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M E Roux

Publications and source records attributed to M E Roux.

At least 37 records · Page 2Linked to original sources
PubMed1992

[Familial amyloidosis].

Familial amyloidosis is characterized by its great clinical and genetic heterogeneity. The most frequent form is amyloidotic neuropathy which may be due to deposits of several amyloid proteins, such as transthyretin, apolipoprotein A1 and gelsolin. Other varieties include predominant lesions of another organ, such as kidney, heart, eye or skin. In most of these lesions, a punctual mutation affects the amyloid protein itself. In other varieties, the amyloid protein is not affected by mutation and, rarely, unknown. The advances achieved in our understanding of transthyretin deposition should improve our knowledge of amyloidosis in general.

Adult↗
PubMed1989

Impaired differentiation of Ig A-B cell precursors in the Peyer's patches of protein depleted rats.

The aim of this study has been set on Ig A plasma cell precursors that are found in the Peyer's patches. In a previous work it has been shown that protein deficiency at weaning led to the presence in the Peyer's patch of very immature B cells, mostly cu+ su- cells. In this report we demonstrate the c mu+ s mu- cells comprise a (c mu OX7)+ s mu- cell population that is predominant in the protein-deprived rats (41.5 versus 16.8 in 39 day-old control rats). Protein refeeding reinitiates the differentiation as follows: (a) the (c mu OX7)+ s mu- cell population was able to differentiate to (cs mu+ as in the normal Peyer's patch (53.6 versus 44.9 in 39 day-old control rats); (b) the switching of sIg M-bearing cells to sIg A-bearing cells occurs in a restricted pattern; only 27.9 versus 47.6 in the 60 day-old control rats; (c) concomitantly, protein-refed rats showed a low absolute number of W3/13+ and W3/25+ T cells. Therefore, this experimental model of immunodeficiency provides further evidence that specialized T helper cells or their soluble factors are needed for Ig A-B cell differentiation "in vivo."

Animals↗
PubMed1989

[The lymphoid system and protein deficiency. Differentiation in the thymus and Peyer's patches].

A: Thymuses from protein deprived rats present: 1) a significant decrease in the absolute number of thymic cells bearing the CD5 phenotype (OX19+), as well as Thy 1.1 (OX7+). The predominant cell population was the one containing TdT (terminal deoxynucleotidyl transferase) as a sole marker: 2) in severely protein deprived rats followed by refeeding during 9 and 21 days, the existence of a small population of cells containing TdT as a sole marker. The TdT+W3/13+ cell population was restored but the CD4+ subpopulation (W3/25+) exists in lower numbers than in the age-matched controls. B: Severe protein deficiency at weaning, led to the presence in the Peyer's patches of very immature B-cells mostly c mu+OX7s mu-. Protein refeeding reinitiated the differentiation process as follows: 1) c mu+OX7+s mu- c mu-OX7-s mu+ as in the normal Peyer's patches; 2) however, switching of sIgM to sIgA-bearing cells was altered; 3) a low absolute number of W3/13+ and W3/25+ T-cells (CD4+) was found. C: Oral tolerance to dextrin evolved due to antigen specific CD8+ T-cells (found in Peyer's patches, mesenteric lymph nodes and spleen) and could be transferred to normal recipients.

Animals↗
PubMed1988

T and B lymphocyte populations in uterus draining lymph nodes at estrus and diestrus in Wistar rats.

In this paper, data are presented on the characterization of uterus draining lymph nodes (UDLN) B and T lymphocytes of virgin rats at estrus (E) and diestrus (D). We established that the T/B lymphocyte relationship in the UDLN is less than one at estrus and more than one at diestrus. This is due to a decrease in the percentage and in the total number of mature T cell population in association with a decrease in the percentage of the OX8 subset in the UDLN at estrus. This situation may be related to an increase in estrogens known to produce thymic involution. These changes were not observed when we studied peripheral (popliteal) lymph nodes. The changes observed in the UDLN T cell population at estrus could be under hormonal control and we think that this condition may be important to prepare the immune system for an eventual pregnancy.

Animals↗
PubMed1987

Hypothesis on the time course of antigen dependent changes in lymphoid organs proved by experimental data of depleted growing rats' mesenteric lymph nodes.

The results described in this paper partially agree with the hypothesis that mesenteric lymph nodes (MLN) of depleted growing rats recover their antigen specific determinants after the oral administration of 20% casein for 5-9 days following the time course of antigen dependent changes observed in virgin lymph nodes. With respect to the 39 days old control group, depleted MLN showed a highly diminished number of mature T cells (W3/13+) as well as surface and intracellular alpha heavy chain (alpha s and alpha cit). The oral administration of a 20% casein diet during 5 days tends to restore the appearance of these determinants; however, normal values were not attained even if refeeding was continued for 9 days. The discrepancy between the proposed hypothesis and the observed results might be ascribed to: a) defective migration of T cells from thymus; b) the diminished number of TH cells involved in terminal differentiation; c) inability of B cells to respond to T cell-derived factors.

Animals↗
PubMed1979

Organ and isotype distribution of plasma cells producing specific antibody after oral immunization: evidence for a generalized secretory immune system.

Mice were induced to produce IgA antibodies against ferritin after oral immunization. Such antibodies were detected by immunofluorescence in plasma cells in the intestinal mucosa as well as in secretory sites located elsewhere, such as the lactating mammary gland, salivary gland, and respiratory tract. The observation suggested that cells immunized locally via the gut could home to distant secretory sites. To confirm this hypothesis, lymphocyte transfer studies were done with mesenteric node (MN) versus peripheral node (PN) cells from orally immunized donors into nonimmunized recipients. IgA anti-ferritin cells from MN homed to exocrine targets, whereas IgM and IgG anti-ferritin cells homed to PN. The findings overall support the concept of a generalized and interrelated secretory immune system.

Animals↗
PubMed1978

Development of the IgA system in the mammary gland.

1) Lymphoblasts in gut-associated lymphoid tissue, committed to the production of IgA, can home to the mammary glands of syngeneic mice and differentiate there into IgA-containing plasmablasts. The phenomenon is limited to near term and lactating recipients. 2) The ability of lymphocytes originating in gut-associated lymphoid tissue and sensitized to intestinal antigens to migrate to the mammary gland can account for the specificity of milk IgA toward intestinal microorganisms and the consequent passive protection offered to suckling infants. 3) The secretory immune system of the mammary gland is apparently under hormonal control since mammotropic hormones given to virgin females can induce morphological and functional characteristics seen naturally only during pregnancy and lactation. Examples are increased numbers of IgA plasma cells and the ability to trap their circulating precursors taken from mesenteric lymph nodes.

Animals↗
PubMed1978

Hormonal induction of the secretory immune system in the mammary gland.

The secretory immune system of the mammary gland is undeveloped in virgin mice but becomes active at term and during lactation. This change appears to depend on migration to the mammary gland of precursors of IgA-secreting cells derived from the gut-associated lymphoid tissue, an origin which explains the specificity of milk IgA antibodies for enteric organisms. Because development of the epithelial components of the mammary gland is clearly under hormonal control, we examined the effect of mammotropic hormones on differentiation of the immune elements. Under a combined regimen of progesterone, estrogen, and prolactin, development of the glandular epithelium occurs with concomitant increments in the number of IgA-secreting plasma cells and amount of intraepithelial IgA. These increases appear to be due to enhanced capacity of the gland to attract or retain precursors of IgA plasma cells derived from gut-associated lymphoid tissue. Testosterone, which antagonizes lactation, also antagonizes development of the secretory immune system and decreases cellular trapping in the lactating gland. The ability of the gland to trap IgA immunoblasts is probably contingent upon a hormone-induced increase in receptors.

Animals↗
PubMed1977

Origin of IgA-secreting plasma cells in the mammary gland.

Lymphoblasts from the mesenteric lymph nodes (MN) of mice home to the mammary glands of syngeneic recipients late in pregnancy and during lactation, and within hours of transfer most can be shown to contain IgA. Homing does not occur in virgins, in early pregnancy, or after weaning. Homing MN lymphoblasts are sensitive to antiserum to IgA plus complement, but not to other class-specific antisera. Thus, lymphoblasts in MN with the potential to home to the mammary gland are already committed to IgA synthesis and bear surface IgA before reaching their destination. These results explain observations, made by others, of specific IgA antibodies and IgA plasma cells in milk and colostrum after oral immunization. Under natural conditions it is likely that IgA precursor cells, after stimulation in the gut-associated lymphoid tissue by intestinal antigens, migrate to the mammary gland where they secrete antibodies which constitute an important defense mechanism of the newborn. In the absence of lactation, these cells probably form part of the normal traffic to the lamina propria of the small intestine.

Animals↗
PubMed1977

Plasma cells and epithelial immunoglobulins in the mouse mammary gland during pregnancy and lactation.

Mammary glands of virgin, pregnant, lactating, and post-weaning CAF1 mice were studied by immunofluorescence for epithelial immunoglobulins and stromal plasma cells. In normal virgins, both females and males, only occasional plasma cells and but scanty intraepithelial immunoglobulins were present. During pregnancy and the early days of lactation, an increase in the number of plasma cells occurs, and by 1 week of lactation, there is a marked increase in the number, and most are synthesizing IgA. This increment parallels the development and proliferation of the glandular epithelium, in anatomical relation to which the plasma cells are observed. The intraepithelial content of IgA is also maximal when the glandular epithelium is most developed. These findings are consistent with a local production of the IgA in milk. Weaning, or deliberate interruption of suckling for more than 10 days results in a sheep decrease in the number of IgA plasma cells and an involution of the epithelium, whose content of immunoglobulin also declines. The changes in the secretory IgA system which occur locally during lactation are thought to be hormone-dependent.

Animals↗
PubMed1976

Clonal dominance and the preservation of clonal memory cells mediated by antigen-antibody.

Selected B-cell clones and their well characterized monoclonal antibody products were used to analyse the role of antibody in clonal dominance and the regulation of memory cell supplies. The experimental design was to permit contact between spleen cells and antigen in vitro, and to administer antibody to DNP prior to or following cell transfers into irradiated recipients. The anti-hapten response was strongly suppressed by the clone's own antibody or higher affinity antibody administered on day 0. Antigen-antibody inhibited memory cell generation. The suppressive effect was temporary, and reversible with time and further antigen and the same clone could be induced to produce antibody again, analysed by isoelectric focusing. We were therefore not dealing with clonal deletion. Change in the source of clonal anti-hapten excluded possible effects of antibody to carrier protein or idiotypic determinants in this system. The timing of antibody administration indicates that clones already triggered in the first 4 days after antigen contact could not be suppressed by antibody. Passive antibody to DNP only suppressed when both B and T cells had been permitted contact with hapten-carrier protein. Alteration of the carrier protein enabled us to study the effect of antigen-antibody on B and T cells separately. B cells binding antigen and antibody to hapten were triggered more efficiently by fresh T cells recognizing the carrier protein than after antigen uptake alone. Antibody to DNP suppressed only when both B and T cells had taken up hapten-protein, suggesting that antigen-antibody acts centrally at the level of both B memory cells and T helper cells. This reversible antigen-antibody blockade appears to favour the preservation of a pool of long-lived memory cells rather than the priming of new clones developing from short lived precursor cells; clonal dominance ensues.

Animals↗