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Biomedical subjects

M Chopin

Publications and source records attributed to M Chopin.

10 recordsLinked to original sources
PubMed2001

Spontaneous retinopathy in HLA-A29 transgenic mice.

Humans who have inherited the class I major histocompatibility allele HLA-A29 have a markedly increased relative risk of developing the eye disease termed birdshot chorioretinopathy. This disease affecting adults is characterized by symmetrically scattered, small, cream-colored spots in the fundus associated with retinal vasculopathy and inflammatory signs causing damage to the ocular structures, leading regularly to visual loss. To investigate the role of HLA-A29 in this disease, we introduced the HLA-A29 gene into mice. Aging HLA-A29 transgenic mice spontaneously developed retinopathy, showing a striking resemblance to the HLA-A29-associated chorioretinopathy. These results strongly suggest that HLA-A29 is involved in the pathogenesis of this disease. Elucidation of the role of HLA-A29 should be assisted by this transgenic model.

Animals↗
PubMed2001

Analysis of six prophages in Lactococcus lactis IL1403: different genetic structure of temperate and virulent phage populations.

We report the genetic organisation of six prophages present in the genome of Lactococcus lactis IL1403. The three larger prophages (36-42 kb), belong to the already described P335 group of temperate phages, whereas the three smaller ones (13-15 kb) are most probably satellites relying on helper phage(s) for multiplication. These data give a new insight into the genetic structure of lactococcal phage populations. P335 temperate phages have variable genomes, sharing homology over only 10-33% of their length. In contrast, virulent phages have highly similar genomes sharing homology over >90% of their length. Further analysis of genetic structure in all known groups of phages active on other bacterial hosts such as Escherichia coli, Bacillus subtilis, MYCOBACTERIUM: and Streptococcus thermophilus confirmed the existence of two types of genetic structure related to the phage way of life. This might reflect different intensities of horizontal DNA exchange: low among purely virulent phages and high among temperate phages and their lytic homologues. We suggest that the constraints on genetic exchange among purely virulent phages reflect their optimal genetic organisation, adapted to a more specialised and extreme form of parasitism than temperate/lytic phages.

Bacteriophages↗
PubMed2000

Suppression of arthritis and protection from bone destruction by treatment with TNP-470/AGM-1470 in a transgenic mouse model of rheumatoid arthritis.

OBJECTIVE: We assessed the clinical and histologic features of angiogenesis inhibition in a transgenic mouse model of arthritis that closely resembles rheumatoid arthritis (RA) in humans. METHODS: KRN/NOD mice, which spontaneously develop arthritis, were treated with TNP-470, an angiogenesis inhibitor. Disease was monitored by use of clinical indices and histologic examinations; circulating blood levels of vascular endothelial growth factor were determined by enzyme-linked immunosorbent assay. RESULTS: In the preventive protocol, with TNP-470 administration at a dosage of 60 mg/kg of body weight, the onset of arthritis was delayed and its clinical intensity was rather mild; 100% of placebo-treated transgenic mice developed arthritis that led to severe articular destruction. At a dosage of 90 mg/kg of TNP-470, the appearance of clinical signs was delayed for a longer period of time and disease was almost abolished. The therapeutic regimen alleviated clinical signs only when given during the very early stage of disease. Reductions in cartilage and bone destruction by TNP-470 treatment were observed histologically, a feature that was still evident at 30 and 80 days after injections were withdrawn. CONCLUSION: Our demonstration that in vivo administration of an angiogenesis inhibitor suppresses arthritis and protects from bone destruction provides new insight into the pathogenesis of the disease and opens new possibilities in the treatment of RA in humans.

Angiogenesis Inhibitors↗
PubMed1998

Differential in vitro and in vivo effects of all-trans retinoic acid on the growth of human myeloma cells.

The effects of all trans retinoic acid (ATRA) on human myeloma cells growth were studied in vitro and in vivo using immunodeficient mice engrafted with malignant plasma cells. ATRA inhibited the in vitro proliferation of plasma cells originating from two patients with multiple myeloma whereas it had no effect on the in vivo growth of plasma cell grafts as assessed by the serial study of human Ig levels in mouse serum. Thus, the efficacy of ATRA for the treatment of human multiple myeloma remains to be ascertained.

Animals↗
PubMed1996

The absence of human beta 2-microglobulin increases the occurrence of ankylosing enthesopathy in HLA-B27 transgenic mice.

HLA-B27 transgenic mice develop a spontaneous ankylosing enthesopathy (ANKENT). We have investigated the occurrence of ANKENT in transgenic mice carrying transgenes for human beta 2-microglobulin (M TGM), HLA-B27-heavy chain (27 TGM), or both (27M TGM). An unexpected finding was the increase in ANKENT occurrence among the HLA-B27 transgenic mice lacking the human beta 2-microglobulin transgene (27 TGM): 33% of such mice were found to develop ANKENT, whereas 19% of 27M mice were diseased. In addition, the expression of HLA-B27 molecules in individual 27 TGM was highly variable, ranging from no expression to a level similar to that observed in 27M TGM. Our results confirm that in mice the HLA-B27 transgene is a relative risk factor for ANKENT. The increase of ANKENT occurrence is HLA-B27 transgenics in the absence of human beta 2-microglobulin suggests a possible role for impaired cell surface expression of HLA-B27. The absence of human beta 2-microglobulin might entail an accumulation of unassembled HLA-B27 heavy chains. Exposure of these mice to an environmental trigger could then lead to an inappropriate immune response which might result in disease development.

Animals↗
PubMed1988

Immune response to H-2 class I antigens on platelets. I. Immunogenicity of platelet class I antigens.

Purified allogeneic murine platelet suspensions were found unable to induce primary anti-H-2 class I antibody or T cell proliferative responses. In contrast, the same platelet suspensions could elicit secondary anti-class I responses. The secondary responses were not due to contaminating leucocytes. Possible explanations, the lack of acolyte determinants (class II or non- H-2) on platelets or inappropriate layout and/or structure of their class I antigens, are discussed. These findings emphasize the importance of sufficient leucocyte depletion before platelet transfusion in the human.

Animals↗
PubMed1988

Immune response to H-2 class I antigens on platelets. II. Specific decrease of H-2 class I-specific antibody response induced by treatment with allogeneic platelets.

Mice pretreated with injections of allogeneic platelets were found to mount a decreased antibody response upon challenge by lymphocytes of the same donor strain. This decrease was mediated by platelets themselves, and not by leucocytes and red cells contaminating the platelet suspension. It affected specifically antibodies reactive with H-2 class I antigens present on donor platelets. This phenomenon may be related to the lack of class II or some non-H-2 antigens on platelets, and/or to properties of their class I antigens (soluble molecules adsorbed from the plasma). These findings emphasize the potential usefulness of purified platelet transfusions preceding organ transplantation in man.

Animals↗