Immune cell profiling in normal pregnancy, partial and complete molar pregnancy

Nagymanyoki, Zoltan; Callahan, Michael J.; Parast, Mana M.; Fülöp, Vilmos; Mok, Samuel C.; Berkowitz, Ross S.

doi:10.1016/j.ygyno.2007.06.028

Cited by 20 publications

(25 citation statements)

References 36 publications

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“…However, our result was based on a very limited GTN sample size. In another study, FoxP3 + Treg infiltration was significantly higher at the implantation site of HM (CM and PM) compared to the implantation site in NP, but they did not perform comparisons to CCA cases (7).…”

Section: Discussionmentioning

confidence: 96%

“…Although several studies have previously investigated the presence of immune cells in HM and CCA cases (7,(24)(25)(26), this was the first study to assess whether these particular immune and proliferative cells together may be useful markers for these cases.…”

Section: Discussionmentioning

confidence: 99%

“…It may be postulated that the high number of CD3 + T cells in the GTN, CM and PM groups was due to increased recruitment, local proliferation or increased turnover rates of these T cells in response to the molar trophoblasts (7). Another study that investigated the presence of CD3 + T cells in gestational trophoblastic diseases reported that the number of CD3 + T cells was high in HM and CCA cases, although it was not mentioned which type of HM was included in the study (24,25).…”

Section: Discussionmentioning

confidence: 99%

“…The level of aggressiveness varies according to mole type; they may lead to persistent disease or post-molar gestational trophoblastic neoplasia (GTN). Thus, HMs are considered the pre-cancerous lesions of GTN (3,7).…”

Section: Introductionmentioning

confidence: 99%

“…In contrast to CMs, PMs are generally triploid; PMs retain maternal chromosomes, but also have an excess set of paternal chromosomes. PMs result from fertilization of a normal haploid ovum (23X) by two haploid spermatozoa (3,4,7). In CMs, the complete allograft conceptus is expected to provoke a maternal immune response, with immune cell invasion leading to rejection.…”

Section: Introductionmentioning

confidence: 99%

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Decidual infiltration of FoxP3+ regulatory Tï¿½cells, CD3+ Tï¿½cells, CD56+ decidual natural killer cells and Ki-67 trophoblast cells in hydatidiform mole compared to normal and ectopic pregnancies

et al. 2011

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Abstract. Hydatidiform moles are considered pre-cancerous lesions of gestational trophoblastic neoplasia and are associated with an aberrant immune response. This preliminary study aimed to evaluate the feasibility of measuring the presence of immune cells as potential prognostic markers for hydatidiform moles. + trophoblast cells were highest in the gestational trophoblastic neoplasias (688/1,000 trophoblast cells) and lowest in the partial moles (87/1,000 trophoblast cells). Our results suggest that regulatory T cells may be involved in the progression of complete hydatidiform moles. A larger cohort study is required to assess whether immune cells are effective prognostic markers in gestational trophoblastic diseases. IntroductionHydatidiform moles (HM) or molar pregnancy is a unique entity among gestational trophoblastic diseases (GTDs), characterized by abnormal proliferation of placental trophoblasts accompanied by an excess of paternal genes. This pathological form of pregnancy persists until the 1st trimester before clinical symptoms become evident (1-4). The incidence of HM is highest in Asian countries and comparatively low in Western countries (5,6). HM appears as complete moles (CM) or partial moles (PM), based on histopathological features and karyotypes that confer the potential for local invasion and widespread metastasis. The level of aggressiveness varies according to mole type; they may lead to persistent disease or post-molar gestational trophoblastic neoplasia (GTN). Thus, HMs are considered the pre-cancerous lesions of GTN (3,7).Most CMs are cytogenetically diploid with a 46XX karyotype. Both sets of chromosomes are of paternal origin, since the CM results from fertilization of an empty ovum by a haploid (23X) spermatozoa; alternatively, dispermic CMs develop from an empty ovum fertilized by two haploid (23X and/or 23Y) spermatozoa. Both types of CMs are totally paternally derived and represent a complete intrauterine allograft in the mother. In contrast to CMs, PMs are generally triploid; PMs retain maternal chromosomes, but also have an excess set of paternal chromosomes. PMs result from fertilization of a normal haploid ovum (23X) by two haploid spermatozoa (3,4,7). In CMs, the complete allograft conceptus is expected to provoke a maternal immune response, with immune cell invasion leading to rejection. PMs may also provoke an altered immune response compared to normal pregnancy (NP), due to the excess paternal genetic material.Ectopic pregnancy (EP) is another type of first trimester abnormal pregnancy. It is the most common early pregnancy

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Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%