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)

In order to analyze relation of immunological abnormalities to the development of lupus glomerulonephritis (LGN) at an early stage, various immunological parameters were examined in BXSB and MRL/lpr mice at 8 and 13 weeks of age. The following results were obtained. (a) Male BXSB mice showed slight LGN already at 8 weeks of age and the disease became obvious at 13 weeks of age. On the other hand, glomerular change of MRL/lpr mice became apparent at 13 weeks. (b) Immunofluorescent studies to semiquantify degree of the deposition of immune complexes (IC) at glomeruli revealed that there were no difference in fluorescence intensities among BXSB mice at 8 and 13 weeks and 13-week-old MRL/lpr mice. (c) MRL/lpr mice had much higher level of serum IC than male BXSB mice at 13 weeks as assessed by fluid- and solid-phase C1q-binding assays. Both strains showed almost the same level of Raji cell-binding IC which might be related to glomerular depositing ones. (d) Spleen of 13-week-old MRL/lpr mice contained extraordinary number of IgG-producing cells in spleen as compared with 8-week-old mice or male BXSB mice at 8 or 13 weeks. There were no differences in IgM-producing cell numbers among the strains and ages of mice. These results indicate that MRL/lpr and male BXSB mice have different immunological backgrounds for the development of LGN. It was noticeable that male BXSB mice showed some degree of LGN already at 8 weeks of age, without apparent polyclonal B cell activation and enhanced serum level of IC, as compared with MRL/lpr mice of the same age.
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PMID:Studies on the mechanisms of the development of lupus nephritis in BXSB mice. II. Comparative studies between male BXSB and MRL/lpr mice at the onset period. 325 31

Factor I (FI) is a regulatory serine protease of the complement system which cleaves three peptide bonds in the alpha-chain of C3b and two bonds in the alpha-chain of C4b thereby inactivating these proteins. The human protein and the recently characterized mouse factor I are heterodimers of about 88,000 MW which consist of a non-catalytic heavy chain of 50,000 MW which is linked to a catalytic light chain of 38,000 MW by a disulphide bond. For the screening of a rat liver cDNA library we used a hybridization probe produced by polymerase chain reaction (PCR) using degenerated primers which corresponded to conserved parts of the human and the murine factor I nucleotide sequences. One of the identified sequences, which had a length of 2243 base pairs (bp), contained the complete coding region and the whole 3' untranslated region. The length of the coding region in rat consisted of 1812 bp followed by a 3' untranslated region of 207 bp including the polyadenylation signal and the beginning of the poly A tail. Comparison of the rat cDNA-derived coding sequence revealed identities of 87% to the mouse and of 78% to the human FI nucleotide sequence. The translation product of rat FI mRNA was 604 amino acid residues (aa) in length with an identity of 85% to the mouse (603 aa) and 69% to the human protein (583 aa). The comparison of the molecular mass predicted by the primary structure and derived from rat FI isolated from rat serum as detected in immunoblot analyses suggested a glycosylation of more than 20% of the total mass of the FI protein. Expression studies using reverse transcription (RT)-PCR assays indicated that FI-specific mRNA could neither be identified in B cells, nor in T cells, monocytes or granulocytes from rat and human peripheral blood nor in rat peritoneal macrophages. These data were in agreement with the results of RT-PCR obtained with several human lymphoma cell lines (Jurkat, MOLT-4, HUT102, Wil 2-NS, Ramos, Raji, U937) all of which were devoid of FI-specific mRNA. In accord with our data from two rat hepatoma cell lines (FAO and H4IIE) and one from man (HepG2) only isolated rat hepatocytes (HC) but neither Kupffer cells (KC), hepatic stellate cells (HSC; Ito cells) nor sinusoidal endothelial cells (SEC) expressed FI-specific mRNA. FI mRNA was also detected in human umbilical vein endothelial cells (HUVEC) and in the uterus and small intestine of the rat. Spleen and lymph nodes did not contain any detectable FI-specific mRNA.
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PMID:Rat complement factor I: molecular cloning, sequencing and expression in tissues and isolated cells. 1058 9