Search results for "autoimmuniteetti"
showing 5 items of 5 documents
Parvovirus B19V Nonstructural Protein NS1 Induces Double-Stranded Deoxyribonucleic Acid Autoantibodies and End-Organ Damage in Nonautoimmune Mice
2018
Abstract Background Viral infection is implicated in development of autoimmunity. Parvovirus B19 (B19V) nonstructural protein, NS1, a helicase, covalently modifies self double-stranded deoxyribonucleic acid (dsDNA) and induces apoptosis. This study tested whether resulting apoptotic bodies (ApoBods) containing virally modified dsDNA could induce autoimmunity in an animal model. Methods BALB/c mice were inoculated with (1) pristane-induced, (2) B19V NS1-induced, or (3) staurosporine-induced ApoBods. Serum was tested for dsDNA autoantibodies by Crithidia luciliae staining and enzyme-linked immunosorbent assay. Brain, heart, liver, and kidney pathology was examined. Deposition of self-antigens…
Fungal Dysbiosis and Intestinal Inflammation in Children With Beta-Cell Autoimmunity
2020
Although gut bacterial dysbiosis is recognized as a regulator of beta-cell autoimmunity, no data is available on fungal dysbiosis in the children at the risk of type 1 diabetes (T1D). We hypothesized that the co-occurrence of fungal and bacterial dysbiosis contributes to the intestinal inflammation and autoimmune destruction of insulin-producing beta-cells in T1D. Fecal and blood samples were collected from 26 children tested positive for at least one diabetes-associated autoantibody (IAA, GADA, IA-2A or ICA) and matched autoantibody-negative children with HLA-conferred susceptibility to T1D (matched for HLA-DQB1 haplotype, age, gender and early childhood nutrition). Bacterial 16S and funga…
Human parvovirus B19 induced apoptotic bodies contain altered self-antigens that are phagocytosed by antigen presenting cells.
2013
Human parvovirus B19 (B19V) from the erythrovirus genus is known to be a pathogenic virus in humans. Prevalence of B19V infection has been reported worldwide in all seasons, with a high incidence in the spring. B19V is responsible for erythema infectiosum (fifth disease) commonly seen in children. Its other clinical presentations include arthralgia, arthritis, transient aplastic crisis, chronic anemia, congenital anemia, and hydrops fetalis. In addition, B19V infection has been reported to trigger autoimmune diseases such as systemic lupus erythematosus and rheumatoid arthritis. However, the mechanisms of B19V participation in autoimmunity are not fully understood. B19V induced chronic dise…
Pathogenesis and autoimmunity initiated by a viral protein-induced apoptotic bodies
2016
Ihmisen parvovirus B19 (B19) on laajalle levinnyt, yleinen virus, joka aiheuttaa lapsissa parvorokkoa (viides tauti). Aikuisille B19 aiheuttaa erinäisiä sairauksia, muun muassa nivelkipuja ja – tulehdusta, anemiaa, sekä raskaana oleville sikiöpöhöä. Lisäksi B19 infektio saattaa johtaa autoimmuunisairauksiin, kuten punahukkaan (systemic lupus erythematosus, SLE), nivelreumaan ja sydänlihastulehdukseen. Toisaalta infektio voi olla myös täysin oireeton. Mekanismit, jotka johtavat B19 tartunnasta autoimmuunisairauteen, ovat vielä tuntemattomia. Kuitenkin tiedetään, että B19:n ei-rakenteellinen proteiini NS1 on soluille tuhoisa ja aiheuttaa niiden kuoleman (apoptoosin) muodostaen solunjäännösten…
Pathogenic mechanisms of how human parvovirus breaks self-tolerance
2017
It is known that viral infections can cause acute, chronic, and autoimmune diseases (ADs). However, the mechanism of how a persistent viral infection contributes to ADs remains still unclear. In this thesis, pathological and immunological aspects of how common viruses can initiate autoimmunity were investigated, and human parvovirus B19 (B19V) was employed as a model virus. B19V non-structural protein 1 (NS1), a superfamily 3 (SF3) helicase, initiated DNA damage resulting in cellular apoptosis. The apoptotic bodies (ApoBods) induced by B19V NS1 were purified and characterized. These ApoBods contained viral NS1 proteins with modified autoimmune-associated self-antigens, e.g. DNA, Smith, Apol…