in inbred mice to detect pathways highly correlated with albuminuria. Expression analysis also identified Glcci1, a gene known to affect podocyte structure and function in zebrafish, as a strong candidate gene for the albuminuria QTL on Chromosome 6. Overall, these findings greatly enhance our understanding of the genetic basis of albuminuria in mice and may guide future studies into the genetic basis of kidney disease in humans.

The Putative Oncogene Pim-1 in the Mouse: Its Linkage and Variation Among t Haplotypes

Genetics ◽  
1987 ◽  
Vol 117 (3) ◽  
pp. 533-541
Author(s):  
Joseph H Nadeau ◽  
Sandra J Phillips
Keyword(s):  
Restriction Fragment ◽  
Inbred Mice ◽  
Globin Gene ◽  
Inbred Strains ◽  
Chromosome 17 ◽  
Wild Type ◽  
Alpha Crystallin ◽  
T Complex ◽  
Variant Alleles ◽  
Apparent Association

ABSTRACT Pim-1, a putative oncogene involved in T-cell lymphomagenesis, was mapped between the pseudoalpha globin gene Hba-4ps and the alpha-crystallin gene Crya-1 on mouse chromosome 17 and therefore within the t complex. Pim-1 restriction fragment variants were identified among t haplotypes. Analysis of restriction fragment sizes obtained with 12 endonucleases demonstrated that the Pim-1 genes in some t haplotypes were indistinguishable from the sizes for the Pim-1b allele in BALB/c inbred mice. There are now three genes, Pim-1, Crya-1 and H-2 I-E, that vary among independently derived t haplotypes and that have indistinguishable alleles in t haplotypes and inbred strains. These genes are closely linked within the distal inversion of the t complex. Because it is unlikely that these variants arose independently in t haplotypes and their wild-type homologues, we propose that an exchange of chromosomal segments, probably through double crossingover, was responsible for indistinguishable Pim-1 genes shared by certain t haplotypes and their wild-type homologues. There was, however, no apparent association between variant alleles of these three genes among t haplotypes as would be expected if a single exchange introduced these alleles into t haplotypes. If these variant alleles can be shown to be identical to the wild-type allele, then lack of association suggests that multiple exchanges have occurred during the evolution of the t complex.

scholarly journals CYTODYNAMICS OF THE IMMUNE RESPONSE IN TWO LINES OF MICE GENETICALLY SELECTED FOR "HIGH" AND "LOW" ANTIBODY SYNTHESIS

1972 ◽  
Vol 135 (5) ◽  
pp. 1071-1094 ◽  
Author(s):  
G. Biozzi ◽  
C. Stiffel ◽  
D. Mouton ◽  
Y. Bouthillier ◽  
C. Decreusefond
Keyword(s):  
Immune Response ◽  
Cellular Response ◽  
Doubling Time ◽  
Selective Breeding ◽  
Plasma Cells ◽  
Serum Antibody ◽  
Optimal Dose ◽  
Target Cells ◽  
Blast Cells ◽  
Low Responder

Two lines of mice have been separated by selective breeding for the character "agglutinin production to heterologous erythrocytes." Around the 18th generation of selection the two lines could be considered as homozygous for the character investigated. This trait is under the control of a group of additive genes. The interline difference in the production of anti-SE agglutinins was verified for the range of antigen doses from subimmunogenic to maximal. After intravenous immunization with an optimal dose of SE, the duration of the exponential rise in serum antibody was 4–5 days in both lines. At this time most of the interline difference in responsiveness is already expressed. A cytodynamic study carried out in terms of plaque-forming cells (PFC) and rosette-forming cells (RFC) in the spleen during the exponential phase showed that the principal interline difference is found in the doubling time of cells engaged in the immune response. More precise cytodynamic analysis made in terms of RFC showed that the doubling time of RFC is 9 hr in high responder and 16 hr in low responder mice. The duration of the exponential rise and the number of target cells stimulated by antigen is the same in both lines. The interline difference at the end of the exponential rise (4 days postimmunization) is larger in terms of serum antibody (30–40-fold) than in terms of PFC or RFC (20- and 11-fold, respectively). A morphological study of RFC in nonimmunized mice showed that about 90% of rosettes were formed by small lymphocytes in both lines. The remainder were medium-sized lymphocytes. At the peak of the cellular response the RFC have differentiated into large lymphocytes, blast cells, and plasma cells. The contribution of plasma cells to RFC is much greater in the high than in the low line. The cytodynamic and morphologic results presented in this article are compatible with the hypothesis that the group of genes segregated in each line during the selective breeding control and regulate the rate of multiplication and differentiation of the antibody-producing cells.

scholarly journals The Resistance of BALB/cJ Mice to Yersinia pestis Maps to the Major Histocompatibility Complex of Chromosome 17

2008 ◽  
Vol 76 (9) ◽  
pp. 4092-4099 ◽  
Author(s):  
Joshua K. Turner ◽  
Milton M. McAllister ◽  
John L. Xu ◽  
Richard I. Tapping
Keyword(s):  
Major Histocompatibility Complex ◽  
Yersinia Pestis ◽  
Genetic Locus ◽  
Inbred Strains ◽  
Chromosome 17 ◽  
Surrounding Tissue ◽  
Resistance Locus ◽  
Major Histocompatibility ◽  
Histocompatibility Complex ◽  
Trait Locus

ABSTRACT Yersinia pestis, the causative agent of plague, has been well studied at the molecular and genetic levels, but little is known about the role that host genes play in combating this highly lethal pathogen. We challenged several inbred strains of mice with Y. pestis and found that BALB/cJ mice are highly resistant compared to susceptible strains such as C57BL/6J. This resistance was observed only in BALB/cJ mice and not in other BALB/c substrains. Compared to C57BL/6J mice, the BALB/cJ strain exhibited reduced bacterial burden in the spleen and liver early after infection as well as lower levels of serum interleukin-6. These differences were evident 24 h postinfection and became more pronounced with time. Although a significant influx of neutrophils in the spleen and liver was exhibited in both strains, occlusive fibrinous thrombi resulting in necrosis of the surrounding tissue was observed only in C57BL/6J mice. In an effort to identify the gene(s) responsible for resistance, we measured total splenic bacteria in 95 F2 mice 48 h postinfection and performed quantitative trait locus mapping using 58 microsatellite markers spaced throughout the genome. This analysis revealed a single nonrecessive plague resistance locus, designated prl1 (plague resistance locus 1), which coincides with the major histocompatibility complex of chromosome 17. A second screen of 95 backcrossed mice verified that this locus confers resistance to Y. pestis early in infection. Finally, eighth generation backcrossed mice harboring prl1 were found to maintain resistance in the susceptible C57BL/6J background. These results identify a novel genetic locus in BALB/cJ mice that confers resistance to Y. pestis.

scholarly journals Redirecting the Humoral Immune Response against Streptococcus mutans Antigen P1 with Monoclonal Antibodies

2004 ◽  
Vol 72 (12) ◽  
pp. 6951-6960 ◽  
Author(s):  
Monika W. Oli ◽  
Nikki Rhodin ◽  
William P. McArthur ◽  
L. Jeannine Brady
Keyword(s):  
Immune Response ◽  
Streptococcus Mutans ◽  
Serum Antibody ◽  
Antibody Responses ◽  
Vaccine Antigen ◽  
Immunomodulatory Activity ◽  
Mucosal Immunization ◽  
Biologically Relevant ◽  
Humoral Immune ◽  
Inhibition Response

ABSTRACT The adhesin P1 of Streptococcus mutans has been studied as an anticaries vaccine antigen. An anti-P1 monoclonal antibody (MAb) bound to S. mutans prior to mucosal immunization of mice was shown previously to alter the amount, specificity, isotype, and biological activity of anti-P1 antibodies. The present study was undertaken to screen this and four additional anti-P1 MAbs for immunomodulatory activity when complexed with S. mutans and administered by a systemic route and to evaluate sera from immunized mice for the ability to inhibit adherence of S. mutans to immobilized human salivary agglutinin. All five MAbs tested influenced murine anti-P1 serum antibody responses in terms of subclass distribution and/or specificity. The effects varied depending on which MAb was used and its coating concentration. Two MAbs promoted a more effective, and two others a less effective, adherence inhibition response. An inverse relationship was observed between the ability of the MAbs themselves to inhibit adherence and the ability of antibodies elicited following immunization with immune complexes to inhibit adherence. Statistically significant correlations were demonstrated between the levels of anti-P1 serum immunoglobulin G2a (IgG2a) and IgG2b, but not of IgG1 or IgG3, and the ability of sera from immunized animals to inhibit bacterial adherence. These results indicate that multiple anti-P1 MAbs can mediate changes in the immune response and that certain alterations are potentially more biologically relevant than others. Immunomodulation by anti-P1 MAbs represents a useful strategy to improve the beneficial immune response against S. mutans.

scholarly journals Antibody Responses to SARS-CoV-2 mRNA Vaccines Are Detectable in Saliva

2021 ◽  
Vol 6 (1) ◽  
pp. 116-134
Author(s):  
Thomas J. Ketas ◽  
Devidas Chaturbhuj ◽  
Victor M. Cruz Portillo ◽  
Erik Francomano ◽  
Encouse Golden ◽  
...  
Keyword(s):  
Immune Responses ◽  
Serum Antibody ◽  
Cross Sectional Study ◽  
Antibody Responses ◽  
Target Cells ◽  
Receptor Binding Domain ◽  
Sectional Study ◽  
Cross Sectional ◽  
S Protein ◽  
Iga Antibodies

The approved Pfizer and Moderna mRNA vaccines are well known to induce serum antibody responses to the SARS-CoV-2 Spike (S)-protein. However, their abilities to elicit mucosal immune responses have not been reported. Saliva antibodies represent mucosal responses that may be relevant to how mRNA vaccines prevent oral and nasal SARS-CoV-2 transmission. Here, we describe the outcome of a cross-sectional study on a healthcare worker cohort (WELCOME-NYPH), in which we assessed whether IgM, IgG, and IgA antibodies to the S-protein and its receptor-binding domain (RBD) were present in serum and saliva samples. Anti-S-protein IgG was detected in 14/31 and 66/66 of saliva samples from uninfected participants after vaccine doses-1 and -2, respectively. IgA antibodies to the S-protein were present in 40/66 saliva samples after dose 2. Anti-S-protein IgG was present in every serum sample from recipients of 2 vaccine doses. Vaccine-induced antibodies against the RBD were also frequently present in saliva and sera. These findings may help our understanding of whether and how vaccines may impede SARS-CoV-2 transmission, including to oral cavity target cells.

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