HLA‐G: expression in human keratinocytes in vitro and in human skin in vivo

Abstract

Classical, polymorphic major histocompatibility complex class I molecules are expressed on most nucleated cells. They present peptides at the cell surface and, thus, enable the immune system to scan peptides for their antigenicity. The function of the other, nonclassical class I molecules in man is controversial. HLA-G which has been shown by transfection experiments to be expressed at the cell surface, is only transcribed in placental tissue and in the fetal eye. Therefore, a role of HLA-G in the control of rejection of the allogeneic fetus has been discussed. We found that HLA-G expression is induced in keratinocytes by culture in vitro. Three different alternative splicing products of HLA-G can be detected: a full length transcript, an mRNA lacking exon 3 and a transcript devoid of exon 3 and 4. Reverse transcription followed by polymerase chain reaction also revealed the presence of HLA-G mRNA in vivo in biopsies of either diseased or healthy skin.

Amniotic fluid soluble human leukocyte antigen-G in term and preterm parturition, and intra-amniotic infection/inflammation

“…[108] However, HLA-G expression can be induced in cancers,[109,110] organ transplant,[111] multiple sclerosis,[112] inflammatory diseases,[113,114] and viral infections. [115,116] The mRNA for HLA-G has been detected in several embryonic an adult tissues, including adult and fetal thymus,[117,118] fetal liver and eye,[56,119] adult spleen,[120] skin and keratinocytes,[121] but the protein has been reported to be restricted to trophoblast and choriocarcinoma cells. [92,122,123]…”

HLA-G protein up-regulation in primary cutaneous lymphomas is associated with interleukin-10 expression in large cell T-cell lymphomas and indolent B-cell lymphomas

“…23,24 We have shown the full-length HLA-G transcript in all of the samples, confirming that this is the most commonly transcribed HLA-G form in PBMCs and keratinocytes. 24,44 Only in situations in which the translation of the HLA-G1 protein is impaired (ie, individuals homozygous for the null allele HLA-G*0105N), the other shorter isoforms might serve as a "biological back-up" undertaking necessary HLA-G functions, although the HLA-G transcription and splicing are not affected. 45 Therefore, we have focused our quantitative PCR primarily on this isoform.…”

“…44 Because the lymphocytes are the predominant cell population within the lymphomatous lesions, the end PCR result is likely to reflect the transcription of the infiltrate rather than the one of solely active epidermal basal cell layer. On the other hand, observed significant case-to-case differences in HLA-G1 levels are probably reflecting the interindividual differences of patients, unique biology of the lesions, or various clinical stages of the disease.…”

HLA-G as a Tolerogenic Molecule in Transplantation and Pregnancy

“…It is also expressed by amnion epithelial cells [8, 9], erythroid, and endothelial cells of fetal blood vessels in the placenta [10, 11], as well as in the thymus [12], cornea [13], pancreas [14], and nail matrix [15]. Although marginal, the levels of HLA-G specific transcripts are found in nearly all tissues analysed, for example, fetal liver, myelomonocytic cells, fetal and adult eye tissue, skin and keratinocytes, and peripheral blood lymphocytes [16]. The latter can release substantial amounts of soluble HLA-G (sHLA-G) into the blood circulation [17–19].…”