Cord blood B cells are mature in their capacity to switch to IgE-producing cells in response to interleukin-4 <i>in vitro</i>

Pastorelli, G.; Rousset, F; Pène, Jérôme; Péronne, Catherine; Roncarolo, MG; Tovo, Pier-Angelo; Vries, J E de

doi:10.1111/j.1365-2249.1990.tb05413.x

Cited by 38 publications

(5 citation statements)

References 33 publications

(1 reference statement)

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“…These results provide evidence that the decreased GL activity in the cord blood lymphocytes may be due to functional immaturity which can be overcome with appropriate stimuli. Similar conclusions were also drawn by other investigators using different experimental approaches [35,36].…”

Section: Discussionsupporting

confidence: 79%

In vivo expression of human immunoglobulin germ-line mRNA in normal and in immunodeficient individuals

Islam

Baskin

Christensson

et al. 1994

Clinical and Experimental Immunology

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SUMMARYPrevious in vitro studies suggest that transcription of the unrearranged immunoglobulin switch region and its 5' flanking region precedes isotype switching. These [1][2][3][4][5][6][7][8][9][10][11][12]. The GL mRNA which lacks a variable region is formed by the direct splice of I region exon(s) to the constant region gene. According to the accessibility model for immunoglobulin class switching [2,3], alterations in the chromatin structure and transcriptional activity result in an accessible state in which the recombinatory machinery gets access to the genomic sequences involved in class switching. Recently, evidence for a functional role of the I-region has been obtained by

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Section: Discussionsupporting

confidence: 79%

In vivo expression of human immunoglobulin germ-line mRNA in normal and in immunodeficient individuals

Islam

Baskin

Christensson

et al. 1994

Clinical and Experimental Immunology

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“…No detectable levels of IL-4 were found in culture supernatants of cord blood cells after stimulation with mitogen, immobilized anti-CD3 antibody or combination of mitogen and the phorbol ester TPA [36][37][38], and no IL-4 gene transcription could be detected in activated cord blood T cells [37.38]. In one study, the production of both IFN-'y and I L-4 by activated cord blood cells was found to be absent (38].…”

Section: Discussionmentioning

confidence: 99%

High numbers of autoantigen-reactive mononuclear cells expressing interferon-gamma (IFN-γ), IL-4 and transforming growth factor-beta (TGF-β) are present in cord blood

Fredrikson

Link

et al. 1995

Clinical and Experimental Immunology

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SUMMARYUtnbilical cord blood of neonates and peripheral blood of healthy adults were analysed by in situ hybridization for numbers of mononuclear cells (MNC) expressing the cytokines IFN-7, TGF-/? and IL-4 mRNA without culture and after culture in the presence of acetylcholine receptor (AChR), myelin basic protein (MBP) and peripheral myelin protein P2. These antigens were chosen since they represent autoanljgens in putatively immune-mediated neurological diseases, The numbers of cells expressing cytokine mRNA after 72 h culture in the presence of AChR, MBP and P2 were higher in cord blood than in peripheral blood of healthy adults. IFN-7, TGF-^ and IL-4 were always elevated in parallel. In cord blood there was a pronounced reactivity to several of the lested antigens, while such broad reactivity was not found in peripheral blood of healthy adults. No differences in cytokine mRNA expression were found between cord blood and peripheral blood of adults when cells were analysed without culture. The results show a capacity of cord blood cells to react to several autoantigens by the up-regulation of cytokine mRNA expression.

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“…Despite the early burst of Ig production during fetal life, newborns have low quantities of IgM, IgA and IgE. The neonatal immune system responds to antigens mainly by producing IgM with low affinities (131). At birth, the majority of innate and adaptive cells are immature (132) but the immune system is functional and complete.…”

Section: Ontogeny Of the Human Immune System During Fetal Lifementioning

confidence: 99%

Relevance of the Materno-Fetal Interface for the Induction of Antigen-Specific Immune Tolerance

et al. 2020

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In humans, maternal IgGs are transferred to the fetus from the second trimester of pregnancy onwards. The transplacental delivery of maternal IgG is mediated by its binding to the neonatal Fc receptor (FcRn) after endocytosis by the syncytiotrophoblast. IgGs present in the maternal milk are also transferred to the newborn through the digestive epithelium upon binding to the FcRn. Importantly, the binding of IgGs to the FcRn is also responsible for the recycling of circulating IgGs that confers them with a long half-life. Maternally delivered IgG provides passive immunity to the newborn, for instance by conferring protective anti-flu or anti-pertussis toxin IgGs. It may, however, lead to the development of autoimmune manifestations when pathological autoantibodies from the mother cross the placenta and reach the circulation of the fetus. In recent years, strategies that exploit the transplacental delivery of antigen/IgG complexes or of Fc-fused proteins have been validated in mouse models of human diseases to impose antigen-specific tolerance, particularly in the case of Fc-fused factor VIII (FVIII) domains in hemophilia A mice or pre-pro-insulin (PPI) in the case of preclinical models of type 1 diabetes (T1D). The present review summarizes the mechanisms underlying the FcRn-mediated transcytosis of IgGs, the physiopathological relevance of this phenomenon, and the repercussion for drug delivery and shaping of the immune system during its ontogeny.

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Cord blood B cells are mature in their capacity to switch to IgE-producing cells in response to interleukin-4 in vitro

Cited by 38 publications

References 33 publications

In vivo expression of human immunoglobulin germ-line mRNA in normal and in immunodeficient individuals

In vivo expression of human immunoglobulin germ-line mRNA in normal and in immunodeficient individuals

High numbers of autoantigen-reactive mononuclear cells expressing interferon-gamma (IFN-γ), IL-4 and transforming growth factor-beta (TGF-β) are present in cord blood

Relevance of the Materno-Fetal Interface for the Induction of Antigen-Specific Immune Tolerance

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