scholarly journals Genetic control of susceptibility to infection with Plasmodium chabaudi chabaudi AS in inbred mouse strains

2011 ◽  
Vol 13 (2) ◽  
pp. 155-163 ◽  
Author(s):  
A Laroque ◽  
G Min-Oo ◽  
M Tam ◽  
I Radovanovic ◽  
M M Stevenson ◽  
...  
Keyword(s):  
Genetic Control ◽  
Inbred Mouse ◽  
Mouse Strains ◽  
Inbred Mouse Strains ◽  
Plasmodium Chabaudi ◽  
Susceptibility To Infection

scholarly journals Variation and Genetic Control of Gene Expression in Primary Immunocytes across Inbred Mouse Strains

2014 ◽  
Vol 193 (9) ◽  
pp. 4485-4496 ◽  
Author(s):  
Sara Mostafavi ◽  
Adriana Ortiz-Lopez ◽  
Molly A. Bogue ◽  
Kimie Hattori ◽  
Cristina Pop ◽  
...  
Keyword(s):  
Gene Expression ◽  
Genetic Control ◽  
Inbred Mouse ◽  
Mouse Strains ◽  
Inbred Mouse Strains ◽  
Control Of Gene Expression

A comparative study of susceptibility of inbred and outbred mouse strains compared with hamsters to infection with New World cutaneous leishmaniases

Parasitology ◽  
1983 ◽  
Vol 87 (1) ◽  
pp. 7-13 ◽  
Author(s):  
R. A. Neal ◽  
C. Hale
Keyword(s):  
Comparative Study ◽  
New World ◽  
Inbred Mouse ◽  
Mouse Strains ◽  
Inbred Mouse Strains ◽  
Leishmania Mexicana ◽  
Susceptibility To Infection ◽  
Outbred Mouse ◽  
Intermediate Response ◽  
Cd1 Mice

SUMMARYOne stock of each of Leishmania mexicana mexicana and L. m. amazonesis together with two stocks of L. braziliensis panamensis and L. b. braziliensis were tested for infectivity in inbred mouse strains Balb/c and CBA/H. The infectivity was compared with hamsters and the outbred CD1 mice. Balb/c mice were more susceptible than hamsters to L. mexicaba and L. braziliensis panamensis. Balb/c mice were not susceptible to L. b. braziliensis. CBA/H mice showed a low susceptibility to infection while CD1 mice showed an intermediate response

Genetic control of platelet activation in inbred mouse strains

Platelets ◽  
1997 ◽  
Vol 8 (4) ◽  
pp. 235-242 ◽  
Author(s):  
Kenneth A. Ault ◽  
Cathy Knowles ◽  
Jane Mitchell ◽  
Christine L. Brown ◽  
Kathy L. Schultz ◽  
...  
Keyword(s):  
Genetic Control ◽  
Platelet Activation ◽  
Inbred Mouse ◽  
Mouse Strains ◽  
Inbred Mouse Strains

scholarly journals Expression of Murine APOBEC3 Alleles in Different Mouse Strains and Their Effect on Mouse Mammary Tumor Virus Infection

2009 ◽  
Vol 83 (7) ◽  
pp. 3029-3038 ◽  
Author(s):  
Chioma M. Okeoma ◽  
Josiah Petersen ◽  
Susan R. Ross
Keyword(s):  
Mammary Tumor ◽  
Mouse Mammary Tumor Virus ◽  
Inbred Mouse ◽  
Mouse Strains ◽  
Inbred Mouse Strains ◽  
Mammary Tumor Virus ◽  
Susceptibility To Infection ◽  
Mouse Mammary Tumor ◽  
Tumor Virus

ABSTRACT Recent work has shown that mouse APOBEC3 restricts infection by mouse mammary tumor virus (MMTV) and murine leukemia virus (MLV) and that there are polymorphic APOBEC3 alleles found in different inbred mouse strains. For example, C57BL/6 mice, which are resistant to Friend MLV (F-MLV), encode a APOBEC3 gene different from that encoded by F-MLV-susceptible BALB/c mice; the predominant RNA produced in C57BL/6 mice lacks exon 5 (mA3−5) and encodes a protein with 15 polymorphic amino acids. It has also been reported that BALB/c mice produce only a variant RNA that lacks exon 2 (mA3−2). In this study, we examined the effect of these polymorphic APOBEC3 proteins on MMTV infection. We found that the major RNA made in C57BL/6 and B10.BR mice lacks exon 5 but that BALB/c and C3H/HeN mice predominantly express an RNA that contains all nine exons. In addition to producing the splice variant, C57BL/6 and B10.BR cells and tissues had levels of mA3 RNA fivefold higher than those from BALB/c and C3H/HeN mice. A cloned C57BL/6-derived mA3 protein lacking exon 5 inhibited MMTV infection better than a cloned full-length protein derived from 129/Ola RNA when packaged into MMTV virions. We also tested dendritic cells derived from different inbred mouse strains for their abilities to be infected by MMTV and showed that susceptibility to infection correlated with the presence of the exon 5-encoding allele. In vivo susceptibility to infection cosegregated with the inherited mA3 allele in a C57BL/6 × BALB/c backcross analysis. Moreover, virus produced in vivo in the mammary tissue of mA3 knockout and BALB/c mice was more infectious than that produced in the tissue of C57BL/6 mice. These data indicate that mA3 plays a role in the genetics of susceptibility and resistance to MMTV infection.

scholarly journals THE NATURE OF THE ANTIGENIC DETERMINANT IN A GENETIC CONTROL OF THE ANTIBODY RESPONSE

1969 ◽  
Vol 130 (3) ◽  
pp. 493-504 ◽  
Author(s):  
Edna Mozes ◽  
Hugh O. McDevitt ◽  
Jean-Claude Jaton ◽  
Michael Sela
Keyword(s):  
Amino Acids ◽  
Immune Responses ◽  
Genetic Control ◽  
Antigenic Determinant ◽  
Inbred Mouse ◽  
Side Chain ◽  
Mouse Strains ◽  
Inbred Mouse Strains ◽  
Antibody Assay ◽  
Similar Series

The response of inbred mouse strains to two polypeptides derived from multichain polyprolines, (T,G)-Pro--L and (Phe,G)-Pro--L, is different from the response of the same mouse strains to a similar series of polymers built on multi-poly-D,L-alanyl--poly-L-lysine, although the same short sequences of amino acids are attached to the side chains of the polypeptides in the two series. These results indicate that a portion of the side chain (e.g. polyalanine or polyproline) participates in the antigenic determinant. This was confirmed by studying the response of different mouse strains to two kinds of polypeptides: (T,G)-Pro-A--L 717 and 718 and (T,G)-A-Pro--L 719 and 721. Antibody assay of antisera to (Phe,G)-Pro--L with the cross-reacting antigens (T,G)-Pro--L and (Phe,G)-A-L indicates that different inbred mouse strains make antibodies specific for different parts of the same polypeptide. Thus, antibody from DBA/1 mice reacts almost exclusively with the (Phe,G) sequence, while SJL antisera bind only (T,G)-Pro--L and fail to bind (Phe,G)-A-L. The immune responses to the same amino acids on two different polypeptides (i.e. A--L and Pro--L) appear to be under separate genetic control.

scholarly journals Differences in the response of inbred mouse strains to the factor increasing monocytopoiesis.

1984 ◽  
Vol 159 (2) ◽  
pp. 524-536 ◽  
Author(s):  
W Sluiter ◽  
I Elzenga-Claasen ◽  
A van der Voort van der Kley-van Andel ◽  
R van Furth
Keyword(s):  
Bone Marrow ◽  
Listeria Monocytogenes ◽  
Inflammatory Response ◽  
Genetic Control ◽  
Inflammatory Reaction ◽  
Inbred Mouse ◽  
Mouse Strains ◽  
Inbred Mouse Strains ◽  
Soluble Extract ◽  
Cba Mice

Previous studies have shown that monocyte production during an inflammatory response is controlled by the factor increasing monocytopoiesis (FIM), secreted by macrophages at the site of inflammation. The inflammatory reaction to latex particles and a saline-soluble extract of Listeria monocytogenes (SEL), expressed as the number of monocytes in the circulation and of macrophages at the site of inflammation, was about twice as strong in C57BL/10 mice compared with CBA mice. This raised the question as to the mechanism underlying these differences. One possibility might be that these mouse strains differ with respect to the production of FIM, but this cannot be the case because the maximum levels of FIM activity in the serum of both C57BL/10 and CBA mice given latex or SEL intraperitoneally were almost the same; however, the courses of FIM activity in the two strains after intraperitoneal latex were not exactly synchronous. Another possibility is that the sensitivity of monocyte precursor cells for FIM differs. Evidence for the latter was provided by the finding that the intravenous injection of sera with FIM activity obtained from C57BL/10 and from CBA mice into the C57BL/10 mice evoked monocytosis, whereas CBA mice did not respond to these sera. Earlier studies showed that an increase of monocytes after the injection of serum containing FIM reflects increased monocyte production. Taken together, the results of the present study demonstrate that one of the mechanisms underlying the genetic control of the inflammatory response is, rather than enhanced FIM synthesis, the ability of monocyte precursors in the bone marrow to respond to FIM by increased monocyte production.

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