Mahdi Alimoradi Fard; Mehri Ghafourian; Abdolah Mousavi-Salehi; Farideh Moramazi; Nastaran Ranjbari
Abstract
Background: Endometriosis is a medical condition that can cause infertility in women. Women with endometriosis experience a decrease in NK cell cytotoxic activity against endometrial cells, ultimately contributing to the spread of these cells.Objective: To assess the frequency of NK cells and the expression ...
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Background: Endometriosis is a medical condition that can cause infertility in women. Women with endometriosis experience a decrease in NK cell cytotoxic activity against endometrial cells, ultimately contributing to the spread of these cells.Objective: To assess the frequency of NK cells and the expression of the NKP46 receptor in endometrial tissue from patients with endometriosis using immunohistochemistry.Methods: 30 endometrial tissue specimens were collected from three groups of cases with mild (n=11), moderate (n=10), and severe endometriosis (n=9), respectively. Additionally, 20 normal endometrial tissue specimens were collected as the control group. Immunohistochemical staining was carried out using specific human monoclonal antibodies against CD56 and NKP46 molecules.Results: Cases with severe endometriosis had a significantly higher number of CD56+ uterine NK cells (26.19±2.50) compared to fertile women (15.02±0.622) and women with mild to moderate endometriosis (p<0.001). However, there was no significant difference between the mild to moderate patients compared with the healthy women (p>0.05). Endometrial NKp46 expression was lower in women with severe endometriosis (0.447±0.0829) compared to fertile women (0.987±0.115, p=0.03). The NKp46+/CD56+ cell ratio was also lower in women with severe endometriosis (0.019±0.003) compared to fertile women (0.072±0.011, p=0.01).Conclusion: Women with severe endometriosis demonstrated an increased rate of infiltrated uterine NK cells and a significant decrease in NKP46 expression compared to fertile women. Therefore, NK cells and the NKp46 receptor may be involved in the development of endometriosis.
Abdolah Mousavi Salehi; Mehri Ghafourian; Afshin Amari; Mahvash Zargar
Abstract
Background: Women afflicted with recurrent spontaneous abortion (RSA) and repeated implantation failure (RIF) may have immune abnormalities. The role of vitamin D has been demonstrated in the function of the immune system. Objective: To assess the percentage and function of CD3+ T cells and their ...
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Background: Women afflicted with recurrent spontaneous abortion (RSA) and repeated implantation failure (RIF) may have immune abnormalities. The role of vitamin D has been demonstrated in the function of the immune system. Objective: To assess the percentage and function of CD3+ T cells and their relationship with the level of the serum vitamin D or 1,25-dihydroxy vitamin D3 (the active form of the vitamin) in women with RSA and RIF. Methods: In this case-control study, peripheral blood was obtained from the patient and the healthy control groups. The ratio of CD3+T cell and activated CD3+ CD69+T cell was investigated using flow cytometry. The serum levels of Interferon-γ (IFN-γ) and vitamin D were measured by ELISA. Results: The mean proportion of CD3+T cells in women with RSA increased significantly compared with the healthy control group (p<0.04). However, no significant difference was observed in RIF women compared with the control group. There was no significant difference in the ratio of activated CD3+CD69+T cells between the patient and the healthy control groups. Serum IFN-γ levels in women with RSA showed a significant increase compared to the control group (p<0.031); however, no significant difference was observed between women with RIF and the control group. Serum levels of vitamin D showed a significant reduction in both RSA (p<0.01) and RIF (p<0.04) groups in comparison with the control. Conclusion: An increase in the percentage and inflammatory function of T cells was associated with RSA. Decreased vitamin D levels may contribute to immune dysfunction and pregnancy loss.
Nahid Daraei; Mehri Ghafourian; Ata Ghadiri; Afshin Amari; Mahin Najafian; Saber Rokhafrooz
Abstract
Background: The development of a maternal immune response to fetal antigens and deficiency in regulatory T-cells (Tregs) may lead to preeclampsia. A plausible explanation for the reduced Treg cell function in women with preeclampsia is the presence of exhausted Treg cells which express CD279 or programmed ...
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Background: The development of a maternal immune response to fetal antigens and deficiency in regulatory T-cells (Tregs) may lead to preeclampsia. A plausible explanation for the reduced Treg cell function in women with preeclampsia is the presence of exhausted Treg cells which express CD279 or programmed cell death receptor-1 (PD-1), a negative regulatory molecule associated with limited proliferative capacity and reduced immune suppression. Objective: To assess the number of Treg CD4+ CD25high and exhausted Treg CD4+ CD25high CD279+ cells in women with preeclampsia (PE group) and healthy pregnant women (HP group) during the third trimester of pregnancy. Methods: Three-color flow cytometry was used to determine the proportion of Treg and exhausted Treg cells in 40 women in the PE group and 37 women in the HP group. Participants’ blood samples were placed in EDTA blood collection tubes. Peripheral mononuclear cells were separated from the samples and stained with flurochrome-conjugated antibodies against human CD4, CD25 and CD279 markers, and subsequently analyzed by flow cytometry. Results: The PE group had fewer Tregs compared to the HP group (p=0.011). There was a significant increase in the percentage of exhausted PD-1+(CD279) Tregs (p=0.035) in the PE group comparisons with the HP group. Conclusion: The increased number of PD-1 (CD279) molecules on the Treg cells may play a role in preeclampsia, hence it recommendation as a therapeutic target for the disease.
