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Biomedical subjects

X Mariette

Publications and source records attributed to X Mariette.

At least 91 records · Page 5Linked to original sources
PubMed1993

Detection of human T lymphotropic virus type I tax gene in salivary gland epithelium from two patients with Sjögren's syndrome.

OBJECTIVE: To investigate whether human T lymphotropic virus type I (HTLV-I) could be involved in the pathogenesis of Sjögren's syndrome (SS). METHODS: Labial salivary gland (LSG) biopsy specimens from 9 patients with SS (4 with primary SS and 5 with SS secondary to rheumatoid arthritis) and 9 controls were studied for the presence of the tax gene of HTLV-I using in situ hybridization, and for the presence of tax, gag, pol, and env genes of HTLV-I using the polymerase chain reaction (PCR). Testing for antibodies to HTLV-I and examination of lymphocytes on blood smears were performed to determine whether systemic viral infection was present. RESULTS: Using in situ hybridization and PCR, we detected the tax gene, but not the gag, pol, or env genes, of HTLV-I in LSG sections from 2 of 9 patients with SS and from none of the control subjects. Tax DNA was present mostly in nuclei of epithelial cells, but also in some lymphoid cells. Serum of the 2 affected patients did not contain antibodies to HTLV-I. In 1 patient, examination of blood smears revealed rare convoluted lymphocytes, sometimes with the appearance of "flower cells," as observed in the blood of HTLV-I-infected patients. CONCLUSION: None of the known endogenous retroviral sequences is homologous to the tax gene. Thus, we suggest that HTLV-I (or another related retrovirus) can infect salivary epithelium. Transactivation properties of the tax protein could be implicated in the pathogenesis of SS. Alternatively, viral infection could cause de novo expression of HLA-DR antigens and favor the presentation of antigens by epithelial cells, leading, in some genetically predetermined subjects, to lymphoid infiltration of the gland.

Antibodies, Viral↗
PubMed1993

Nucleotidic sequence analysis of the variable domains of four human monoclonal IgM with an antibody activity to myelin-associated glycoprotein.

We determined the nucleotide sequence of the VL and VH regions of four human monoclonal IgM directed to myelin-associated glycoprotein (MAG) and a nerve glycolipid, the sulfated glucuronic paragloboside (SGPG). Clonal lymphoblastoid cell lines (three cases) and an heterohybridoma (one case) secreting anti-MAG IgM were derived from patients' blood B cells. V kappa genes derived from the single germinal V kappa IV (two cases), the V kappa Id and the V kappa IIIa Humkv328h5 genes. VH genes derived from the VHIII 9.1 germinal gene (or a closely related gene) in two cases, whereas two others possibly represent new members of the VHIII or VHI variability subgroups. There was no obvious restriction in the use of J kappa, JH and DH segments. Somatic mutations were predominantly found in the CDR3 of the V kappa IV genes with an overall ratio of replacement over silent mutations of 7/0. The sequence of two VHIII genes exhibited five replacement mutations in CDR in comparison to that of the germ-line 9.1 gene. Although some V genes are likely to be overrepresented among anti-MAG IgM, the diversity of the immune repertoire for MAG and SGPG explains the lack of easily detectable public idiotopes among these IgM. This last finding, as well as a high ratio of replacement versus silent nucleotide mutations in the CDR of VL and probably VH genes, suggest that the pathogenesis of these monoclonal antibodies (and of the associated lymphoplasmocytic disorder) differs from that of other previously characterized monoclonal autoantibodies such as rheumatoid factors and cold agglutinins.

Amino Acid Sequence↗
PubMed1993

Nodular lymphocyte predominance Hodgkin's disease featuring blood atypical polyclonal B-cell lymphocytosis.

The nodular lymphocyte predominance form of Hodgkin's disease (NLPHD) is considered as a B cell derived lymphoproliferative disease. A patient with NLPHD presented with an absolute increase in blood B cells with cytological features of mantle zone cells; these B cells were polyclonal, did not exhibit bcl-2 gene rearrangement, and some of them displayed non-clonal chromosomal aberrations. EB virus genome was not detected by Southern analysis. Thus, this study, taking advantage of the presence of an unusual population of blood atypical B cells, confirms data obtained on lymph nodes where, however, malignant cells may be scarce, indicating that NLPHD is a polyclonal B cell lympho-proliferative disease of mantle zone origin.

Adult↗
PubMed1993

Characterization of a human monoclonal autoantibody directed to cardiolipin/beta 2 glycoprotein I produced by chronic lymphocytic leukaemia B cells.

We determined the specificity and sequence of immunoglobulin molecules synthesized by monoclonal B cells from a patient with chronic lymphocytic leukaemia (CLL) who presented with a number of clinical and biological autoimmune symptoms. Heterohybrids obtained by fusion of CLL cells with the mouse X63-Ag 8.653 myeloma produced IgM lambda MoAbs directed to the cardiolipin/beta 2 glycoprotein I (beta 2GPI) complex and ssDNA. They were devoid of polyreactivity. Nucleotide sequence analysis of the variable domain of the mu chain indicated the utilization of the VH4 71.2 gene or one allotypic variant, DXP4 and JH3 segments. The lambda light chain used the single gene from the V lambda 8 subfamily, J lambda 3 and C lambda 3 genes. The VH gene displayed 11 nucleotide changes in comparison with its putative germline counterpart. However, these nucleotide changes correspond to variations observed in other published VH4 sequences, suggesting gene polymorphism rather than somatic mutation. DXP4 and JH3 were also in germline configuration. The VL gene exhibited a single replacement mutation in CDR1. These data suggest that the monoclonal CLL B cells in this patient retained VH and VL genes in germline configuration although they secreted a pathogenic anti-cardiolipin antibody associated with clinical symptoms, vasculitis and thrombosis, which may be provoked by antibodies to the phospholipid/beta 2GPI complex.

Amino Acid Sequence↗
PubMed1992

Bone densitometry in patients with multiple myeloma.

PURPOSE, PATIENTS, AND METHODS: We performed dual-energy x-ray absorptiometry in 10 selected patients with aggressive multiple myeloma in whom substantial tumor mass reduction was achieved after high-dose chemoradiotherapy followed by autologous blood stem cell transplantation. RESULTS: In most cases, bone mineral density (BMD) of the spine was initially low (Mean Z score: -2.69, SEM 0.76) and dramatically increased after treatment (mean increase 16.4%; 7.7% with 95% confidence interval 2.2 to 12.2, excluding one patient whose spine BMD increased by 94.8%). In contrast, skeletal roentgenograms, computed tomographic scans, and magnetic resonance imaging did not reveal any significant improvement of patients' bone lesions. CONCLUSIONS: In patients with multiple myeloma, bone densitometry could be a useful way to assess the efficacy of treatment on bone status.

Absorptiometry, Photon↗
PubMed1992

Determination of the affinity of monoclonal human IgM for myelin-associated glycoprotein and sulfated glucuronic paragloboside.

We determined the association constant of eight monoclonal IgM with two of their targets, i.e. the myelin-associated glycoprotein (MAG) or the sulfated glucuronic paragloboside (SGPG). All IgM had a 10- to 100-fold higher affinity for MAG than for SGPG. The affinity of the different IgM for MAG ranged from 1.3 x 10(-6) to 7 x 10(-9) mol/liter. The Scatchard plots for MAG were curvilinear, half of the sites being of high or low affinity. In contrast, the plots were linear in the assay using SGPG. No obvious correlations were found between the fine specificity of these IgM for the glucuronyl sulfate epitope and their affinity, although most IgM with a high affinity reacted exclusively with SGPG derivatives retaining a sulfate group. There was no parallelism between the severity of the neuropathy and the affinity of the IgM for MAG or SGPG.

Globosides↗
PubMed1992

Pulmonary Hodgkin's disease in HIV-infected patient. Diagnosis by bronchoalveolar lavage.

We report herein the pulmonary recurrence of Hodgkin's disease coincidental with a marked decrease in the peripheral blood CD4 lymphocyte count in an HIV-seropositive patient with alveolar consolidation on chest roentgenogram. The diagnosis of lung parenchyma involvement was made by bronchoalveolar lavage cell analysis and illustrates the reliability of Reed-Sternberg cell identification in bronchoalveolar lavage for the diagnosis of pulmonary localization of Hodgkin's disease.

Adult↗
PubMed1991

Detection of Epstein-Barr virus DNA by in situ hybridization and polymerase chain reaction in salivary gland biopsy specimens from patients with Sjögren's syndrome.

PURPOSE: To determine whether Epstein-Barr virus (EBV) could be involved in the pathogenesis of Sjögren's syndrome (SS). PATIENTS AND METHODS: In situ hybridization using the BamH1-W fragment of EBV DNA was performed using labial salivary gland biopsy specimens from 14 patients with SS (eight with primary SS and six with secondary SS) and 39 control subjects. Furthermore, labial salivary gland biopsy specimens from 12 patients with SS (seven with primary SS and five with secondary SS) and 24 control subjects were submitted to the polymerase chain reaction to detect EBV DNA. RESULTS: In situ hybridization detected EBV DNA in epithelial cells of labial salivary gland biopsy specimens from four of eight (50%) patients with primary SS, zero of six patients with secondary SS, and three of 39 (8%) control subjects. The difference between patients with primary SS and control subjects was statistically significant (p less than 0.02). The polymerase chain reaction detected EBV DNA in six of seven (86%) patients with primary SS, three of five (60%) patients with secondary SS, and seven of 24 (29%) control subjects. The difference between patients with primary SS and control subjects was statistically significant (p less than 0.01). CONCLUSION: Both newly developed techniques showed that the presence of EBV DNA was significantly increased in patients with primary SS in comparison with control subjects. In all the positive SS patients who underwent in situ hybridization, epithelial cells of the labial salivary gland were the target of EBV infection. Our results suggest that this virus may play a role in the pathogenesis of SS. We cannot yet determine whether EBV is directly responsible for the destruction of the gland, or if its presence is a secondary event following gland injury.

Adult↗