Mariagiulia Spazzapan, Silvia Pegoraro, C. Agostinis, R. Bulla
The complement component C1q plays a role as a pro-angiogenic factor in different contexts, acting in a complement-independent way. For example, this molecule is able to foster the remodeling of the spiral arteries for a physiological pregnancy and to promote the wound healing process. It is also involved in angiogenesis after post-stroke ischemia. Furthermore, it has a role in supporting the tumor vessel growth. Given its role in promoting angiogenesis both under physiological and pathological situations, other studies are needed to understand its potential therapeutic implications.
{"title":"The role of complement component C1q in angiogenesis","authors":"Mariagiulia Spazzapan, Silvia Pegoraro, C. Agostinis, R. Bulla","doi":"10.37349/ei.2023.00122","DOIUrl":"https://doi.org/10.37349/ei.2023.00122","url":null,"abstract":"The complement component C1q plays a role as a pro-angiogenic factor in different contexts, acting in a complement-independent way. For example, this molecule is able to foster the remodeling of the spiral arteries for a physiological pregnancy and to promote the wound healing process. It is also involved in angiogenesis after post-stroke ischemia. Furthermore, it has a role in supporting the tumor vessel growth. Given its role in promoting angiogenesis both under physiological and pathological situations, other studies are needed to understand its potential therapeutic implications.","PeriodicalId":93552,"journal":{"name":"Exploration of immunology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138971554","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
L. Karalashvili, D. Chakhunashvili, M. Kakabadze, T. Paresishvili, Zurab Kakabadze
Aim: Non-healing wounds are one of the most substantial and difficult problems to treat. Wound healing involves a sequence of complex biological processes, but often the oral cavity microbiota adversely affects healing and forms a chronic non-healing wound. Methods: In this study, a biologically active membrane (BAM) is present, consisting of decellularized human amniotic membrane and bone marrow stem cells (BMSCs). The efficacy of BAM was evaluated in a model of non-healing oral wounds in rats with streptozotocin (STZ)-induced diabetes mellitus. Results: Studies have shown that BAM enhanced the healing of chronic oral wounds in animals with induced diabetes mellitus, reduced scarring, and reduced risk of infection. Paracrine freeze-dried BMSCs stimulated angiogenesis and improved wound conditions. Conclusions: BMSCs may lower glucose levels in rats with STZ-induced diabetes mellitus and improve the healing process of chronic diseases. However, more studies are needed to study the paracrine factors of BMSCs and their role in the treatment of non-healing wounds.
{"title":"Treatment of a non-healing oral wound in diabetic-induced rats","authors":"L. Karalashvili, D. Chakhunashvili, M. Kakabadze, T. Paresishvili, Zurab Kakabadze","doi":"10.37349/ei.2023.00121","DOIUrl":"https://doi.org/10.37349/ei.2023.00121","url":null,"abstract":"Aim: Non-healing wounds are one of the most substantial and difficult problems to treat. Wound healing involves a sequence of complex biological processes, but often the oral cavity microbiota adversely affects healing and forms a chronic non-healing wound. Methods: In this study, a biologically active membrane (BAM) is present, consisting of decellularized human amniotic membrane and bone marrow stem cells (BMSCs). The efficacy of BAM was evaluated in a model of non-healing oral wounds in rats with streptozotocin (STZ)-induced diabetes mellitus. Results: Studies have shown that BAM enhanced the healing of chronic oral wounds in animals with induced diabetes mellitus, reduced scarring, and reduced risk of infection. Paracrine freeze-dried BMSCs stimulated angiogenesis and improved wound conditions. Conclusions: BMSCs may lower glucose levels in rats with STZ-induced diabetes mellitus and improve the healing process of chronic diseases. However, more studies are needed to study the paracrine factors of BMSCs and their role in the treatment of non-healing wounds.","PeriodicalId":93552,"journal":{"name":"Exploration of immunology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-12-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138588310","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Tiffany Pascreau, Sara Zia-Chahabi, T. Andriamandimbisoa, Marc Vasse
Protein Z (PZ) is a vitamin K-dependent protein that acts as a cofactor for the inhibition of activated factor X by the PZ-dependent protease inhibitor, an anticoagulant protein of the serpin superfamily. The presence of antibodies against PZ (aPZ-Abs) was first described in women with unexplained recurrent embryo loss, pre-eclampsia, or foetal death, independently from habitual antiphospholipid/anti-cofactor antibodies. Other studies suggested that aPZ-Ab could be associated with a small birthweight for the gestational age. The mechanism of action of these antibodies is not yet understood. At this time, even aPZ-Abs are frequently observed in patients with lupus anticoagulant or anticardiolipin antibodies, there is no evidence that aPZ-Abs increase systemic venous or arterial thrombotic risk. The comparison of the various published studies shows that the threshold suggesting an obstetric risk is not clearly defined. At present, it is not known whether one isotype of immunoglobulin (G or M, or both) is particularly involved in certain obstetric manifestations, or these antibodies persist during time, or can be induced by infectious diseases. Consequently, detection of these antibodies is not routinely warranted and should only be performed in randomized clinical trials.
{"title":"An update on anti-protein Z antibodies","authors":"Tiffany Pascreau, Sara Zia-Chahabi, T. Andriamandimbisoa, Marc Vasse","doi":"10.37349/ei.2023.00120","DOIUrl":"https://doi.org/10.37349/ei.2023.00120","url":null,"abstract":"Protein Z (PZ) is a vitamin K-dependent protein that acts as a cofactor for the inhibition of activated factor X by the PZ-dependent protease inhibitor, an anticoagulant protein of the serpin superfamily. The presence of antibodies against PZ (aPZ-Abs) was first described in women with unexplained recurrent embryo loss, pre-eclampsia, or foetal death, independently from habitual antiphospholipid/anti-cofactor antibodies. Other studies suggested that aPZ-Ab could be associated with a small birthweight for the gestational age. The mechanism of action of these antibodies is not yet understood. At this time, even aPZ-Abs are frequently observed in patients with lupus anticoagulant or anticardiolipin antibodies, there is no evidence that aPZ-Abs increase systemic venous or arterial thrombotic risk. The comparison of the various published studies shows that the threshold suggesting an obstetric risk is not clearly defined. At present, it is not known whether one isotype of immunoglobulin (G or M, or both) is particularly involved in certain obstetric manifestations, or these antibodies persist during time, or can be induced by infectious diseases. Consequently, detection of these antibodies is not routinely warranted and should only be performed in randomized clinical trials.","PeriodicalId":93552,"journal":{"name":"Exploration of immunology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138599147","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Since 2019, notable global viral outbreaks have occurred necessitating further research and healthcare system investigations. Following the coronavirus disease 2019 (COVID-19) pandemic, in 2022, whilst severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) strains evolved, monkeypox virus (MPXV) infections became more evident. MPXV is of the Orthopoxviridae genus, belonging to the family Poxviridae. Zoonotic transmission (animal-to-human transmission) may occur. The Orthopoxviridae genus includes other orthopoxviruses (OPXVs) present in animal host reservoirs that include cowpox viruses (CPXVs), vaccinia virus (VACV), and variola virus (VARV), with the latter being a causal agent of smallpox and excessive mortality. This review aims to present facts about MPXV-specific pathogenesis, epidemiology, and immunology alongside historical perspectives. MPXV was rarely reported outside Africa before April 2000. Early research since 1796 contributed towards the eradication of VARV leading to immunisation strategies. The World Health Organisation (WHO) announcement that VARV had been eradicated was confirmed in 1980. On the 23rd of July 2022, the WHO announced MPXV as a health emergency. Therefore, concern due to the propagation of MPXV causing monkeypox (mpox) disease requires clarity. Infected hosts display symptoms like extensive cellular-initiated rashes and lesions. Infection with MPXV makes it difficult to differentiate from other diseases or skin conditions. Antiviral therapeutic drugs were typically prescribed for smallpox and mpox disease; however, the molecular and immunological mechanisms with cellular changes remain of interest. Furthermore, no official authorized treatment exists for mpox disease. Some humans across the globe may be considered at risk. Historically, presenting symptoms of mpox resemble other viral diseases. Symptoms include rashes or lesions like Streptococcus, but also human herpes viruses (HHVs), including Varicella zoster virus (VZV).
{"title":"Immunopathogenesis of Orthopoxviridae: insights into immunology from smallpox to monkeypox (mpox)","authors":"Brent Brown, Ingo Fricke, Chinua Imarogbe, Alexander Ariel Padrón González, Osvaldo Aguilera Batista, Pascal Mensah, Enrique Chacon-Cruz","doi":"10.37349/ei.2023.00119","DOIUrl":"https://doi.org/10.37349/ei.2023.00119","url":null,"abstract":"Since 2019, notable global viral outbreaks have occurred necessitating further research and healthcare system investigations. Following the coronavirus disease 2019 (COVID-19) pandemic, in 2022, whilst severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) strains evolved, monkeypox virus (MPXV) infections became more evident. MPXV is of the Orthopoxviridae genus, belonging to the family Poxviridae. Zoonotic transmission (animal-to-human transmission) may occur. The Orthopoxviridae genus includes other orthopoxviruses (OPXVs) present in animal host reservoirs that include cowpox viruses (CPXVs), vaccinia virus (VACV), and variola virus (VARV), with the latter being a causal agent of smallpox and excessive mortality. This review aims to present facts about MPXV-specific pathogenesis, epidemiology, and immunology alongside historical perspectives. MPXV was rarely reported outside Africa before April 2000. Early research since 1796 contributed towards the eradication of VARV leading to immunisation strategies. The World Health Organisation (WHO) announcement that VARV had been eradicated was confirmed in 1980. On the 23rd of July 2022, the WHO announced MPXV as a health emergency. Therefore, concern due to the propagation of MPXV causing monkeypox (mpox) disease requires clarity. Infected hosts display symptoms like extensive cellular-initiated rashes and lesions. Infection with MPXV makes it difficult to differentiate from other diseases or skin conditions. Antiviral therapeutic drugs were typically prescribed for smallpox and mpox disease; however, the molecular and immunological mechanisms with cellular changes remain of interest. Furthermore, no official authorized treatment exists for mpox disease. Some humans across the globe may be considered at risk. Historically, presenting symptoms of mpox resemble other viral diseases. Symptoms include rashes or lesions like Streptococcus, but also human herpes viruses (HHVs), including Varicella zoster virus (VZV).","PeriodicalId":93552,"journal":{"name":"Exploration of immunology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139252385","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Célia Dos Santos, Jesica Trinidad, Santiago Castera, Laura Alconcher, Paula Alejandra Coccia, Federico Javie Manni, María Fabiana Alberto, Analía Sánchez-Luceros
Aim: To describe the clinical characteristics and frequency of anti-factor H (FH) autoantibody-associated atypical hemolytic uremic syndrome (aHUS) in the first cohort of Argentine patients. Methods: The presence of anti-FH autoantibodies in 70 pediatric patients with suspected aHUS was investigated between 2013 and 2022. Clinical and laboratory parameters were collected and compared between patients who were positive and negative for anti-FH antibodies. Results: The 70 patients screened for anti-FH autoantibodies presented clinical features of non-immune microangiopathic hemolytic anemia, thrombocytopenia and renal injury. Positive titers were found in 14 children [mean: 1,938 arbitrary units per mL (AU/mL), range 179–8,500]. Due to missing clinical data, two patients who tested positive for anti-FH and 20 patients who tested negative for anti-FH were excluded from the data analysis. The laboratory features and clinical manifestations of anti-FH-positive aHUS cases (n = 12) were very similar to those of subjects with no autoantibodies detected (n = 36). Treatment administration was heterogeneous among the 12 patients analyzed. Dialysis was performed in six patients in total. Five children received plasmapheresis, while three patients were treated with plasma exchange followed by administration of eculizumab. Two patients received eculizumab only and one showed significant improvement solely through supportive care. Eight patients in total received immunosuppressive therapy. Follow-up of three patients showed a significant decrease of anti-FH autoantibody titers in 2/3 after treatment and during clinical remission. Conclusions: The cohort of 70 pediatric patients in this study demonstrated that the frequency of anti-FH autoantibody-associated aHUS in Argentina is 20%. The implementation of anti-FH testing in the country can potentially contribute to improved treatment and follow-up for patients with autoimmune aHUS.
{"title":"Anti-factor H autoantibody-associated hemolytic uremic syndrome in an Argentine pediatric cohort","authors":"Célia Dos Santos, Jesica Trinidad, Santiago Castera, Laura Alconcher, Paula Alejandra Coccia, Federico Javie Manni, María Fabiana Alberto, Analía Sánchez-Luceros","doi":"10.37349/ei.2023.00118","DOIUrl":"https://doi.org/10.37349/ei.2023.00118","url":null,"abstract":"Aim: To describe the clinical characteristics and frequency of anti-factor H (FH) autoantibody-associated atypical hemolytic uremic syndrome (aHUS) in the first cohort of Argentine patients. Methods: The presence of anti-FH autoantibodies in 70 pediatric patients with suspected aHUS was investigated between 2013 and 2022. Clinical and laboratory parameters were collected and compared between patients who were positive and negative for anti-FH antibodies. Results: The 70 patients screened for anti-FH autoantibodies presented clinical features of non-immune microangiopathic hemolytic anemia, thrombocytopenia and renal injury. Positive titers were found in 14 children [mean: 1,938 arbitrary units per mL (AU/mL), range 179–8,500]. Due to missing clinical data, two patients who tested positive for anti-FH and 20 patients who tested negative for anti-FH were excluded from the data analysis. The laboratory features and clinical manifestations of anti-FH-positive aHUS cases (n = 12) were very similar to those of subjects with no autoantibodies detected (n = 36). Treatment administration was heterogeneous among the 12 patients analyzed. Dialysis was performed in six patients in total. Five children received plasmapheresis, while three patients were treated with plasma exchange followed by administration of eculizumab. Two patients received eculizumab only and one showed significant improvement solely through supportive care. Eight patients in total received immunosuppressive therapy. Follow-up of three patients showed a significant decrease of anti-FH autoantibody titers in 2/3 after treatment and during clinical remission. Conclusions: The cohort of 70 pediatric patients in this study demonstrated that the frequency of anti-FH autoantibody-associated aHUS in Argentina is 20%. The implementation of anti-FH testing in the country can potentially contribute to improved treatment and follow-up for patients with autoimmune aHUS.","PeriodicalId":93552,"journal":{"name":"Exploration of immunology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-11-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135137506","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Victor Ivanovich Seledtsov, Galina V. Seledtsova, Alexei A. von Delwig
Immunotherapeutic treatment of autoimmune diseases should aim to inactivate autoaggressive memory T-cells and restore immune tolerance. It is envisaged that three approaches could be used to achieve this goal: stimulation of anti-idiotypic immune responses by vaccination with pathogenic T-cells; administration of suboptimal doses of antibodies (Abs) against two or more surface T-cell markers to provide selective Ab-mediated destruction of activated pathogenic memory T-cells; and induction of oral immune tolerance. The proposal entails the use of T-cell vaccination (TCV) or Ab-based therapy as an initial approach to reduce autoantigenic T-cell sensitization. Subsequently, the implementation of oral immunotherapy (OIT) is recommended to reinstate a consistent immune tolerance.
{"title":"Immune-based, multifaceted inactivation of pathogenic T lymphocytes in treating autoimmune diseases","authors":"Victor Ivanovich Seledtsov, Galina V. Seledtsova, Alexei A. von Delwig","doi":"10.37349/ei.2023.00117","DOIUrl":"https://doi.org/10.37349/ei.2023.00117","url":null,"abstract":"Immunotherapeutic treatment of autoimmune diseases should aim to inactivate autoaggressive memory T-cells and restore immune tolerance. It is envisaged that three approaches could be used to achieve this goal: stimulation of anti-idiotypic immune responses by vaccination with pathogenic T-cells; administration of suboptimal doses of antibodies (Abs) against two or more surface T-cell markers to provide selective Ab-mediated destruction of activated pathogenic memory T-cells; and induction of oral immune tolerance. The proposal entails the use of T-cell vaccination (TCV) or Ab-based therapy as an initial approach to reduce autoantigenic T-cell sensitization. Subsequently, the implementation of oral immunotherapy (OIT) is recommended to reinstate a consistent immune tolerance.","PeriodicalId":93552,"journal":{"name":"Exploration of immunology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136102391","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The concept and assessment of immune fitness","authors":"Joris C. Verster, Emina Išerić, Johan Garssen","doi":"10.37349/ei.2023.00116","DOIUrl":"https://doi.org/10.37349/ei.2023.00116","url":null,"abstract":"","PeriodicalId":93552,"journal":{"name":"Exploration of immunology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136261565","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Miguel Angel Pardiño-Vega, Norma Estela Herrera-González
One of the greatest challenges in the study of coronavirus disease 2019 (COVID-19) has been to establish the determining factors in the severity of the disease. Through extensive research efforts, a crucial factor responsible for disease control or exacerbation in COVID-19 has been identified—the regulation of the immune response. The abnormal release of interleukin-1 (IL-1), IL-6, and tumor necrosis factor-alpha (TNF-α) has been extensively studied in the context of the altered immune response observed in severe cases of COVID-19. However, recent attention has turned towards the excessive release of IL-17 and the increased presence of T helper 17 (Th17) cells, the main secretory cells of this cytokine. These factors have garnered interest due to their potential involvement in the cytokine storm observed in severe cases of COVID-19. In this review, it will be delved into the intricate mechanisms by which IL-6 contributes to the differentiation of Th17 cells, resulting in an increase in the population of Th17 cells. Moreover, it will be explored the proportional relationship between the increase of these lymphocytes and the release of IL-17 and other chemokines, which all together play a key role in promoting the chemotaxis and activation of neutrophils. Ultimately, this cascade of events culminates in the generation of tissue damage by neutrophils. Additionally, therapeutic options targeting these lymphocytes and cytokines are explored, providing insights into potential avenues for intervention.
{"title":"Loss of regulation of T helper 17 cells: a definitive factor for critical cases of coronavirus disease 2019","authors":"Miguel Angel Pardiño-Vega, Norma Estela Herrera-González","doi":"10.37349/ei.2023.00115","DOIUrl":"https://doi.org/10.37349/ei.2023.00115","url":null,"abstract":"One of the greatest challenges in the study of coronavirus disease 2019 (COVID-19) has been to establish the determining factors in the severity of the disease. Through extensive research efforts, a crucial factor responsible for disease control or exacerbation in COVID-19 has been identified—the regulation of the immune response. The abnormal release of interleukin-1 (IL-1), IL-6, and tumor necrosis factor-alpha (TNF-α) has been extensively studied in the context of the altered immune response observed in severe cases of COVID-19. However, recent attention has turned towards the excessive release of IL-17 and the increased presence of T helper 17 (Th17) cells, the main secretory cells of this cytokine. These factors have garnered interest due to their potential involvement in the cytokine storm observed in severe cases of COVID-19. In this review, it will be delved into the intricate mechanisms by which IL-6 contributes to the differentiation of Th17 cells, resulting in an increase in the population of Th17 cells. Moreover, it will be explored the proportional relationship between the increase of these lymphocytes and the release of IL-17 and other chemokines, which all together play a key role in promoting the chemotaxis and activation of neutrophils. Ultimately, this cascade of events culminates in the generation of tissue damage by neutrophils. Additionally, therapeutic options targeting these lymphocytes and cytokines are explored, providing insights into potential avenues for intervention.","PeriodicalId":93552,"journal":{"name":"Exploration of immunology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136113945","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Fariza A. Cheldieva, Anastasiia A. Shumilova, Mariya V. Cherkasova, Svetlana I. Glukhova, Aleksander M. Lila, Evgeny L. Nasonov, Tatiana M. Reshetnyak
Aim: The study aims to evaluate the incidence of recurrent thromboses in patients with primary antiphospholipid syndrome (PAPS) and its association with the presence of different antiphospholipid antibodies (aPLs) and known thrombogenic risk factors. Methods: This retrospective study included 52 patients. The median age of the patients was 38.5 years [31.5; 43.5], and the duration of the disease was 9.0 years [3.1; 13.0]. aPLs, including IgG/IgM/IgA antibodies to cardiolipin (aCLs), IgG/IgM/IgA anti-beta2-glycoprotein I (anti-β2-GPI), IgG anti-domain I-β2-GPI (anti-β2-GPI DI) antibodies, IgG/IgM antibodies to the phosphatidylserine/prothrombin complex (aPS/PT), and other thrombosis risk factors were included for analysis. Results: Recurrent thrombosis was reported in 34 (65%) out of 52 patients and 18 (35%) did not have it. The main reason for the recurrence of thrombosis was the lack of anticoagulant therapy: in 18 (52.9%) out of 34 patients with recurrent thrombosis. Three patients were taking warfarin at the time of thrombosis recurrence, but target international normalized ratio (INR) levels were not achieved. Other patients with recurrent thrombosis were taking direct oral anticoagulants (DOACs). The risk of recurrent thrombotic events with positive IgG aCL was 10.33 (P = 0.002) and 21 (P = 0.007) times higher were examined in enzyme-linked immunoassay (ELISA) and chemiluminescent assay (CLA), respectively. The risk of thrombosis was 4.58 times higher in patients who were IgA aCL-positive (P = 0.01). Compared with other antibodies, with positive IgG values of anti-β2-GPI and IgG aPS/PT by ELISA, a lower probability of thrombosis recurrence was observed: 7.56 and 7.25, respectively. A high risk of recurrent thrombosis [odds ratio (OR) = 32.0] was observed in IgG anti-β2-GPI (CLA). The combination of IgG aCL with IgG anti-β2-GPI and with IgG anti-β2-GPIDI is more informative with respect to the risks of thrombosis recurrence compared to double positivity for aCL with anti-β2-GPI (OR = 20.71 vs. OR = 10.18). Triple positivity for IgG aCL with IgG anti-β2-GPI and with IgG aPS/PT also shows better results compared to positivity for aCL with anti-β2-GPI (OR = 6.06 vs. OR = 5.79). Among other risk factors, arterial hypertension (AH) and obesity were significant in relation to the recurrence of thrombosis. AH occurred in 22 (42%) of 52 patients with PAPS. AH was associated with recurrent thrombosis in PAPS patients: 18 (53%) out of 34 with recurrent thrombosis had AH versus 4 out of 18 without recurrent thrombosis (P = 0.003). Conclusions: Recurrent thrombosis in antiphospholipid syndrome (APS) is largely associated with IgG aCL, IgG anti-β2-GPI, IgG anti-β2-GPIDI, IgG aPS/PT, and IgA aCL positivity. AH was a significant risk factor for recurrent thrombosis.
{"title":"Risk factors and recurrent thrombosis in primary antiphospholipid syndrome","authors":"Fariza A. Cheldieva, Anastasiia A. Shumilova, Mariya V. Cherkasova, Svetlana I. Glukhova, Aleksander M. Lila, Evgeny L. Nasonov, Tatiana M. Reshetnyak","doi":"10.37349/ei.2023.00114","DOIUrl":"https://doi.org/10.37349/ei.2023.00114","url":null,"abstract":"Aim: The study aims to evaluate the incidence of recurrent thromboses in patients with primary antiphospholipid syndrome (PAPS) and its association with the presence of different antiphospholipid antibodies (aPLs) and known thrombogenic risk factors. Methods: This retrospective study included 52 patients. The median age of the patients was 38.5 years [31.5; 43.5], and the duration of the disease was 9.0 years [3.1; 13.0]. aPLs, including IgG/IgM/IgA antibodies to cardiolipin (aCLs), IgG/IgM/IgA anti-beta2-glycoprotein I (anti-β2-GPI), IgG anti-domain I-β2-GPI (anti-β2-GPI DI) antibodies, IgG/IgM antibodies to the phosphatidylserine/prothrombin complex (aPS/PT), and other thrombosis risk factors were included for analysis. Results: Recurrent thrombosis was reported in 34 (65%) out of 52 patients and 18 (35%) did not have it. The main reason for the recurrence of thrombosis was the lack of anticoagulant therapy: in 18 (52.9%) out of 34 patients with recurrent thrombosis. Three patients were taking warfarin at the time of thrombosis recurrence, but target international normalized ratio (INR) levels were not achieved. Other patients with recurrent thrombosis were taking direct oral anticoagulants (DOACs). The risk of recurrent thrombotic events with positive IgG aCL was 10.33 (P = 0.002) and 21 (P = 0.007) times higher were examined in enzyme-linked immunoassay (ELISA) and chemiluminescent assay (CLA), respectively. The risk of thrombosis was 4.58 times higher in patients who were IgA aCL-positive (P = 0.01). Compared with other antibodies, with positive IgG values of anti-β2-GPI and IgG aPS/PT by ELISA, a lower probability of thrombosis recurrence was observed: 7.56 and 7.25, respectively. A high risk of recurrent thrombosis [odds ratio (OR) = 32.0] was observed in IgG anti-β2-GPI (CLA). The combination of IgG aCL with IgG anti-β2-GPI and with IgG anti-β2-GPIDI is more informative with respect to the risks of thrombosis recurrence compared to double positivity for aCL with anti-β2-GPI (OR = 20.71 vs. OR = 10.18). Triple positivity for IgG aCL with IgG anti-β2-GPI and with IgG aPS/PT also shows better results compared to positivity for aCL with anti-β2-GPI (OR = 6.06 vs. OR = 5.79). Among other risk factors, arterial hypertension (AH) and obesity were significant in relation to the recurrence of thrombosis. AH occurred in 22 (42%) of 52 patients with PAPS. AH was associated with recurrent thrombosis in PAPS patients: 18 (53%) out of 34 with recurrent thrombosis had AH versus 4 out of 18 without recurrent thrombosis (P = 0.003). Conclusions: Recurrent thrombosis in antiphospholipid syndrome (APS) is largely associated with IgG aCL, IgG anti-β2-GPI, IgG anti-β2-GPIDI, IgG aPS/PT, and IgA aCL positivity. AH was a significant risk factor for recurrent thrombosis.","PeriodicalId":93552,"journal":{"name":"Exploration of immunology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136014392","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The etiology of recurrent spontaneous abortion (RSA) is extremely complex, as there are 40–50% of patients with unexplained miscarriages, known as unexplained RSA (URSA). URSA affects approximately 1–2% of females of childbearing age and has a massive impact on the physical and mental conditions of both patients and their families. The pathogenesis of the disease remains unclear, making its treatment complicated. In recent years, considerable progress has been made in the exploration of the URSA immune balance mechanism and it has been universally acknowledged that a balanced immune response (as abnormal immunity) may be the root cause of poor pregnancy outcomes. This review discussed and summarized the effects of immune cells and blocking antibodies (BAs) on URSA based on the current state of knowledge in this area. Additionally, molecular genetics also plays an essential role in the incidence rate of URSA since the role of genetic polymorphism in the pathogenesis of URSA has been thoroughly studied. Nonetheless, the outcomes of these studies are inconsistent, particularly across populations. This paper reviewed previous studies on URSA and maternal genetic polymorphism, focusing on and synthesizing the most important findings to date, and providing diagnostic recommendation for URSA patients with clinical symptoms.
{"title":"Research progress of immune balance and genetic polymorphism in unexplained recurrent abortion","authors":"Yafei Kang, Qinying Xie, Shuting Chen, Qinlan Li, Xinyi Dong, Tianyu Zhang, Sen Fu, Qinghua Lei, Donghui Huang","doi":"10.37349/ei.2023.00113","DOIUrl":"https://doi.org/10.37349/ei.2023.00113","url":null,"abstract":"The etiology of recurrent spontaneous abortion (RSA) is extremely complex, as there are 40–50% of patients with unexplained miscarriages, known as unexplained RSA (URSA). URSA affects approximately 1–2% of females of childbearing age and has a massive impact on the physical and mental conditions of both patients and their families. The pathogenesis of the disease remains unclear, making its treatment complicated. In recent years, considerable progress has been made in the exploration of the URSA immune balance mechanism and it has been universally acknowledged that a balanced immune response (as abnormal immunity) may be the root cause of poor pregnancy outcomes. This review discussed and summarized the effects of immune cells and blocking antibodies (BAs) on URSA based on the current state of knowledge in this area. Additionally, molecular genetics also plays an essential role in the incidence rate of URSA since the role of genetic polymorphism in the pathogenesis of URSA has been thoroughly studied. Nonetheless, the outcomes of these studies are inconsistent, particularly across populations. This paper reviewed previous studies on URSA and maternal genetic polymorphism, focusing on and synthesizing the most important findings to date, and providing diagnostic recommendation for URSA patients with clinical symptoms.","PeriodicalId":93552,"journal":{"name":"Exploration of immunology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135969460","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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