Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0153470 (Spleen)
 4,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

CBA/N female mice, which express an X-linked defect in B-lymphocyte function, were mated with C3H/HeJ male mice, which are unresponsive to lipopolysaccharide (LPS). The resulting F1 hybrid females were mated to C3H/HeJ males. Approximately one-half of the backcross (BC.1) males obtained from this mating expressed a more profound immunologic defect than either of the parental strains. Spleen cells from these mice were unresponsive to a series of B-cell mitogens including LPS prepared from Escherichia coli K235 and from E. coli 0111:B4, lipoprotein mitogen from E. coli, and Nocardia water-soluble mitogen (NWSM). They failed to give in vitro antibody responses to the thymus-independent type 2 (TI-2) antigen trinophenylated Ficoll and most were unresponsive to the TI-1 antigens trinitrophenylated Brucella abortus, trinitrophenylated LPS, and trinitrophenylated NWSM. This synergistic defect in B-lymphocyte function depended on the presence of the CBA/N xid gene but the critical gene(s) from the C3H strain was not the defective Lps gene (Lpsd). These mice should provide a valuable tool for the elucidation of B-lymphocyte ontogeny, heterogeneity, and function.
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PMID:Synergistic genetic defect in B-lymphocyte function. I. Defective responses to B-cell stimulants and their genetic basis. 696 7

CBA/N mice have an X-linked B cell defect which prevents them from responding to nonmitogenic thymic independent (TI-2) antigens such as dinitrophenylated DNP-Ficoll (1,2). The F1 male progeny of CBA/N female mice express the same defect. Spleen cell suspensions from such defective mice (CBA/N X C3H/HeN F1 males) could not respond to DNP-Ficoll following in vitro immunization and subsequent transfer into irradiated, syngeneic, F1 male recipients as expected. In contrast, normal CBA/N X C3H/HeN F1 female spleen cells could respond and effect a "rescue"; they mounted strong plaque-forming cell responses 7 days after in vitro exposure to DNP-Ficoll and subsequent transfer into irradiated F1 male recipients. Defective F1 male spleen cells, however, could bind significant quantities of 125I-DNP-Ficoll after in vitro exposure. Extensive washing of these spleen cells could not reverse this binding. Such DNP-Ficoll-exposed and washed F1 male spleen cells could, after transfer, aid normal untreated F1 female cells in their rescue function. The defective F1 male spleen cells could convey immunogenic quantities of DNP-Ficoll to the "rescuing" F1 female cells. Mitomycin treatment of F1 male cells did not interfere with their conveyor function. Goat anti-mouse mu serum impeded the passive antigen conveyor function of defective F1 male cells as did prior exposure to high concentrations of free DNP hapten. Our data support the view that the B cell defect of CBA/N X C3H/HeN F1 male mice does not relate to antigen binding, but rather to an inability to be effectively triggered by certain cell-bound polymeric antigens.
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PMID:Functional antigen binding by the defective B cells of CBA/N mice. 698 43

A synthetic serum thymic factor (FTS) augmented the lipopolysaccharide (LPS)-induced polyclonal B-cell responses in vitro of CBA/N mice and their F1 hybrids having an X-linked B-cell defect. For this augmentation, FTS should be injected in vivo. Splenic B cells derived from FTS-treated mice with the CBA/N defect were receptive to T-cell help from normal or immunodeficient mouse T cells. Thus, the inability of B cells from mice with the CBA/N defect to accept T -cell help may not be caused by an intrinsic T-cell defect, but by a functional B-cell defect that can be corrected by treatment with FTS in vivo. Spleen cells from ATXBM CBA/N mice treated with FTS 3 weeks after cell transfer did not increase the B-cell response. B cells from FTS-treated male F1 mice with the CBA/N defect still have characteristics of neonatal mouse B cells as revealed by inhibition with antimouse Ig and anti-Ia sera. These findings suggest that FTS may act on generation of a B-cell acceptor for T -cell help, rather than on the maturation of a B-cell subset.
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PMID:Activation of polyclonal antibody responses by a synthetic serum thymic factor (FTS) in CBA/N mice. 703 18

Phex is the gene whose mutation is the cause of X-linked hypophosphatemia in humans and mice. The organs expressing Phex in normal animals, and their possible sensitivity to stimulation by low phosphate diets, are unknown. In this study, Phex expression was measured in 6-wk-old normal B6C3H male and female mice and in 135 g Sprague-Dawley rats fed a normal phosphate diet or a low phosphate diet with deionized water ad libitum for 7 d. The animals were then anesthetized, and a variety of organs were collected and frozen in liquid nitrogen. Phex mRNA expression was measured in each organ by reverse transcription-polymerase chain reaction (RT-PCR) with primers specific for both Phex and glyceraldehyde-3-phosphate dehydrogenase (G3PDH). Southern blots were prepared, hybridized with 32P-labeled internal oligonucleotides, and quantified with a phosphor imager. The Phex/G3PDH ratio was computed, and the data were compiled as the mean +/- SEM. In these growing animals, the highest Phexexpression levels were found in the gonads, brain, and lung. In contrast, Phex expression in calvaria and femur was markedly less. Two significant changes were found in animals that were fed a low phosphate diet. Spleen showed a significant decrease in Phex mRNA levels on low phosphate diet (60+/-10% of normal P diet, n = 12/group, p = 0.002). The pituitary gland showed a significant increase in Phex expression with low phosphate diet (851+/-127% of G3PDH) over normal P diet (569+/-78%, n = 24 - 25/group, p = 0.03). No significant change was found in femur, calvaria, or a variety of soft tissues. In summary, Phex mRNA was found in most tissues examined. Expression levels varied by two orders of magnitude from highest to lowest with more in gonads, brain, and lung and with less in bone. Increased Phex mRNA was found in the pituitary gland of animals that were fed a low phosphate diet.
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PMID:MRNA expression of Phex in mice and rats: the effect of low phosphate diet. 1105 Oct 50


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