Search PubMed⌕ Search

Biomedical subjects

M C Boissier

Publications and source records attributed to M C Boissier.

At least 37 records · Page 2Linked to original sources
PubMed1996

Attenuation of collagen-induced arthritis in mice by treatment with vector cells engineered to secrete interleukin-13.

The anti-inflammatory effects of the recently identified cytokine interleukin (IL)-13 on collagen-induced arthritis (CIA) was explored and compared to those of IL-4 using systemic administration of these cytokines via two injections of xenogeneic vector cells transfected with a plasmid construct. CIA was induced in DBA/I mice by immunization with native bovine type II collagen (CII). Chinese hamster ovary (CHO) fibroblasts transfected with the mouse IL-13 or IL-4 genes were inoculated subcutaneously on days 10 and 25 post-priming with CII and mice were monitored for signs of arthritis by observers unaware of the status of the animal. Incidence and severity of CIA were significantly reduced in the groups of mice treated with IL-13 and IL-4 gene-transfected CHO cells compared to control groups receiving nontransfected cells. Expression of various cytokines in spleen cells from individual mice was assessed by quantitative reverse transcriptase-polymerase chain reaction at different times after immunization. Our data show that IL-13-induced suppression of CIA coincided with a decreased TNF-alpha mRNA expression in the spleen of treated animals. This may explain at least partially the anti-inflammatory effects of IL-13 in CIA. Thus, our results may have important implications for the clinical use of T helper (Th)1/TH2 modulatory cytokines as therapeutic agents in the treatment of autoimmune diseases.

Animals↗
PubMed1996

Comparative study of 6 types of criteria in adult Still's disease.

OBJECTIVE: To compare the sensitivity of 6 sets of criteria proposed for adult Still's disease in published papers in a well defined patient population. METHODS: For inclusion we required a diagnosis of adult Still's disease established by a senior internist or senior rheumatologist. Sensitivity was evaluated in 65 new cases of adult Still's disease from a multicenter study based on signs and symptoms (1) in the first 6 months of illness, (2) in the same period in patients followed more than one year (52 patients), and (3) at any time in patients followed more than one year. RESULTS: The Yamaguchi criteria are most sensitive (93.5%), followed by those of Calabro and Londino. Medsger et al (80.6%), Kahn (69.3%), Reginato (55.2%), and Goldman (43.7%). Sensitivity was high even from the first 6 months, except for the 2 less sensitive criteria. CONCLUSION: Awareness of these discrepancies in adult Still's disease criteria are crucial to ensure comparability of different series of this condition.

Adult↗
PubMed1996

[Experimental gene therapy in models of inflammatory arthritis].

Gene therapy is rheumatoid arthritis is presently in an experimental phase. Genes encoding for antiinflammatory proteins can be transfected in joint cells. Therefore gene encoding for interleukin-1 receptor antagonist has been transfected into synovial cells or into chondrocytes. Gene expression can be maintained as long as 8 weeks after cell transfer. We have reported that clinical and histopathological parameters of collagen-induced arthritis (an animal model of rheumatoid arthritis) can be reduced by engraftment of CHO cells transfected with genes encoding for antiinflammatory cytokines such as interleukine-4 or interleukine-13. Some of the questions which need to be assessed before planning clinical trial are the choice of vectors and the most efficient target cells; and the genes to be transfected have to be chosen among many candidates.

Animals↗
PubMed1995

Biphasic effect of interferon-gamma in murine collagen-induced arthritis.

Interferon-gamma (IFN-gamma) exerts both enhancing and suppressing influences on collagen-induced arthritis (CIA), depending on the route and protocol of administration. To study the role of IFN-gamma on the autoimmune process of CIA, we treated DBA/1 mice with two different rat monoclonal antibodies (mAb) to murine IFN-gamma. Treatments, given twice weekly for 4 weeks, consisted of intraperitoneal injections of either mAb. In early treatments, starting from the day of immunization with type II collagen (CII), the severity of arthritis was reduced in both groups of anti-IFN-gamma-treated mice compared with control groups. Moreover, anti-CII antibody levels decreased in the sera of these mice. CIA was also down-regulated in mice treated from days 14 or 28 post immunization. In contrast, late treatments with anti-IFN-gamma mAb either induced aggravating effects, or did not affect the course of the disease. On the other hand, administration of high doses (8 x 10(4) U three times/week) of rat recombinant IFN-gamma exerted a transient increase of CIA severity. These findings suggest that IFN-gamma may play a critical role during both the induction and the course of CIA, first enhancing the immune response, and then regulating the arthritis process.

Animals↗
PubMed1995

[Treatment of inflammation with anti-inflammatory cytokines: example in models of auto-immune diseases].

Cytokines may exert anti-inflammatory properties, allowing the hypothesis of their potential therapeutic use. Targeting the cytokines balance may modify the course of subsequent inflammatory events in an autoimmune disease. Many data are available. Interferon-gamma can be blocked by an anti-interferon-gamma monoclonal antibody: if the treatment is administered in the early phase of an autoimmune disease such as collagen-induced arthritis, the course of the disease is worsened; if the treatment is given later, the disease can be improved; these results are mirrored by treatment with high doses of the cytokine itself. Pharmacologic effects of antiinflammatory cytokines such as interleukin (IL)-4, IL-10 or IL-13 are a protection against several experimental autoimmune diseases. The very short half-life of cytokines makes them difficult and expensive to use directly; in such occurrence, high quantities have to be frequently injected. In this context, gene therapy appears as an effective alternative solution: the transfection of cells with cytokines genes (e.g. either IL-4 or IL-13) then the engraftment of these vectors in animals, permit the in vivo secretion of high levels of cytokines, and result in the protection of the animals from the development of the disease.

Animals↗
PubMed1995

Adult Still's disease: part I. Manifestations and complications in sixty-five cases in France.

DESIGN: a retrospective multicenter study conducted in France identified 65 cases of adult Still's disease. Data were recorded on a standardized questionnaire validated by the Inflammatory Joint Disease and Immunorheumatology Committee of the Société Française de Rhumatologie. OBJECTIVES: (1) To compare clinical and laboratory findings in our patients with those reported in earlier studies, particularly two large series from Canada and Japan, respectively; (2) to describe the systemic and visceral complications associated with adult Still's disease. RESULTS: as compared with the two above-mentioned series, our study group included more patients who had experienced onset of their disease after the age of 35 years and fewer patients with involvement of the liver, spleen, or lymph nodes. Rates of occurrence of arthritis, myalgia, sore throat, pleuritis, pericarditis, and abdominal pain were significantly higher in the Canadian series than in the other two series. Arthritis was absent in one fourth of our patients. Life-threatening complications included "Still's hepatopathy", disseminated intravascular coagulation (with hemophagocytosis in some cases), and "Still's myocarditis". CONCLUSION: differences in the expression of adult Still's disease were found between patients from Canada, France, and Japan. Adult Still's disease can be responsible for life-threatening complications.

Adolescent↗
PubMed1995

Adult Still's disease. Part II. Management, outcome, and prognostic factors.

DESIGN: a multicenter study conducted in France identified 65 cases of adult Still's disease. Follow-up exceeded one year in 52 cases. OBJECTIVES: were as follows: 1) to describe treatments used; 2) to analyze disease course patterns; 3) to study joint alterations; 4) to determine whether any characteristics present within the first six months of onset were of prognostic significance. RESULTS: aspirin was ineffective. Indomethacin ensured satisfactory control in eight patients. Corticosteroid therapy was required in 88% of cases. Among patients followed up for more than one year, half developed radiologic joint alterations; 23% had monocyclic systemic disease, 38.5% had polycyclic systemic disease and 38.5% had chronic articular disease. More than half of the patients (58%) had more than one systemic flare. Polyarthritis at onset and involvement of the proximal limb joints were significantly predictive of chronic articular disease, whereas isolated arthralgia was predictive of monocyclic or polycyclic systemic disease. Oligoarthritis was not predictive of the outcome. CONCLUSION: the knowledge that polyarthritis or proximal limb joint involvement within six months of onset is predictive of chronic joint disease may have important therapeutic implications.

Anti-Inflammatory Agents↗
PubMed1994

[Clinical pitfalls in the diagnosis of microcrystalline arthritis].

Diagnosis of microcrystalline arthritis often is based on joint punctures, performed whenever possible. The clinical features of the crises may suggest diagnosis, but is not decisive. The course before or during treatment is not indicative and cannot fully exclude infection when the patient is seen during a crisis; arthritis with one or several microcrystals is possible, as in forms associated with joint infection. For well-oriented management, good knowledge of such diagnostic difficulties is necessary.

Arthritis↗
PubMed1994

[Rheumatoid polyarthritis. Immunopathological mechanisms, contribution of experimental arthritis].

Rheumatoid arthritis is an auto-immune disease the autoantigen of which has not yet been identified. Induction and maintenance of the disease may involve environmental factors (bacteria, viruses) and autoantigens directly issued from the articular tissue (collagens, proteoglycans). T cells play a crucial role in rheumatoid arthritis; after the antigen has been recognized, they secrete lymphokines and enable other T and B lymphocytes to be activated. The synovial cells themselves can produce large amounts of lymphokines and enzymes which contribute to the destruction of joints. The immunopathology of rheumatoid arthritis is now much better known owing to studies of experimental arthritis which are the animal models of the disease. These models have helped in validating therapeutic approaches based on immunointervention.

Animals↗
PubMed1994

T cell regulation of collagen-induced arthritis in mice. III. Is T cell vaccination a valuable therapy?

Since T cells play a critical role in collagen-induced arthritis (CIA), CD4+ T cell hybridomas were derived from DBA/1 mice immunized with bovine type II collagen (CII). The hybrid clones selected were Thy-1-2+, CD4+, CD8-, T cell receptor (TcR) alpha beta + and produced interleukin-2 in response to CII peptides presented by I-Aq molecules. The clones were collagen type-specific and recognized CII from many species except the mouse. More precisely, the reactivity was directed against the immunodominant cyanogen bromide-cleaved fragment CB11(II). Analysis of the TcR carried by the T cell hybridomas showed that they used identical V alpha and J alpha (V alpha BMB, J alpha 20) gene segments and two distinct V beta (V beta 1 and V beta 4) associated with the J beta 2.5 gene segment. Interestingly, the junctional regions were highly conserved in structure and length. These findings may indicate a strong in vivo selection by the antigen for a particular combination of both alpha and beta chains of the TcR. Inoculation of irradiated anti-CII T cell hybrids into DBA/1 mice, before priming with CII, altered the course of the disease resulting in either a long-lasting suppression or an exacerbation of CIA whereas a control CD4+ hybridoma with an unrelated specificity did not influence the development of arthritis. However, the regulatory effect of anti-CII T cell clones was unpredictable, suggesting that the TcR structure may not solely account for the modulation of CIA and that T cell vaccination is not a reliable method for inducing suppression of CIA.

Amino Acid Sequence↗
PubMed1994

A peripheral protein associated with the cis-Golgi network redistributes in the intermediate compartment upon brefeldin A treatment.

Human autoantibodies offer unique tools for the study of cellular constituents since they usually recognize highly conserved components, the most difficult to detect due to their low immunogenicity. The serum from a patient with Sjögren's syndrome (RM serum) showing a very high reactivity to the Golgi complex has been shown to immunoprecipitate and to immunodetect by Western blotting experiments a protein mol wt 210,000 (p210) that was shown to be peripheral and cytoplasmically disposed. A close examination of the p210 labeling revealed some differences with Golgi markers: RM serum staining was slightly more extensive than several Golgi markers and showed a discontinuous or granular appearance. Nocodazole induced a specific and early segregation of many p210-associated vesicles or tubules from Golgi apparatus. Upon brefeldin A treatment, p210 did not redistribute in the ER as did other Golgi proteins. In contrast, it exhibited a vesicular pattern reminiscent to that displayed by proteins residing in the intermediate compartment. Double staining immunofluorescence using the RM serum and the marker of the intermediate compartment, p58, revealed segregation of both proteins in control conditions but colocalization in BFA-treated cells. We have further demonstrated by combining different drug treatments that p210-containing elements in brefeldin A-treated cells belong indeed to the intermediate compartment. Experiments on brefeldin A recovery suggested that these p210 elements might play a role in reformation and repositioning of the Golgi apparatus. Ultrastructural localization performed by immunoperoxidase staining allowed us to establish that p210 interacted with the external side of an abundant tubulo-vesicular system on the cis side of the Golgi complex which extended to connecting structures and vesicles between saccules or stacks of cisternae, p210 appears to be a novel protein residing in the cis-Golgi network that may cycle between the Golgi apparatus and the intermediate compartment.

Autoantigens↗
PubMed1993

T cell regulation of collagen-induced arthritis in mice. II. Immunomodulation of arthritis by cytotoxic T cell hybridomas specific for type II collagen.

Injection of native type II collagen (CII) to susceptible strains of mice (H-2q) induces a rheumatoid arthritis-like disease. To study the role of CD8+ T cells in the collagen-induced arthritis (CIA), we generated CII-specific T cell hybridomas by fusion of cells from arthritic C3H. Q mice and an AKR thymoma. Two hybrid clones (P3G8 and P2D9) were selected for their ability to lyse syngeneic CII-pulsed macrophages and recognize different antigenic epitopes in association with Kq molecules. When these T cell clones were irradiated and inoculated into (C3H.Q x AKR)F1 mice 21 days prior to priming with native CII/complete Freund's adjuvant, the incidence and the duration of CIA were significantly reduced in comparison to groups receiving saline or control T cell hybridoma. Furthermore, both anti-CII T cell hybridomas were able to attenuate CIA in highly susceptible inbred strains of mice and this suppression was antigen and disease specific. The protective activity seems to require intact cells as neither membrane fractions nor cytosolic preparations of the hybridoma T cells retained the vaccinating activity. Most importantly, one of the hybrid clones (P3G8) had a therapeutic effect on CIA since its administration to arthritic DBA/1 mice on day 30 after priming down-regulated the ongoing disease. Taken together, these findings suggest that anti-CII cytotoxic T cell clones can vaccinate against CIA and even reverse the disease.

Adjuvants, Immunologic↗
PubMed1992

[Acute renal insufficiency associated with lymphoma. A new case].

We report on a case of acute renal failure secondary to relapse of a centrocytocentroblastic non-Hodgkin's lymphoma. Twenty-seven cases of acute renal failure due to lymphomatous infiltration of the kidneys have been so far reported. The clinical presentation is non-specific; the size of the kidneys appears normal or enlarged; diagnosis is confirmed by renal biopsy and/or CT scan examination. Chemotherapy and/or radiotherapy sometimes lead to dramatic improvement of renal function. However, prognosis is poor, mostly due to lymphomatous evolution.

Acute Kidney Injury↗
PubMed1992

Combination of cyclosporine A and calcitriol in the treatment of adjuvant arthritis.

We investigated combination treatment with cyclosporine A (CsA) and calcitriol (CT), 2 immunomodulatory agents, in vivo in the adjuvant arthritis (AA) model in rats. Treatment initiated at priming with complete Freund's adjuvant consisted of daily administration of CsA and CT during the prearthritic phase (14 days). CsA given alone delayed the onset of the disease, whereas the severity was either not affected or paradoxically enhanced. Injection of CT alone reduced the severity of arthritis. The association of low doses of CsA (5 mg/kg) and CT (0.2 micrograms/kg) further delayed the onset of AA and abolished the aggravating effect. Our findings suggest that low doses of CsA and CT in association exhibit the additive beneficial effects of either agent alone.

Administration, Oral↗