PubMed Health⌕ Search

Biomedical subjects

E Rabin

Publications and source records attributed to E Rabin.

12 recordsLinked to original sources
PubMed1992

Loss of CD23 is a consequence of B-cell activation. Implications for the analysis of B-cell lineages.

When splenic CD5- B cells are stimulated with antiimmunoglobulin they become CD5+ and have a prolonged in vitro life. Further treatment with IL-6 induces a loss of surface CD23 and IgD; that is, they resemble freshly isolated peritoneal CD5+ cells. These data suggest that the CD5 phenotype is induced after sIg-mediated B-cell activation. Additional support for this view arises from the observation that the loss of CD23 and IgD can be induced by another activation inducer, LPS, although in this case CD5 is not expressed. Thus, activation by anti-Ig plus IL-6 or by LPS induces CD23 loss. Consistent with the hypothesis that the loss of CD23 is a consequence of activation, we now report that the surface expression of CD23 varies inversely with the amount of total cellular RNA. We also find both CD23 positive and negative B cells among freshly isolated splenic CD5- B cells. In young mice a proportion of small splenic CD5+ B cells are CD23+, providing additional evidence that CD23 is present on all B cells prior to activation. A comparison of the features of CD5+ B cells and the antibody responses to thymus-dependent and thymus-independent antigens leads us to hypothesize that the CD5 phenotype arises as a consequence of thymus-independent type 2 (TI-2) stimulation. The relationship of CD5 expression to B-cell lineage (fetal vs. adult bone marrow) is discussed.

Animals↗
PubMed1992

Production of 17.2.25 mu transgenic and endogenous immunoglobulin in X-linked immune deficient mice.

In M54 mice transgenic for a completely rearranged mu(a) heavy chain there is a decrease in total B cells and the rearrangement of endogenous immunoglobulin genes is partially inhibited. Surprisingly, however, endogenous immunoglobulin gene rearrangement and significant heavy chain polypeptide production does occur. We tested the hypothesis that only CD5+ B cells produce endogenous immunoglobulin by taking advantage of the fact that X-linked immune deficient (xid) mice normally are deficient in CD5+ B cells. We found that the frequency of CD5+ splenic B cells was similar in XxidY transgenic and non-transgenic F1 males, and in XxidX transgenic and non-transgenic F1 females. In both XxidX and XxidY transgenic F1 mice some, but not all, splenic B cells are CD11b+. There was a striking deficit of splenic B cells expressing endogenous immunoglobulin in XxidY transgenic mice, although this was not true for peritoneal cells. Thus, the introduction of the 17.2.25 mu transgene does not prevent the development of CD5- B cells nor does it limit endogenous immunoglobulin gene arrangement and expression solely to CD5+ B cells. However, in mice capable of expressing B cell surface CD5 or CD11 this transgene can lead to expansion of the fraction of B cells positive for these molecules. We conclude that while the introduction of the 17.2.25 mu transgene alters the frequencies of B cell populations, maturation is not limited to one subpopulation.

Animals↗
PubMed1991

Treatment of murine CD5- B cells with anti-Ig, but not LPS, induces surface CD5: two B-cell activation pathways.

Anti-Ig stimulated murine B cells express high levels of surface CD5 (ly-1) and increased CD44 while maintaining surface IgD, CD23 and J11d. Sorting of CD5- and CD5+ cells demonstrates that anti-Ig induces CD5 expression rather than the selective expansion of CD5+ cells. Anti Ig plus interleukin-6 (IL-6) induces the CD23, IgD, low ly-5 (B220) (CD45low), J11dhigh phenotype of typical CD5+ peritoneal B cells. In contrast, lipopolysaccharide (LPS)-stimulated B cells have high levels of CD44 but decreased surface IgD, CD23 and J11d and no CD5. Thus LPS and anti-Ig generate activated cells with differing phenotypes. Induced CD5+ cells have increased viability, even in the absence of added exogenous factors, while the viability of CD5- B cells is dependent on factors such as IL-4. We conclude that conventional CD5- B cells can be activated by either of two pathways: one generating CD5+ B cells; the other yielding conventional activated cells. We hypothesize that the first path requires slg cross-linking and corresponds to T-independent (type 2) stimulation, while cognate interaction with helper T cells in the absence of slg cross-linking induces B cells to enter the second path.

Animals↗
PubMed1988

Pathology of laser-induced experimental aneurysms.

Aneurysms were produced in the common carotid artery of 35 rats by milliwatt CO2 laser welding of an adventitia patch over a hole. The aneurysmal sac was formed by collagen; the lumen was covered by an endothelial-like lining and partially thrombosed. The pathology of these aneurysms is similar to spontaneously occurring intracranial human aneurysms. This aneurysm model has properties (reliability, spontaneous bleeding tendency, minimal vessel manipulation, and pathological features) that make it theoretically advantageous for the induction of experimental intracranial aneurysms in larger animals.

Aneurysm↗
PubMed1988

Induction of experimental aneurysms on the rat common carotid artery using a microsurgical CO2 laser.

Aneurysms were produced on the common carotid artery of rats by milliwatt CO2 laser welding of an adventitia patch over a hole. Sixty-nine animals were operated on. Aneurysms were present in 35 animals (51%), 7 of which ruptured spontaneously. The time to aneurysm formation was 1 week or longer. The adventitia patch aneurysm model has features (reliability, minimal vessel manipulation, histology similar to human berry aneurysm, and spontaneous bleeding tendency) that make it theoretically suitable for the induction of intracranial aneurysms in experimental animals. The microsurgical skills required to create and dissect the aneurysm make our experimental aneurysm useful as a teaching model in the development of microneurovascular surgery skills.

Aneurysm↗
PubMed1986

Regulation of B-lymphocyte activation, proliferation, and immunoglobulin secretion.

Lymphocyte growth and differentiation are controlled by signals resulting from the interaction of antigen and cellular products, such as lymphokines, with specific cell membrane receptors. Resting B lymphocytes can be activated by low concentrations (1-5 micrograms/ml) of antibodies to membrane IgM, which is the B-lymphocyte receptor for antigen. The binding of anti-IgM to B cells causes a rapid increase in intracellular free calcium concentration ([Ca2+]i), in inositol phosphate concentration, and in protein kinase activity. Moreover, the effects of anti-IgM on B cells are mimicked by the combined use of calcium ionophores and phorbol esters. Since phorbol esters activate protein kinase c, this suggests that the increase in [Ca2+]i and in phosphatidylinositol metabolism stimulated by anti-IgM are critical events in B-cell activation. The entry into S phase of B cells stimulated with anti-IgM depends on the action of a T-cell-derived factor designated B-cell stimulatory factor (BSF)-1. This is a 20,000-Da protein which is a powerful inducer of class II major histocompatibility complex molecules. Although an important cofactor for B-cell proliferative responses to anti-IgM, its major locus of action is on resting B cells. B cells stimulated with anti-IgM and BSF-1 do not synthesize secretory IgM. However, if two additional T-cell-derived factors, B151-TRF and interleukin-2, are added to cultures, a substantial proportion of stimulated B cells produce secretory IgM. BSF-1 has also been shown to participate in the "switch" in Ig class expression. Resting B cells cultured with lipopolysaccharide will switch to IgG1 secretion in the presence of purified BSF-1.

Animals↗
PubMed1986

Technique of experimental aneurysm formation in the rat common carotid artery using the milliwatt carbon dioxide laser and the adventitia patch model.

Aneurysms were induced in the rat common carotid artery by using the milliwatt carbon dioxide laser to weld an adventitia patch over a hole. This technique proved to be effective and reliable as demonstrated by the 100% incidence of aneurysm formation at the patch site in 28 rats killed 1 week or later after the procedure. It is suggested that this technique may be used to produce intracranial aneurysms in experimental animals due to the minimal vessel manipulation required.

Aneurysm↗
PubMed1986

Umbilical artery catheterization complicated by multiple mycotic aortic aneurysms.

A premature infant had three pseudoaneurysms of the thoracic and abdominal aorta secondary to umbilical artery catheterization and sepsis. The infant had septicemia as the direct result of bacterial contamination of an umbilical artery catheter with Staphylococcus aureus. The thoracic pseudoaneurysm caused massive hemothorax and the infant's death. The upper abdominal aortic aneurysm developed at the level of the renal arteries and caused decreased left renal blood flow and renal hypoplasia. The lower abdominal aneurysm involved the right iliac artery and was complicated by mural thrombosis and ischemia of the right leg. To our knowledge, this is the first published case of multiple mycotic aortic aneurysms after umbilical artery catheterization.

Aorta, Abdominal↗