Distribution of β2 microglobulin and HLA in chorionic villi of human placentae

Faulk, W. Pagé; Temple, Anne

doi:10.1038/262799a0

Cited by 228 publications

(74 citation statements)

References 17 publications

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“…As such, it is a hemiallogeneic graft with respect to the mother but is not rejected, an immunological paradox first pointed out by Medawar in 1953 (1). Twenty-five years later it was discovered that the highly polymorphic class I MHC molecules histocompatibility leukocyte antigen (HLA)-A and -B, potentially the primary immunological obstacle to successful pregnancy, are not expressed on the extraembryonic tissues in direct contact with maternal tissues (2). Villous cytotrophoblasts and syncytiotrophoblasts, which are in direct contact with maternal blood in the intervillous space, express neither class I nor class II MHC molecules.…”

mentioning

confidence: 99%

HLA-G homodimer-induced cytokine secretion through HLA-G receptors on human decidual macrophages and natural killer cells

Houser²,

Nicotra³

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

177

150

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Human decidual CD14 ؉ macrophages and CD56 ؉ NK cells were isolated from material obtained after first-trimester pregnancy terminations. Each cell type expressed a specific surface receptor for histocompatibility leukocyte antigen (HLA)-G (an MHC class Ib protein that is expressed on extravillous trophoblasts), LILRB1 on CD14 ؉ macrophages and KIR2DL4 on CD56 ؉ NK cells. Cross-linking with anti-LILRB1 or anti-KIR2DL4 resulted in up-regulation of a small subset of mRNAs including those for IL-6, IL-8, and TNF␣ detected using a microarray representing 114 cytokines. Incubation with transfectants expressing the HLA-G homodimer (but not with transfectants expressing the HLA-G monomer) resulted in secretion of the same cytokine proteins from both leukocyte sets. Moreover, cytokine secretion from both leukocyte sets was blocked by both the appropriate anti-receptor mAb and by anti-HLA-G. The amount of these cytokines secreted by decidual macrophages was substantially greater than that secreted by decidual NK cells. VEGF was constitutively secreted by both cell types. LILRB1, which contains an immunoreceptor tyrosine-based switch motif, functions here as an activating receptor, although it has been known as an inhibitory receptor. KIR2DL4 also functions as an activating receptor, although it also has the potential to function as an inhibitory receptor. Secretion of proinflammatory and proangiogenic proteins supports a role for these leukocytes in important processes that are essential for successful pregnancy, but they may represent only a portion of the proteins that are secreted.IL-6 ͉ IL-8 ͉ pregnancy ͉ trophoblast ͉ VEGF

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mentioning

confidence: 99%

HLA-G homodimer-induced cytokine secretion through HLA-G receptors on human decidual macrophages and natural killer cells

Houser²,

Nicotra³

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

177

150

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“…Thus, no preferential suppression of the paternal haplotype was observed. The relative-labeling intensities (as given by the median grain count of labeled cells per unit area of 64 #m 2) of individual H-2 antigens were very similar for 14-and 16- In the case of human trophoblasts most studies have been unable to detect HLA (10,11,18,23). Whether they are due to technical limitations or represent a real phenomenon is an open question.…”

Section: Examination Of Anti-paternal Antibodies In Maternal Serummentioning

confidence: 95%

“…The question of the presence or absence of histocompatibility antigens on trophoblast-cell surface still remains a highly controversial issue, as indicated by apparently conflicting data from different laboratories (10,11,(18)(19)(20)(21)(22)(23). Variation in technical sensitivity, as well as a lack of precise identification of the antigen-bearing placental cells in question may account for some of the discrepancies.…”

mentioning

confidence: 98%

“…The various hypotheses that have been forwarded to explain this phenomenon include the following (a) the uterus is an immunologically privileged site (1), (b) there is a general depression of the maternal immune functions possibly resulting from pregnancy-associated humoral factors and hormones (2)(3)(4)(5), (c) a neutral barrier existing at the fetomaternal tissue interface prevents immune interactions between the maternal and fetally-derived cells (6)(7)(8), (d) histocompatibility antigens are absent from the surface of placental trophoblast cells that remain in direct contact with maternal blood (9)(10)(11), (e) there is a blocking of the effector arm of the maternal immune response by noncytotoxic antibodies or antigen-antibody complexes (12,13).…”

mentioning

confidence: 99%

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Localization of H-2 antigens on mouse trophoblast cells.

Chatterjee‐Hasrouni¹,

Lala²

1979

The Journal of Experimental Medicine

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The presence of H-2 antigens of the paternal and maternal haplotypes on mouse trophoblast cells was examined at several stages of pregnancy by using a sensitive immunolabeling technique followed by quantitative radioautography. Results revealed the presence of H-2 antigens (determined by the K or D loci) of both parental haplotypes on the F1 trophoblast cells. At 14-16 d of gestation, the antigen density was equivalent to that on adult thymocytes and there was a further 50% increase on day 18. H-2 antigens of both parental haplotypes are also found to be expressed on 11-13 d trophoblast cells.

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“…Statistical significance was determined by analysis of variance. **, p Յ 0.01; ***, p Յ 0.001. and abetted in trophoblasts by the lack of expression of major histocompatibility complex antigens which present peptides to CD8ϩ cytotoxic T cells (49); the expression of nonclassical, nonpolymorphic HLA-G which inhibits natural killer cells (50,51); the dominance of the type 2 T-helper cells over type 1 T-helper cells (52); the immunosuppressive effect of induced prostaglandin E 2 (53); and induction of apoptosis in Fas-bearing activated lymphocytes by placental expression of Fas ligand (54,55). Similarly, for neoplasms, continued subversion of host surveillance may involve a deficiency or lack of expression of major histocompatibility complex antigens (56,57); dysregulation between HLA class I antigen expression and natural killer cell activity (58); an expansion in type 2 T-helper cells and a malfunction in type 1 T-helper cells (59,60); enhanced production of prostaglandin E 2 (61,62); and neoplastic expression of Fas-ligand (63,64).…”

Section: Figmentioning

confidence: 99%