How rheumatoid arthritis can result from provocation of the immune system by microorganisms and viruses

© 2016 Arleevskaya, Kravtsova, Lemerle, Renaudineau and Tsibulkin.The pathogenesis of rheumatoid arthritis (RA), similar to development of a majority of inflammatory and autoimmune disorders, is largely due to an inappropriate or inadequate immune response to environmental challenges. Among these challenges, infectious agents are the undisputed leaders. Since the 1870s, an impressive list of microorganisms suspected of provoking RA has formed, and the list is still growing. Although a definite causative link between a specific infectious agent and the disease has not been established, several arguments support such a possibility. First, in the absence of a defined pathogen, the spectrum of triggering agents may include polymicrobial communities or the cumulative effect of several bacterial/viral factors. Second, the range of infectious episodes (i.e., clinical manifestations caused by pathogens) may vary in the process of RA development from preclinical to late-stage disease. Third, infectious agents might not trigger RA in all cases, but trigger it in a certain subset of the cases, or the disease onset may arise from an unfortunate combination of infections along with, for example, psychological stress and/or chronic joint tissue microtrauma. Fourth, genetic differences may have a role in the disease onset. In this review, two aspects of the problem of "microorganisms and RA" are debated. First, is there an acquired immune deficiency and, in turn, susceptibility to infections in RA patients due to the too frequent and too lengthy infections, which at last break the tolerance of self antigens? Or, second, is there a congenital deficiency in tolerance and inflammation control, which may occur even with ordinary infection frequency and duration?

ОЦЕНКА ЭФФЕКТИВНОСТИ МОДИФИЦИРОВАННОГО ИФА-МЕТОДА ИДЕНТИФИКАЦИИ ПРОТИВОТУБЕРКУЛЕЗНЫХ АНТИТЕЛ ДЛЯ ПРОГНОЗА РАЗВИТИЯ И ДИАГНОСТИКИ ТУБЕРКУЛЕЗА У БОЛЬНЫХ ВИЧ-ИНФЕКЦИЕЙ

The objective of the study: modification of the standard IFA method aimed to detect antibodies against tuberculosis, assessment of its efficiency as a screening tool for prediction and diagnostics of tuberculosis in HIV patients.Subjects and methods. The modification of the standard IFA method aimed to assess the intensity of humoral anti-tuberculosis immune response included measurement of operational dilution of tested sera in order to enhance its diagnostic value. The modified method was used for the examination in the following groups: 85 active tuberculosis cases, 92 HIV patients with no clinical signs of tuberculosis, and 30 healthy donors.Results: it is possible to use the modified method in HIV positive people in order to detect those with the highest risk of tuberculosis among them; to provide early diagnostics of active tuberculosis, which is especially crucial at the advanced stages of HIV infection. This method cannot replace the classic methods of tuberculosis diagnostics and it is not recommended for mass screening in HIV negative persons.Цель исследования: модификация стандартного ИФА-метода идентификации ПТАТ, оценка его эффективности в качестве скринингового для прогнозирования и диагностики туберкулеза у больных ВИЧ-инфекцией.Материалы и методы. Модификация стандартного ИФА-метода оценки выраженности гуморального противотуберкулезного иммунного ответа включала титрование рабочего разведения исследуемых сывороток для увеличения его диагностической значимости. Модифицированный метод использовался при обследовании в группах из 85 больных активным туберкулезом, 92 больных ВИЧ-инфекцией без клинических признаков туберкулеза и 30 здоровых доноров.Результаты: возможно использовать модифицированный метод у ВИЧ-позитивных лиц для выявления среди них лиц с наибольшим риском развития туберкулеза; для ранней диагностики активного туберкулеза, что особенно актуально на поздних стадиях ВИЧ-инфекции. Метод не заменяет классические способы диагностики туберкулеза и не рекомендуется для использования в качестве массового скрининга ВИЧ-негативных лиц

How rheumatoid arthritis can result from provocation of the immune system by microorganisms and viruses

© 2016 Arleevskaya, Kravtsova, Lemerle, Renaudineau and Tsibulkin.The pathogenesis of rheumatoid arthritis (RA), similar to development of a majority of inflammatory and autoimmune disorders, is largely due to an inappropriate or inadequate immune response to environmental challenges. Among these challenges, infectious agents are the undisputed leaders. Since the 1870s, an impressive list of microorganisms suspected of provoking RA has formed, and the list is still growing. Although a definite causative link between a specific infectious agent and the disease has not been established, several arguments support such a possibility. First, in the absence of a defined pathogen, the spectrum of triggering agents may include polymicrobial communities or the cumulative effect of several bacterial/viral factors. Second, the range of infectious episodes (i.e., clinical manifestations caused by pathogens) may vary in the process of RA development from preclinical to late-stage disease. Third, infectious agents might not trigger RA in all cases, but trigger it in a certain subset of the cases, or the disease onset may arise from an unfortunate combination of infections along with, for example, psychological stress and/or chronic joint tissue microtrauma. Fourth, genetic differences may have a role in the disease onset. In this review, two aspects of the problem of "microorganisms and RA" are debated. First, is there an acquired immune deficiency and, in turn, susceptibility to infections in RA patients due to the too frequent and too lengthy infections, which at last break the tolerance of self antigens? Or, second, is there a congenital deficiency in tolerance and inflammation control, which may occur even with ordinary infection frequency and duration?

How rheumatoid arthritis can result from provocation of the immune system by microorganisms and viruses

© 2016 Arleevskaya, Kravtsova, Lemerle, Renaudineau and Tsibulkin.The pathogenesis of rheumatoid arthritis (RA), similar to development of a majority of inflammatory and autoimmune disorders, is largely due to an inappropriate or inadequate immune response to environmental challenges. Among these challenges, infectious agents are the undisputed leaders. Since the 1870s, an impressive list of microorganisms suspected of provoking RA has formed, and the list is still growing. Although a definite causative link between a specific infectious agent and the disease has not been established, several arguments support such a possibility. First, in the absence of a defined pathogen, the spectrum of triggering agents may include polymicrobial communities or the cumulative effect of several bacterial/viral factors. Second, the range of infectious episodes (i.e., clinical manifestations caused by pathogens) may vary in the process of RA development from preclinical to late-stage disease. Third, infectious agents might not trigger RA in all cases, but trigger it in a certain subset of the cases, or the disease onset may arise from an unfortunate combination of infections along with, for example, psychological stress and/or chronic joint tissue microtrauma. Fourth, genetic differences may have a role in the disease onset. In this review, two aspects of the problem of "microorganisms and RA" are debated. First, is there an acquired immune deficiency and, in turn, susceptibility to infections in RA patients due to the too frequent and too lengthy infections, which at last break the tolerance of self antigens? Or, second, is there a congenital deficiency in tolerance and inflammation control, which may occur even with ordinary infection frequency and duration?

How rheumatoid arthritis can result from provocation of the immune system by microorganisms and viruses

© 2016 Arleevskaya, Kravtsova, Lemerle, Renaudineau and Tsibulkin.The pathogenesis of rheumatoid arthritis (RA), similar to development of a majority of inflammatory and autoimmune disorders, is largely due to an inappropriate or inadequate immune response to environmental challenges. Among these challenges, infectious agents are the undisputed leaders. Since the 1870s, an impressive list of microorganisms suspected of provoking RA has formed, and the list is still growing. Although a definite causative link between a specific infectious agent and the disease has not been established, several arguments support such a possibility. First, in the absence of a defined pathogen, the spectrum of triggering agents may include polymicrobial communities or the cumulative effect of several bacterial/viral factors. Second, the range of infectious episodes (i.e., clinical manifestations caused by pathogens) may vary in the process of RA development from preclinical to late-stage disease. Third, infectious agents might not trigger RA in all cases, but trigger it in a certain subset of the cases, or the disease onset may arise from an unfortunate combination of infections along with, for example, psychological stress and/or chronic joint tissue microtrauma. Fourth, genetic differences may have a role in the disease onset. In this review, two aspects of the problem of "microorganisms and RA" are debated. First, is there an acquired immune deficiency and, in turn, susceptibility to infections in RA patients due to the too frequent and too lengthy infections, which at last break the tolerance of self antigens? Or, second, is there a congenital deficiency in tolerance and inflammation control, which may occur even with ordinary infection frequency and duration?

Interaction of hepatitis C virus with the immune system in pregnant women with chronic hepatitis C

Aim: to analyze the relation between hepatitis C virus (HCV) load, the immune reactivity, and the immune-mediated lesions in the liver during pregnancy in women with chronic hepatitis C (CHC). Materials and methods. The study included 1690 pregnant women, 107 of whom had IgG antibodies to HCV; in addition, 68 women (63.5 %) were diagnosed with chronic hepatitis C and had a positive test for HCV RNA. The diagnosis of CHC was confirmed by determining serum total anti-HCV IgG antibodies using an enzyme immunoassay. The qualitative and quantitative determination of HCV RNA in the blood was performed by polymerase chain reaction. The virus replicative activity was qualitatively assessed by the viral load: low - the level of HCV RNA was up to 103 lU/ml, moderate - from 103 to 106 lU/ml, and high - above 106 lU/ml. To quantify the results, we used the positivity index, i.e, the ratio of the serum optical density to the critical optical density (cut-off) in each test. Results. In the early stages of pregnancy, signs of severe immune-mediated hepatocyte injury persisted. In the II and Ill trimesters, there was an unusual discrepancy between the severity of viral load and the degree of hepatocyte injury as the course of CHC remained usual. Another evidence of the liver involvement in this immune-pathological mechanism was an 87 % decrease in alanine aminotransferase activity with an increase in the viral load in patients with CHC in the Ill trimester of pregnancy. Conclusion. Suppression of anti-HCV humoral immunity, but not cellular immunity, begins from early stages of pregnancy and is accompanied by a significant increase in hepatocyte lesions without an increase in the severity of the inflammatory process

ASSESSMENT OF EFFICIENCY OF THE MODIFIED IFA METHOD AIMED TO DETECT ANTIBODIES AGAINST TUBERCULOSIS FOR DEVELOPMENT AND DIAGNOSTICS OF TUBERCULOSIS IN HIV PATIENTS

The objective of the study: modification of the standard IFA method aimed to detect antibodies against tuberculosis, assessment of its efficiency as a screening tool for prediction and diagnostics of tuberculosis in HIV patients.Subjects and methods. The modification of the standard IFA method aimed to assess the intensity of humoral anti-tuberculosis immune response included measurement of operational dilution of tested sera in order to enhance its diagnostic value. The modified method was used for the examination in the following groups: 85 active tuberculosis cases, 92 HIV patients with no clinical signs of tuberculosis, and 30 healthy donors.Results: it is possible to use the modified method in HIV positive people in order to detect those with the highest risk of tuberculosis among them; to provide early diagnostics of active tuberculosis, which is especially crucial at the advanced stages of HIV infection. This method cannot replace the classic methods of tuberculosis diagnostics and it is not recommended for mass screening in HIV negative persons

How Rheumatoid Arthritis Can Result from Provocation of the Immune System by Microorganisms and Viruses

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