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Biomedical subjects

M Fontaine

Publications and source records attributed to M Fontaine.

At least 217 records · Page 12Linked to original sources
PubMedDate not supplied

Differential modulation of complement factor H and C3 expression by TNF-alpha in the rat. In vitro and in vivo studies.

The biosynthesis of alternative regulatory complement protein factor H was investigated using both an in vivo rat model and an in vitro rat hepatocyte culture system, and compared to that of C3 component. Subcutaneous injection of a single dose of 20 micrograms of recombinant murine tumor necrosis factor-alpha (rmTNF-alpha) had no effect on factor H liver mRNA levels, while it increased C3 mRNA levels. In correlation with this, serum factor H levels remained unchanged after rmTNF-alpha injection, whereas C3 levels were increased. In contrast in vitro studies showed that rmTNF-alpha had no effect on factor H and C3 expression by rat hepatocytes. Recombinant human interleukin-1 alpha (rhIL-1 alpha) did not alter the expression of factor H, whereas it increased C3 expression, and recombinant human interleukin-6 (rhIL-6) stimulated expression of both proteins. This study shows that TNF-alpha is not directly responsible for the increased levels of factor H observed in vivo during induced inflammation in the rat. Its in vivo effect on C3 secretion might be secondary to the TNF-alpha-induced release of IL-1 and/or IL-6.

Animals↗
PubMedDate not supplied

Interactions of the third component of human complement (C3) with tumour cells: evidence for presence of C3b acceptor sites and direct activation of C3 by tumour cells.

The interaction of C3 with different tumour cell lines was investigated. Our results indicated that nearly all the cell lines had C3b acceptors on their membranes. The binding of C3b was visualized by the detection of this protein on the cell surface with fluoresceinated anti-C3c serum. The involvement of proteases in the activation of C3 was demonstrated: complement-membrane fluorescence occurred in the presence of EDTA but was completely abolished with epsilon-aminocaproic acid. Experiments performed with purified C3 led to the conclusion that the protease activity might be the initial event for the activation of the alternative pathway by tumour cells.

Burkitt Lymphoma↗
PubMedDate not supplied

Sensitive one-step haemolytic assays of the fourth (C4) and fifth (C5) components of the human complement system.

In this paper, we describe two simple "one-step" methods to assay the C4 and C5 haemolytic activities of human complement. These methods required fresh normal sera immunochemically depleted of C4 or C5 components of the complement system. These sera, called R4 and R5 respectively, were prepared by affinity chromatography on monospecific anti-C4 Sepharose-4B or monospecific anti-C5 Sepharose-4B. Resins were washed with high-ionic strength solution containing 20% saccharose, which gave this method a very high specificity. These reagents were successfully used in the detection and quantification of C4 and C5 in all preparation steps as well as in normal and pathological sera. Two different kinds of haemolytic assays were developed and optimized: a haemolytic tube assay and a haemolytic agarose plate assay.

Complement C4↗
PubMedDate not supplied

Anti-alpha chain monoclonal antibodies of equine MHC class-II antigens: applications to equine infectious anaemia.

This paper describes the characteristics of a monoclonal antibody (mAb), 6B11C3, that recognises most equine monocytic cells, as well as B- and T-lymphocytes. The T CD4+ and T CD8+ of this latter population are also stained by the 6B11C3 mAb. On the basis of the distribution of membrane antigens on these cell populations, and of immunohistochemistry results, this mAb appears to be an anti-equine class-II major histocompatibility complex (MHC) antigen. In horses, the hyperexpression of the MHC class-II antigen on T cells is an indication of activated lymphocytes. A decrease in the percentage of lymphocytes stained by 6B11C3 was observed in horses with persistent equine infectious anaemia.

Animals↗
PubMedDate not supplied

Partial deficiency of the fourth component of human complement (C4) and autoantibody directed against C4 in a patient with SLE.

The finding of dramatically depressed levels of C4 in a 17-year old patient with severe systemic lupus erythematosus (SLE) prompted a genetic study of her family. This study revealed the existence of a partial C4 deficiency; we found the presence of a C4A3,C4BQo haplotype which was transmitted by the mother to each of her children. This patient possessed, in her serum, an autoantibody with anti-C4 specificity. The immunochemical characterization of this autoantibody revealed that it was IgM and belonged to the immunoconglutinin family. We have studied the effects of this autoantibody on the formation and dissociation kinetics of classical C3-convertase.

Adolescent↗
PubMedDate not supplied

[Ocular symptoms in pituitary adenomas (author's transl)].

The study of 85 patients suffering from pituitary adenoma, amongst which 56 with a visual failure, allowed to show: 1) The importance of the functional loss a revealing sign of the disease (50% cases). 2) The importance of the ophthalmological examination as a diagnostic argument. The latter, however, needs an extremely methodical examination of the visual fields. The combinated use of the Goldman Perimeter, and the Amsler schemes gave us satisfactory results: 87.5% of patent bitemporal hemianopsiae. It has been useful, in several cases to enhance these methodes by using coloured indexes. All of the patients underwent surgery, with complementary radiotherapy. The functional recovery quality has been shown, in the majority of the cases, to be proportionnal to the operation precocity in relation to the first functional symptoms.

Adenoma↗
PubMedDate not supplied

[Two new peptic fragments of human IgA: F(abc)'2Alpha and [F(abc)'2]2alpha (author's transl)].

These experiments were undertaken to study the nature of the fragments produced by pepsin digestion of seric IgA. We describe a new fragment with a MW of 140,000 daltons. This fragment, the first produced during pepsin hydrolysis of monomeric IgA, corresponds to an IgA molecule which has lost its CH3 domain. We propose to call this fragment F(abc)'2alpha. It is gradually digested and transformed into an F(ab)'2alpha fragment. When polymeric IgA are digested, an extra fragment with a MW of 290,000 daltons is produced, which has kept its polymeric structure. It corresponds to a covalent [F(abc)'2]2alpha fragment. These findings suggest that there is an intersubunit disulfide bridge in the Calpha2 domain. These results also indicate that polymeric IgA proteins are more resistant to pepsin digestion than monomeric IgA proteins.

Humans↗
PubMedDate not supplied

A study of the breakdown of the third component of human complement (C3).

This paper reports the description of fragments of human C3, purified from aged sera. Sera were incubated at different temperatures (4 degrees, 20 degrees and 37 degrees C) for 8 days or more. At 4 degrees C, the major isolated fragment was C3b which showed a heterogeneity of structure. Under reducing conditions, it liberated a 40,000 dalton fragment which reacted against an anti-C3d and which we called "C3d-like". At 20 degrees C, C3b was partially destroyed to yield the C3c- and C3d-fragments. At 37 degrees C, C3d and C3c were obtained. C3c presented a structural heterogeneity. It was made either of two chains of 75,000 daltons or of three chains with 75,000, 38,000 and 31,000 dalton MW. The comparison of these fragments with those obtained by tryptic hydrolysis led us to propose a pathway to the degradation of C3 and to bring some informations about the structure of this molecule.

Complement C3↗