Biomedical subjects
J Charreire
Publications and source records attributed to J Charreire.
Allograft enhancement induced by bone marrow cells.
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Significance of antigen binding by T cells.
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[Report on crenotherapy of allergic diseases in French thermal spas].
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[Effect of the gaseous phase of cigarette smoke on lymphoblastic transformation of the small human lymphocyte (preliminary observations)].
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[Value of lymphoblastic transformation test (L.T.T.) in the diagnosis of delayed hypersensitivity and drug intolerance (682 cases)].
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[Functional respiratory examination in asthma].
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[Increased autorosette levels with aging].
The autorosette levels studied in human peripheral blood of 115 normal subjects are shown to be higher in women than in men and to increase along with the age in both sexes. These autorosettes could belong to immature T-cells as they stick to nylon wool and they decreased after E-rosette depletion. The T-cell origin of autorosettes is confirmed by the existence of mixed rosettes using autologous erythrocytes and sheep red blood cells.
[Interest in the treatment of asthma caused by delayed hypersensitivity of an immunosuppressive drug, chlorambucil. Personal experience on 21 cases].
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[Delayed-action effect of a racephedrine, theophylline and phenobarbital combination on asthma. Study on 100 cases].
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[H-2 specificity and auto-reactivity of autologous rosette-forming cells from adult thymectomized mice spleen cells].
We have previously shown that the number of autologous rosette-forming cells (A-RFC) found in adult thymectomized mice (A-Tx) spleens was 15 times higher than that found in spleens of intact controls. We have therefore investigated both the specificity of A-RFC and their relationship with autoreactivity. Immunoadsorption experiments showed that while the incubation on allogeneic monolayers did not bring any modification in A-RFC levels. This result suggests that the formation of autologous rosettes is the manifestation of a true recognition event associated with the H-2 complex. A-Tx mice spleen cells injected into syngeneic recipients induced an enlargement of the afferent popliteal lymph node (LN). Ficoll-Triosil A-RFC depleted A-Tx spleen cells lost their capacity to induce this popliteal proliferation. Conversely, A-RFC recovered spleen cell suspensions obtained from the pellet of the Ficoll Triosil gradient kept their capacity of inducing auto-reactivity. Thus, it seems that A-RFC and lymphocytes stimulating the afferent LN belong to the same sub-population.
Desensitization of the antigen receptor primes B cells for activation by superstimulatory influenza virus.
Interaction of the B cell receptor (BCR) with non-immunogenic receptor ligands can induce a specific state of B cell unresponsiveness as a result of receptor desensitization. Provided it is maintained over time, BCR desensitization may provide the molecular basis for clonal anergy. Using an in vitro model of anti-Ig-mediated BCR desensitization, we assessed the susceptibility of desensitized "anergic" B lymphocytes to activation by B cell superstimulatory influenza virus hemagglutinin (HA). Rabbit anti-mouse Ig antibodies (whole Ig molecule or F(ab')(2)-fragments) totally abolished the response of murine B cells to HA, when added simultaneously with the virus. Pretreatment with the same antibodies, however, yielding a complete unresponsiveness to a subsequent challenge with normally mitogenic anti-Ig reagents, even enhanced the subsequent proliferative response to HA. By contrast, HA-mediated high-rate immunoglobulin synthesis was suppressed after desensitization. BCR-desensitized, HA-stimulated B cells exhibited a hyperexpression of various activation markers (B7, major histocompatibility complex class II, CD25) and served as potent antigen-presenting cells (APC) in a polyclonal model for T lymphocyte activation. These observations suggest a possible scenario for the breaking of natural B cell tolerance, where infections with B cell superstimulatory viruses may lead to the clonal expansion of receptor desensitized, functionally silenced B lymphocytes in vivo.