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M Tardieu

Publications and source records attributed to M Tardieu.

188 records · Page 11Linked to original sources
PubMedDate not supplied

HIV receptors within the brain: a study of CD4 and MHC-II on human neurons, astrocytes and microglial cells.

We have investigated the level of expression of CD4 and MHC-II antigens on CNS cells and compared it to that on monocytes. MHC-II antigens were expressed spontaneously on cultured astrocytes and monocytes, whereas they were detected only after IFN gamma stimulation of microglial cells. In vitro, CD4 receptor was present on monocytes but not on neurons, astrocytes or microglial cells. In normal brain, CD4 antigen was expressed on perivascular microglial cells, a specialized microglia expressing monocytic markers, whereas in HIV1-infected brain, CD4+ cells were numerous and scattered throughout the whole parenchyma. These CD4+ macrophages may be HIV1-infected monocytes which have crossed the blood-brain barrier after infection, or perivascular microglial cells infected by HIV1-infected blood lymphocytes or five virions.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

Effect of interferon gamma and TNF alpha on the differentiation/activation of human glial cells: implication for the TNF alpha receptor 1.

This study focused on the activation/differentiation of human microglial cells and astrocytes, which is a prerequisite for HIV1 replication. In vitro, IFN gamma induced a differentiation-like morphological change in embryonic microglia and astrocytes, in both primary and in purified culture. This effect was enhanced by TNF alpha which in itself had no effect. IFN gamma did not increase the low level of endogenous TNF alpha, which is not secreted by embryonic cells, but stimulated the expression of TNF alpha R1, although to a relatively low extent. IFN gamma facilitated TNF alpha response through an increase in TNF alpha R1 expression, but probably also through interaction with different intracellular signal transduction pathways.

Astrocytes↗
PubMedDate not supplied

Adhesion proteins on human microglial cells and modulation of their expression by IL1 alpha and TNF alpha.

Expression of adhesion proteins on human microglial cells was studied by immunocytochemistry. Both microglial cells and peripheral blood monocytes expressed beta 2 integrins and molecules of the immunoglobulin superfamily at similar levels whereas the expression of the beta 1 integrins (alpha 2-VLA (very late antigen), alpha 4-VLA, alpha 5-VLA, alpha 6-VLA) was higher on microglial cells than on monocytes. Stimulation of microglial cells with interleukin-1 alpha and tumour necrosis factor-alpha, the main cytokines detected in HIV1-infected central nervous system (CNS), increased the microglial expression of alpha 1-VLA, intercellular adhesion molecule-1, vascular cell adhesion molecule-1 and beta 2-LFA-1 (leukocyte-function-associated molecule-1) but not of alpha L-LFA-1. Such an induction of adhesion molecules could facilitate penetration of HIV1-infected monocytes into brain parenchyma and their adhesion to CNS cells, and could maintain a chronic inflammation during human immunodeficiency virus-1 (HIV1) encephalopathy.

Brain↗
PubMedDate not supplied

High concentrations of 2-5A, the interferon intracellular mediator, in the blood of children with acute viral infections.

We measured the concentration of 2-5A (2',5'-oligoadenylate), an intracellular mediator of the antiviral action of interferon, in the blood of children with acute viral and bacterial infectious diseases. 2-5A concentration was found to be elevated in several children with viral diseases. This elevation seemed transient and was not specific for viral infections. We provide arguments for the use of 2-5A as a marker of the evolution of diagnosed viral diseases.

Acute Disease↗
PubMedDate not supplied

[Nervous system involvement in HIV1 infections in infants].

A prospective survey of 38 HIV1-infected infants has been performed. Thirty-four percent of the patients expressed neurological abnormalities. Three main clinical entities of various intensity have been defined: 8 patients had severe intellectual and motor dysfunctions associated with a bucco-lingual dyspraxia; in 4 patients, the intellectual and motor alterations were less intense but were associated with a severe bucco-lingual dyspraxia; finally one patient had no clinical symptomatology but a chronic lymphocytic meningitis. No opportunistic infection of the CNS was observed. The neurological alterations were correlated in intensity with the immunological dysfunction. CT scans were normal or showed cerebral atrophy in most cases. CSF were normal in 12 cases and a pleiocytosis was observed in one case. However, in 4 of the 6 tested cases, anti-HIV antibodies were detected in CSF.

Central Nervous System Diseases↗
PubMedDate not supplied

[Post-infectious Epstein-Barr virus encephalitis].

A case of meningoencephalitis is reported in a 14 year old boy. After an acute onset with fever and coma, the outcome was rapidly favorable. Antibody titers in acute and convalescent sera demonstrated recent infection with EBV. EBV encephalitis appears to be a post-infectious encephalitis with no direct viral invasion of the CNS and no acute viral replication.

Adolescent↗
PubMedDate not supplied

[Disturbances of chemotaxis in protein-calorie malnutrition (author's transl)].

A study of specific and non-specific immune functions was performed in 14 children presenting with severe malnutrition, before and after parenteral hyperalimentation by central catheter. Anomalies of cellular functions (reduction of the percentage of E rosettes and deficient proliferation with mitogens) were rarely found. Measurements for serum immunoglobulins did not show any anomaly; however reduced percentages of EAC rosettes and important increase in "null" cells were found in about one third of the cases. The main finding was a decreased serum chemotactic activity following activation of the classic complement pathway. This was found in 12 children and returned to normal values in all cases after hyperalimentation.

Chemotactic Factors↗