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B Autran

Publications and source records attributed to B Autran.

At least 19 recordsLinked to original sources
PubMed1992

[Amplification of a circulating CD4+CD7- T lymphocytes subset in kidney transplantation].

A minor subset of CD4+ T-cells (10 +/- 4 percent) that does not express the CD7 antigen is detectable in normal individuals. These CD4+CD7- T-cells have lower proliferative capacities than autologous CD4+CD7- T-cells. We observed an expansion of CD4+CD7- peripheral T-cells in 45 kidney transplant recipients. The CD4+CD7- TL expansion (23 +/- 20 percent was observed in both short term (< 6 months, n = 20) and long term transplanted patients (> 3 years, n = 25). These results significantly differed from those observed in patients on dialysis (10 +/- 4 percent, P < 0.002). The percentages of CD4+CD7- TL in kidney recipients are significantly correlated with the percentages of CD4+CD57+ and CD8+CD57+ T-cells subsets. A three-color immunofluorescence analysis indicated that 75 percent of the CD4+CD7- TL express the CD57 molecule contrasting with those in normal individuals (0.3 percent). Purified CD4+CD7- T-cells from kidney recipients have lower proliferative responses after PHA, CD2 and CD3 stimulations than autologous CD4+CD7+ TL. The proliferative response is partially restored by the addition of anti-CD28 moAb or IL2. We have highlighted, in kidney recipients with good graft function, an expansion of CD4+CD7- T lymphocytes which could be associated with CD4+ T-cell anergy and tolerance.

Antigens, CD↗
PubMed1992

Consistency of routine measurements of CD4+, CD8+ peripheral blood lymphocytes.

In order to evaluate the reliability of CD4 and CD8 T lymphocyte counts in large scale studies, a quality control study was performed in 12 French laboratories. CD4 and CD8 counts, assessed by various haematological and immunological techniques, were compared in order to assess possible differences between the laboratories and the techniques used. Our data showed that (a) the consistency of CD4 measurements was satisfactory since the between-laboratory coefficient of variation for absolute CD4 cell numbers above 200/mm3 was around 15% instead of 5-10% for all laboratories but one; (b) the major sources of variability arose from the use of automatic devices in the two-step measurement procedure: immunophenotyping and haematological counting. These data suggest that multicentre assays of CD4 and CD8 counts result in some increase in their variability. Nevertheless the results of large multicentric trials can be extrapolated with confidence in the routine care of HIV+ patients. Together, the results justified the involvement of several experienced laboratories in a clinical trial of HIV-related disease.

CD4 Antigens↗
PubMed1992

Minocycline-induced cell-mediated hypersensitivity pneumonitis.

OBJECTIVE: To identify the cause of a hypersensitivity pneumonitis and to determine its pathogenesis. DESIGN: Case study. SETTING: Intensive care unit of a referral hospital. PATIENT: A 51-year-old man with chronic bronchitis who developed a hypersensitivity pneumonitis within 1 month after exposure to minocycline, amoxicillin, and erythromycin. INTERVENTION: Sequential bronchoalveolar lavages after reexposure to minocycline and amoxicillin. MEASUREMENTS: Immunologic analysis of the phenotype and function of alveolar lymphocytes. RESULTS: Reexposure to minocycline but not to amoxicillin was followed by an interstitial pneumonitis. Sequential bronchoalveolar lavages showed a transient rise of eosinophils and neutrophils and a persistent alveolar lymphocytosis. Alveolar lymphocytes consisted predominantly of CD8+ but also CD4+ cells. Two CD8+ lymphocyte subsets were identified: CD8+ D44+ cytotoxic T cells that increased rapidly after the drug was resumed and CD8+ CD57+ suppressor T cells that predominated 11 days after the drug's withdrawal. In-vitro assays showed the presence of a lymphocyte-mediated specific cytotoxicity against minocycline-bearing alveolar macrophages. CONCLUSION: These results support the hypothesis of a central role of T lymphocytes in the pathogenesis of drug-related hypersensitivity pneumonitis.

Alveolitis, Extrinsic Allergic↗
PubMed1992

CD8 lymphocytosis and pseudotumoral splenomegaly in HIV infection.

Three patients infected with human immunodeficiency virus (HIV) presented with pseudotumoral splenomegaly, CD8 lymphocytosis (3.5-5.1 x 10(9)/l), and hypergammaglobulinaemia. Spleen and bone marrow showed diffuse CD8 lymphocyte and plasma-cell infiltration. Amplification of the T-cell-receptor gamma chain gene did not reveal any clonal T-cell population. Phenotypic analysis showed a predominance of CD8/CD57 suppressor T cells with expression of activation markers (DR and CD38). No cytotoxic T lymphocytes specific for HIV could be detected. The three patients shared the HLA haplotype A1, B8, DR3. The association with this haplotype suggests a genetically determined host immune response to HIV.

Acquired Immunodeficiency Syndrome↗
PubMed1992

[Coronary pathology after heart transplantation].

Graft coronary disease is a frequent and devastating complication with rapid development after heart transplantation. Until now, non-invasive and invasive methods have proved to be insensitive in the prediction and detection of the early stages of this disease. Conventional arteriography is considered as the only reliable means of diagnosis, but it remains insensitive in the accurate evaluation of the severity of graft coronary lesions (obliterative, diffuse and distal lesions). Precise quantitation of coronary lumen changes may be a sensitive method for the accurate evaluation of graft coronary disease and help in the understanding of the natural course of development of this disease. The pathogenesis of the disease is still unclear. It is possible that graft coronary disease is a consequence of non-treated low-grade cellular rejections. In most cases, retransplantation must be considered as the unique solution.

Coronary Angiography↗
PubMed1992

CD4+CD7-CD57+ T cells: a new T-lymphocyte subset expanded during human immunodeficiency virus infection.

CD7 and CD57 are two cell surface molecules related to the differentiation or functional stages of CD4+ T cells. The CD4+CD7- T cells represent a minor subset of CD4+ cells in normal individuals and are considered to contain the normal counterpart of Sézary T cells; the CD4+CD57+ peripheral blood lymphocytes (PBL) are detectable in long-term renal allograft recipients. We compared the cell surface expression of these CD7 and CD57 markers on CD4+ T lymphocytes in peripheral blood and lymphoid organs from normal individuals and human immunodeficiency virus (HIV)-infected patients. Our results indicate that CD4+CD7- T cells in normal PBL do not express CD57 and were poorly responsive to anti-CD3 monoclonal antibody (MoAb), the activation being restored by addition of anti-CD28 MoAb. This CD4+CD7- cell subset is increased in peripheral blood during HIV infection, and its progressive expansion mirrors both the absolute and relative decrease of CD4+ T cells. The lack of CD7 expression is correlated with CD57 acquisition on CD4+ T cells because CD4+CD7-CD57+ cells represent a major component of the CD4+CD7- subset in HIV-infected patients. Our results suggest that the presence and the expansion of CD4+CD7-CD57+ T lymphocytes, which do not behave as previously defined helper subsets, may participate to the immune dysfunction observed during HIV infection.

Antigens, CD↗
PubMed1992

Antibodies raised against peptide fragments of CD16 reacting with membrane and soluble form of CD16. I: Production and characterization.

Monoclonal antibodies (MAbs) were generated against human CD16 (Fc gamma RIII) by fusion of NS1 myeloma cells with spleen cells from BALB/c mice immunized with synthetic peptide sequences derived from the CD16 genes. After screening, four hybridomas secreting MAbs (2 IgM and 2 IgG) were selected, cloned and characterized for their activity against CD16 by ELISA test, flow cytometry, rosette inhibition and immuno-blotting. MAbs reacted strongly in ELISA with a soluble form of CD16 (sCD16) present in human serum and to a lesser degree with soluble recombinant CD16 (srCD16). The binding characteristics of the four antibodies to the sCD16 were different, implying that the antibodies recognize different CD16 epitopes. FACS analysis of peripheral blood from healthy volunteers demonstrated that these MAbs are highly reactive with membrane CD16 of neutrophils cells (70-95%) and with a subset of lymphocytes (6-14%). These MAbs seem interesting and may lead to the purification of the soluble human CD16 and to the knowledge of its functions, its physiological role and the cellular polymorphism.

Amino Acid Sequence↗
PubMed1992

Human trophoblast cells express CD4 and are permissive for productive infection with HIV-1.

The European collaborative study of HIV-infected pregnant women in Europe now indicates a 13% risk of fetal HIV infection (originally thought to be about 30%, and possibly higher in some countries). Several reports suggest trans-placental passage. However, the detailed mechanisms associated with such vertical transmission have not yet been clarified. We have examined the possibility that HIV enters placental tissue from maternal blood via binding to CD4 and Fc receptors (FcR) at the trophoblast level, allowing intraplacental infection. Here we report the detection of several FcR with distinct localization in the placental villus as well as CD4 surface expression on human trophoblast cells. In addition, we show that trophoblastic cells interact specifically with the gp120/gp160 viral envelope protein. By their tissue localization, these receptors could be responsible for the entry of HIV into the fetal placental cells. Furthermore, purified placental cells can be directly infected by HIV in vitro, and the infection is inhibited by soluble CD4. This suggests a crucial role of the CD4 receptor but an additional way of entry cannot be excluded. Such an in vitro model may be suitable for further studies concerning placental HIV transmission and its prevention.

CD4 Antigens↗
PubMed1992

Carboxyl-terminal and central regions of human immunodeficiency virus-1 NEF recognized by cytotoxic T lymphocytes from lymphoid organs. An in vitro limiting dilution analysis.

Cytotoxic T lymphocytes (CTL) specific for human immunodeficiency virus (HIV) proteins have been analyzed in lymphoid organs from seropositive patients. Indeed, an active HIV replication coexists with a major CD8+ lymphocytic infiltration in these organs. We have shown in a previous report that HIV-seropositive patients lungs were infiltrated by HIV specific CD8+ lymphocytes. In the present report, we show that HIV-specific CTL responses can also be detected in lymph nodes and spleens, and were mainly directed against the ENV, GAG, and NEF HIV-1 proteins. The primary NEF-specific CTL responses were further characterized by epitope mapping. Determination of epitope-specific CTL frequencies were performed by limiting dilution analysis. Our results indicated that, in addition to the central region of NEF (AA66-148), a new immunodominant region is recognized by CTL. This region corresponds to the carboxyl-terminal domain of NEF (amino acids 182-206). AA182-206 is recognized in association with at least two common human histocompatibility leukocyte antigen (HLA) molecules (HLA-A1 and B8), with clonal frequencies of one CTL per 10(-5) to 10(-6) splenic lymphocytes. Our data indicate that lymphoid organs may represent a major reservoir for in vivo activated HIV-specific CTL. Furthermore, the carboxyl-terminal domain of NEF was found to be conserved among several HIV strains. Therefore, our finding is of interest for further HIV vaccines development.

Amino Acid Sequence↗
PubMed1992

[Cytotoxic response against human immunodeficiency virus (HIV): control with suppressor factor].

We report a new suppressor function of CD8+ CD57+ lymphocytes from HIV-seropositive patients recipients, on the cytolytic activity of allospecific CTL, NK and LAK cells. This inhibitory effect is mediated by a non-antigen specific soluble factor distinct from PGE2, TGF beta and TNF alpha and beta. Biochemical characterization indicates that the CD8+ CD57+ inhibitory activity: 1) is heat and trypsin resistant but remains sensitive to pronase E hydrolyse, 2) specifically bind to concanavalin A-sepharose column, 3) is mediated by a 20-30 kdaltons glycoprotein.

Chemical Phenomena↗
PubMed1992

[Lymphocytic alveolitis in the early stages of HIV infection: correlation with biological and prognostic factors].

Broncho-alveolar lavage was performed to assess the degree of pulmonary lymphocytic alveolitis in 32 asymptomatic patients who were infected with the Human Immunodeficiency Virus (VIH). The patients were stages II and III of the CDC classification and the aim of the study was to determine the frequency, nature and prognostic role of the findings. 62.5% of the subjects (20/32) presented with a lymphocytic alveolitis which consisted predominantly of CD8 lymphocyte (64.3 +/- 3.5%), in the absence of an opportunistic infection or broncho-pulmonary tumours. Two sub-populations of alveolar CD8 were shown at comparable levels, a) sub-population CD8+D44+ (22.1 +/- 5%), in whom we showed the possession of cytotoxic activity in particular specific for VIH; b) sub-population CD8+CD57+ (19.6 +/- 3%) which we have shown to be capable in vitro of inhibiting the effector phase of cytotoxic activity of CD8+D44+ alveolar cells specific for VIH. In this group of 32 patients the occurrence of an alveolitis was not correlated with the usual prognostic factors of infection by VIH measured simultaneously with broncho-alveolar lavage (the level of CD4+ blood lymphocytes, and the beta 2-plasma microglobulins and the presence of p24 antigenaemia). In addition the level of CD4 lymphocytes supperior to 400/mm3 and of beta 2-microglobulins less then 3 mg/l whether a lymphocytic alveolitis was there or not confirmed the relatively poorly developed state of the VIH infection in these asymptomatic patients. Also the occurrence of a lymphocytic alveolitis did not seem to be linked to progression of the disease in the group of patients studied.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

A soluble factor released by CD8+CD57+ lymphocytes from bone marrow transplanted patients inhibits cell-mediated cytolysis.

We report a new inhibitory activity of CD8+CD57+ peripheral blood lymphocytes from allo-bone marrow transplant patients. Positively selected CD8+CD57+ lymphocytes act as potent inhibitors of allospecific cytolytic T lymphocyte and lymphokine activated killer cell cytolytic activities. These suppressor cells are mature T cells expressing the CD2, 5, 7, CD3-TcR alpha beta complex, and lack natural killer cell markers as well as cytolytic function. Their inhibitory activity on both cytolytic processes and T-cell proliferation is mediated by a non-antigen-specific soluble factor released by CD8+CD57+ cells in culture supernatants. Preliminary characterization suggests that the CD8+CD57+ cells' inhibitory activity is mediated by a low molecular weight, glycosylated factor as indicated by its less than 1S coefficient of sedimentation and its binding to concanavalin A lectin.

Antigens, Differentiation, T-Lymphocyte↗
PubMed1991

A lectin-binding soluble factor released by CD8+CD57+ lymphocytes from AIDS patients inhibits T cell cytotoxicity.

CD8+CD57+ T cells, expanded in peripheral blood lymphocytes of AIDS patients, inhibit the effector phase of HLA-specific cytotoxic T lymphocytes, natural killer and lymphocyte-activated killer cells in a 4-h chromium-release assay. This inhibitory activity present in supernatants of purified sorted CD8+CD57+ cells is mediated by a non-antigen-specific inhibitory factor which is distinct from prostaglandin E2, T cell growth factor (TGF)-beta, latent-TGF-beta, tumor necrosis factor (TNF)-alpha and TNF-beta. Partial biochemical characterization demonstrates that the CD8+CD57+ inhibitory activity (a) is heat, trypsin and acid resistant, (b) binds to concanavalin A columns, indicating its glycosylation state and (c) is mediated by a 20-30-kDa soluble molecule.

Acquired Immunodeficiency Syndrome↗
PubMed1991

Evidence that residual host cells surviving the conditioning regimen to allogeneic bone marrow transplantation inhibit donor hematopoiesis in vitro--the role of TNF-alpha.

Blood cells were obtained from patients selected for allogeneic bone marrow transplantation who had undergone a conditioning regimen (CR) with high-dose chemotherapy and total body irradiation. The majority of residual cells bore CD3 antigen (range: 68-98%), and the CD4/CD8 ratio was normal. The effect of these residual/radioresistant cells on donor bone marrow hematopoiesis was investigated in eleven cases. Growth of donor CFU-GM and BFU-E was inhibited by 22-65% and 29-77%, respectively, when donor marrow was cocultured with residual cells at various ratios. In contrast, blood cells obtained from two patients prior to CR had no inhibitory effect. Supernatants obtained following incubation of residual cells from 9 patients were able to inhibit the growth of CFU-GM and BFU-E from normal unrelated subjects, whereas supernatants obtained before CR and from cultured normal marrow had no inhibitory effect. In addition, in blocking experiments, an anti-TNF-alpha MoAb was able to prevent this inhibition. Thus, TBI might be able to select and/or activate cells responsible for hematopoietic growth inhibition by a mechanism involving, at least in part, TNF-alpha.

Adult↗