Immunopathological events initiated and maintained by pathogenic IgG autoantibodies in an experimental autoimmune kidney disease

Impact of IgG Fc-fragments on experimental glomerulonephritis induced by <i>Streptococcus pyogenes</i> strain binding various immunoglobulin classes

“…Согласно литературным данным и более ранним нашим [4,8,9] исследованиям, постстрептококковый гломерулонефрит известен как мембранозно-пролиферативный процесс, первично проявляющийся отложением IgG или IgG-anti-IgG иммунных комплексов в базальной мембране клубочков [4,9,21], между тем как для IgA-нефропатии свойственны отложения IgA или его полимеров в мезангиальных клетках клубочков, ведущие к мезангиальнопролиферативному гломерулонефриту [3,18,19,20,24]. За этими проявлениями фактически должно стоять реальное распределение соответствующих Fc-рецепторов в структурах гломерул.…”

Impact of IgG Fc-fragments on experimental glomerulonephritis induced by <i>Streptococcus pyogenes</i> strain binding various immunoglobulin classes

“…Согласно литературным данным и более ранним нашим [4,8,9] исследованиям, постстрептококковый гломерулонефрит известен как мембранозно-пролиферативный процесс, первично проявляющийся отложением IgG или IgG-anti-IgG иммунных комплексов в базальной мембране клубочков [4,9,21], между тем как для IgA-нефропатии свойственны отложения IgA или его полимеров в мезангиальных клетках клубочков, ведущие к мезангиальнопролиферативному гломерулонефриту [3,18,19,20,24]. За этими проявлениями фактически должно стоять реальное распределение соответствующих Fc-рецепторов в структурах гломерул.…”

The modified vaccination technique designed to prevent and cure acute and chronic disorders

“…During the chronic phase of the autoimmune kidney disease it was observed that both pathogenic IgG and non-pathogenic IgM aabs were present in the circulation, directed against the nephritogenic ag [37]. The former maintained progression [exacerbation] and the latter aimed to downregulate/terminate the disease [remission].…”

“…The role of the specific IgM aabs is to assist in the removal of the released nephritogenic ag from the system, thereby preventing its toxic accumulation and possible chemical alteration which could, if allowed to stay in the system long enough, cause an autoimmune disease. The released aags, after being removed by the specific IgM aabs, are digested into small molecular weight reusable peptides by mononuclear cells [42,43,72].…”

“…Prevention, progression and treatment of any disease depend upon the presentation of the disease causing ag to the cells of the immune system, whether it is exogenous or endogenous in nature. We have observed in an experimental autoimmune disease – SPHN – that the immune system is continually bombarded by released nephritogenic ags from the renal proximal convoluted tubules’ BB zone of cells and as a result specific IgM aabs are produced against them [35, 37, 71]. The role of the specific IgM aabs is to assist in the removal of the released nephritogenic ag from the system, thereby preventing its toxic accumulation and possible chemical alteration which could, if allowed to stay in the system long enough, cause an autoimmune disease.…”

“…Once such aabs [24, 35, 73, 74] are produced, the target ag in the BB region of the proximal convoluted tubules is damaged causing the autoimmune disease (primary injury by the pathogenic IgG aab) with consequent release of the nephritogenic ag into the circulation and urine. The released aag, by contributing to IC deposition in the glomeruli, together with pathogenic IgG aabs directed against the nephritogenic ag in the presence of complement, caused MGN (secondary injury by the pathogenic IgG aab) [37] [exacerbation]. In the meantime, the released nephritogenic ag contributed to the production of elevated IgM aabs which in turn, by removing both modified and native nephritogenic ags from the system, downregulated/terminated the autoimmune disease causing immunopathological processes [24, 35, 37, 45] [remission].…”

Impact of IgG Fc-fragments on experimental glomerulonephritis induced by <i>Streptococcus pyogenes</i> strain binding various immunoglobulin classes

“…Согласно литературным данным и более ранним нашим [4,8,9] исследованиям, постстрептококковый гломерулонефрит известен как мембранозно-пролиферативный процесс, первично проявляющийся отложением IgG или IgG-anti-IgG иммунных комплексов в базальной мембране клубочков [4,9,21], между тем как для IgA-нефропатии свойственны отложения IgA или его полимеров в мезангиальных клетках клубочков, ведущие к мезангиальнопролиферативному гломерулонефриту [3,18,19,20,24]. За этими проявлениями фактически должно стоять реальное распределение соответствующих Fc-рецепторов в структурах гломерул.…”

The modified vaccination technique designed to prevent and cure acute and chronic disorders

“…During the chronic phase of the autoimmune kidney disease it was observed that both pathogenic IgG and non-pathogenic IgM aabs were present in the circulation, directed against the nephritogenic ag [37]. The former maintained progression [exacerbation] and the latter aimed to downregulate/terminate the disease [remission].…”

“…The role of the specific IgM aabs is to assist in the removal of the released nephritogenic ag from the system, thereby preventing its toxic accumulation and possible chemical alteration which could, if allowed to stay in the system long enough, cause an autoimmune disease. The released aags, after being removed by the specific IgM aabs, are digested into small molecular weight reusable peptides by mononuclear cells [42,43,72].…”

“…Prevention, progression and treatment of any disease depend upon the presentation of the disease causing ag to the cells of the immune system, whether it is exogenous or endogenous in nature. We have observed in an experimental autoimmune disease – SPHN – that the immune system is continually bombarded by released nephritogenic ags from the renal proximal convoluted tubules’ BB zone of cells and as a result specific IgM aabs are produced against them [35, 37, 71]. The role of the specific IgM aabs is to assist in the removal of the released nephritogenic ag from the system, thereby preventing its toxic accumulation and possible chemical alteration which could, if allowed to stay in the system long enough, cause an autoimmune disease.…”

“…Once such aabs [24, 35, 73, 74] are produced, the target ag in the BB region of the proximal convoluted tubules is damaged causing the autoimmune disease (primary injury by the pathogenic IgG aab) with consequent release of the nephritogenic ag into the circulation and urine. The released aag, by contributing to IC deposition in the glomeruli, together with pathogenic IgG aabs directed against the nephritogenic ag in the presence of complement, caused MGN (secondary injury by the pathogenic IgG aab) [37] [exacerbation]. In the meantime, the released nephritogenic ag contributed to the production of elevated IgM aabs which in turn, by removing both modified and native nephritogenic ags from the system, downregulated/terminated the autoimmune disease causing immunopathological processes [24, 35, 37, 45] [remission].…”

Impact of IgG Fc-fragments on experimental glomerulonephritis induced by <i>Streptococcus pyogenes</i> strain binding various immunoglobulin classes

“…Согласно литературным данным и более ранним нашим [4,8,9] исследованиям, постстрептококковый гломерулонефрит известен как мембранозно-пролиферативный процесс, первично проявляющийся отложением IgG или IgG-anti-IgG иммунных комплексов в базальной мембране клубочков [4,9,21], между тем как для IgA-нефропатии свойственны отложения IgA или его полимеров в мезангиальных клетках клубочков, ведущие к мезангиальнопролиферативному гломерулонефриту [3,18,19,20,24]. За этими проявлениями фактически должно стоять реальное распределение соответствующих Fc-рецепторов в структурах гломерул.…”

The modified vaccination technique designed to prevent and cure acute and chronic disorders

“…During the chronic phase of the autoimmune kidney disease it was observed that both pathogenic IgG and non-pathogenic IgM aabs were present in the circulation, directed against the nephritogenic ag [37]. The former maintained progression [exacerbation] and the latter aimed to downregulate/terminate the disease [remission].…”

“…The role of the specific IgM aabs is to assist in the removal of the released nephritogenic ag from the system, thereby preventing its toxic accumulation and possible chemical alteration which could, if allowed to stay in the system long enough, cause an autoimmune disease. The released aags, after being removed by the specific IgM aabs, are digested into small molecular weight reusable peptides by mononuclear cells [42,43,72].…”

“…Prevention, progression and treatment of any disease depend upon the presentation of the disease causing ag to the cells of the immune system, whether it is exogenous or endogenous in nature. We have observed in an experimental autoimmune disease – SPHN – that the immune system is continually bombarded by released nephritogenic ags from the renal proximal convoluted tubules’ BB zone of cells and as a result specific IgM aabs are produced against them [35, 37, 71]. The role of the specific IgM aabs is to assist in the removal of the released nephritogenic ag from the system, thereby preventing its toxic accumulation and possible chemical alteration which could, if allowed to stay in the system long enough, cause an autoimmune disease.…”

“…Once such aabs [24, 35, 73, 74] are produced, the target ag in the BB region of the proximal convoluted tubules is damaged causing the autoimmune disease (primary injury by the pathogenic IgG aab) with consequent release of the nephritogenic ag into the circulation and urine. The released aag, by contributing to IC deposition in the glomeruli, together with pathogenic IgG aabs directed against the nephritogenic ag in the presence of complement, caused MGN (secondary injury by the pathogenic IgG aab) [37] [exacerbation]. In the meantime, the released nephritogenic ag contributed to the production of elevated IgM aabs which in turn, by removing both modified and native nephritogenic ags from the system, downregulated/terminated the autoimmune disease causing immunopathological processes [24, 35, 37, 45] [remission].…”