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Biomedical subjects

B Salomon

Publications and source records attributed to B Salomon.

At least 19 recordsLinked to original sources
PubMed2005

Structural and distributional variation of mitochondrial rps2 genes in the tribe Triticeae (Poaceae).

The mitochondrial rps2 gene from barley, like that of rice, wheat, and maize, has an extended open reading frame (ORF) at the 3'-region when compared to that from lower plants. However, the extended portions are variable among these cereals. Since barley and wheat belong to the same tribe (Triticeae), it would be interesting to know when and where the two types of rps2 were generated during evolution. To determine this, we utilized the mitochondrial (mt) DNA sequence to examine variations of the rps2 genes in the tribe Triticeae. By means of the variable 3'-region, the distribution of barley (B)-type and wheat (W)-type rps2 sequences was studied in 19 genera of the tribe. The B-type sequence was identified in 10 of the 19 genera, whereas the W-type sequence was present in all 19 genera. Thus, ten of the examined genera have both types of rps2 sequences due to the presence of two copies of the gene. The W-type sequence was also present in the tribe Bromeae and the B-type sequence was also found in Aveneae and Poeae. Phylogenetic trees based on the B-type and W-type sequences were different from those based on other molecular data. This suggests that the mitochondrial genome in Triticeae has a unique evolutionary history.

Amino Acid Sequence↗
PubMed2001

Division rate and phenotypic differences discriminate alloreactive and nonalloreactive T cells transferred in lethally irradiated mice.

After non-T-cell-depleted allogeneic hematopoietic stem cell transplantation (HSCT), both alloreactive and homeostatic signals drive proliferation of donor T cells. Host-reactive donor T cells, which proliferate on alloantigen stimulation, are responsible for the life-threatening graft-versus-host disease. Non-host-reactive donor T cells, which proliferate in response to homeostatic signals, contribute to the beneficial peripheral T-cell reconstitution. The elimination of alloreactive T cells is a major therapeutic challenge for HSCT and would greatly benefit from their specific identification. After T-cell transfer in lymphopenic recipients, the present results show that alloreactive T cells rapidly divided; up-regulated CD69, CD25, and CD4 molecules; and down-regulated CD62L. In contrast, nonalloreactive T cells started to divide later and did not up-regulate CD69, CD25, and CD4. Thus, these 2 cell populations can be effectively discriminated. This should facilitate the specific depletion of alloreactive T cells in allogeneic HSCT.

Animals↗
PubMed2001

Development of spontaneous autoimmune peripheral polyneuropathy in B7-2-deficient NOD mice.

An increasing number of studies have documented the central role of T cell costimulation in autoimmunity. Here we show that the autoimmune diabetes-prone nonobese diabetic (NOD) mouse strain, deficient in B7-2 costimulation, is protected from diabetes but develops a spontaneous autoimmune peripheral polyneuropathy. All the female and one third of the male mice exhibited limb paralysis with histologic and electrophysiologic evidence of severe demyelination in the peripheral nerves beginning at 20 wk of age. No central nervous system lesions were apparent. The peripheral nerve tissue was infiltrated with dendritic cells, CD4(+), and CD8(+) T cells. Finally, CD4(+) T cells isolated from affected animals induced the disease in NOD.SCID mice. Thus, the B7-2-deficient NOD mouse constitutes the first model of a spontaneous autoimmune disease of the peripheral nervous system, which has many similarities to the human disease, chronic inflammatory demyelinating polyneuropathy (CIDP). This model demonstrates that NOD mice have "cryptic" autoimmune defects that can polarize toward the nervous tissue after the selective disruption of CD28/B7-2 costimulatory pathway.

Aging↗
PubMed2001

Reversal of spontaneous autoimmune insulitis in nonobese diabetic mice by soluble lymphotoxin receptor.

One striking feature of spontaneous autoimmune diabetes is the prototypic formation of lymphoid follicular structures within the pancreas. Lymphotoxin (LT) has been shown to play an important role in the formation of lymphoid follicles in the spleen. To explore the potential role of LT-mediated microenvironment in the pathogenesis of insulin-dependent diabetes mellitus (IDDM), an LTbeta receptor-immunoglobulin fusion protein (LTbetaR-Ig) was administered to nonobese diabetic mice. Early treatment with LTbetaR-Ig prevented insulitis and IDDM, suggesting that LT plays a critical role in the insulitis development. LTbetaR-Ig treatment at a late stage of the disease also dramatically reversed insulitis and prevented diabetes. Moreover, LTbetaR-Ig treatment prevented the development of IDDM by diabetogenic T cells in an adoptive transfer model. Thus, LTbetaR-Ig can disassemble the well established lymphoid microenvironment in the islets, which is required for the development and progression of IDDM.

Animals↗
PubMed2001

The diagnosis.

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Adult↗
PubMed2001

Performance.

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Adult↗
PubMed2001

Trigenomic origin of the hexaploid Psammopyrum athericum (Triticeae: Poaceae) revealed by in-situ hybridization.

The genomic constitution of the hexaploid Psammopyrum athericum was studied with in-situ DNA hybridization using both genomic DNA and isolated cloned sequences as probes. A genomic probe from Thinopyrum bessarabicum (E genome) hybridized successfully to 14 chromosomes of Ps. athericum and a probe from Festucopsis serpentinii (L genome) hybridized to another 14 chromosomes. The remaining chromosomes did not hybridize, apart from in the centromeric region, to any of the genomic probes used. It is thus proposed that Ps. athericum contains the genomes E, L and X where X stands for a so-far unknown genome. Psammopyrum athericum has three pairs of pTa71 sites and approximately 30 pSc119:2 sites. The origin of the third genome will be a matter for further research using genomic and genome-specific probes.

Biological Evolution↗
PubMed2001

Suppressor T cells--they're back and critical for regulation of autoimmunity!

Regulation of the immune response to self-antigens is a complex process that depends on maintaining self-tolerance while retaining the capacity to mount a robust immune response to foreign antigens. Autoreactive T cells specific for these autoantigens are present in most normal individuals but are kept under control by multiple diverse peripheral tolerance mechanisms. In the last few years, there has been a re-emergence of suppressor cells as among the most central of these regulatory mechanisms. These cells, which express CD4, CD25, and CD62L, develop in the thymus and survive in a CD28-dependent manner in the periphery to maintain the homeostatic equilibrium of immunity and tolerance. In this review, we will summarize studies of these regulatory cells as they relate to autoimmune diseases and more specifically to type 1 diabetes and attempt to address some of the many outstanding questions. Finally, evidence is provided to support the ability of anti-CD3 mAbs to stimulate the regulatory T cells and reset the rheostat of immune tolerance in an animal model of autoimmune diabetes, the NOD mouse.

Animals↗
PubMed2001

Admission.

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Emergencies↗
PubMed2001

Complexities of CD28/B7: CTLA-4 costimulatory pathways in autoimmunity and transplantation.

Recent advances in the understanding of T cell activation have led to new therapeutic approaches in the treatment of immunological disorders. One attractive target of intervention has been the blockade of T cell costimulatory pathways, which result in more selective effects on only those T cells that have encountered specific antigen. In fact, in some instances, costimulatory pathway antagonists can induce antigen-specific tolerance that prevents the progression of autoimmune diseases and organ graft rejection. In this review, we summarize the current understanding of these complex costimulatory pathways including the individual roles of the CD28, CTLA-4, B7-1 (CD80), and B7-2 (CD86) molecules. We present evidence that suggests that multiple mechanisms contribute to CD28/B7-mediated T cell costimulation in disease settings that include expansion of activated pathogenic T cells, differentiation of Th1/Th2 cells, and the migration of T cells into target tissues. Additionally, the negative regulatory role of CTLA-4 in autoimmune diseases and graft rejection supports a dynamic but complex process of immune regulation that is prominent in the control of self-reactivity. This is most apparent in regulation of the CD4(+)CD25(+)CTLA-4(+) immunoregulatory T cells that control multiple autoimmune diseases. The implications of these complexities and the potential for use of these therapies in clinical immune intervention are discussed.

Abatacept↗
PubMed2000

A critical role for B7/CD28 costimulation in experimental autoimmune encephalomyelitis: a comparative study using costimulatory molecule-deficient mice and monoclonal antibody blockade.

The B7/CD28 pathway provides critical costimulatory signals required for complete T cell activation and has served as a potential target for immunotherapeutic strategies designed to regulate autoimmune diseases. This study was designed to examine the roles of CD28 and its individual ligands, B7-1 and B7-2, in experimental autoimmune encephalomyelitis (EAE), a Th1-mediated inflammatory disease of the CNS. EAE induction in CD28- or B7-deficient nonobese diabetic (NOD) mice was compared with the effects of B7/CD28 blockade using Abs in wild-type NOD mice. Disease severity was significantly reduced in CD28-deficient as well as anti-B7-1/B7-2-treated NOD mice. B7-2 appeared to play the more dominant role as there was a moderate decrease in disease incidence and severity in B7-2-deficient animals. EAE resistance was not due to the lack of effective priming of the myelin peptide-specific T cells in vivo. T cells isolated from CD28-deficient animals produced equivalent amounts of IFN-gamma and TNF-alpha in response to the immunogen, proteolipid protein 56-70. In fact, IFN-gamma and TNF-alpha production by Ag-specific T cells was enhanced in both the B7-1 and B7-2-deficient NOD mice. In contrast, peptide-specific delayed-type hypersensitivity responses in these animals were significantly decreased, suggesting a critical role for CD28 costimulation in in vivo trafficking and systemic immunity. Collectively, these results support a critical role for CD28 costimulation in EAE induction.

Amino Acid Sequence↗
PubMed2000

B7/CD28 costimulation is essential for the homeostasis of the CD4+CD25+ immunoregulatory T cells that control autoimmune diabetes.

CD28/B7 costimulation has been implicated in the induction and progression of autoimmune diseases. Experimentally induced models of autoimmunity have been shown to be prevented or reduced in intensity in mice rendered deficient for CD28 costimulation. In sharp contrast, spontaneous diabetes is exacerbated in both B7-1/B7-2-deficient and CD28-deficient NOD mice. These mice present a profound decrease of the immunoregulatory CD4+CD25+ T cells, which control diabetes in prediabetic NOD mice. These cells are absent from both CD28KO and B7-1/B7-2KO mice, and the transfer of this regulatory T cell subset from control NOD animals into CD28-deficient animals can delay/prevent diabetes. The results suggest that the CD28/ B7 costimulatory pathway is essential for the development and homeostasis of regulatory T cells that control spontaneous autoimmune diseases.

Abatacept↗
PubMed2000

In memoriam.

So here's the case: a 41-year-old respiratory therapist comes in with a history of a bad headache, now much better. She looks like a rose in the emergency department. Goes for a head computed tomographic (CT) scan, which shows a subarachnoid hemorrhage. Returns to the department and promptly crashes, needs intubation, and starts posturing. She dies about 1 week later.

Adult↗
PubMed2000

Patterns and levels of genetic differentiation in North American populations of the Alaskan wheatgrass complex.

Levels and distribution of genetic variation were assessed using six allozymes in 27 populations of Alaskan wheatgrass (Elymus alaskanus) from different locations in Canada, USA, Greenland and Russia to obtain information on the genetic structure of these populations. The enzyme systems were ACO, DIA, GPI, MDH, PGM and SKD. Allozyme variation at the species level was high, with 64.3% (Ps) of the loci being polymorphic, an average number of alleles per locus of 1.9 (As), and an average genetic diversity of 0.17 (Hes). Differentiation was found in the populations studied, with the following findings: (1) statistically significant differences were found in allele frequencies among populations for every polymorphic locus (P < 0.001); (2) 63% of the total allozyme variation at polymorphic loci was partitioned among populations (GST = 0.63); (3) relatively low mean genetic distances between the populations were obtained (mean D = 0.029); (4) the genetic structure of Russian populations are clearly distinct from the other populations, the cluster and principal component analyses revealed the same genetic patterns of relationships among populations. This study also indicates that E. alaskanus contains different levels of allozyme variation in its populations. Furthermore, some banding patterns at the loci Aco-1, Aco-2, Gpi-2, Mdh-1, Skd-1, Skd-2 can be used as markers to identify individual populations.

Canada↗