Autoantibodies in Nonautoimmune Individuals during Infections

Abstract

Infections can act as environmental triggers inducing or promoting autoimmune disease in genetically predisposed individuals. Identification of microbial peptides similar to self-tissues may by molecular mimicry, provide the inducing mechanism for an immune response. The aim of this study was to identify autoantibodies (autoAbs) in nonautoimmune individuals during acute bacterial, viral, or parasitic infections. Specific Abs or specific infections with an increased autoAb load may shed insight into the mechanisms of autoimmune disease. Sera from 88 patients with acute infections (41 bacterial, 23 viral, 17 parasitic, and 7 rickettsial) were tested by the ELISA method for antinuclear antibodies (ANA) 8 Pro, and Abs to thyroid peroxidase (TPO), thyroglobulin, phospholipids, annexin-V, laminin, anti-Saccharomyces cervisiae (ASCA), and prothrombin, along with 80 normal controls. Elevated titers of Abs to annexin-V and prothrombin were the most prevalent in viral, parasitic, and rickettsial infections and to laminin in viral and parasitic infections. Elevated titers of ASCA and ANA were found in viral and bacterial infections. Antiphospholipid Abs were found in parasitic and Q-fever infections. Thirty-four individuals harbored elevated titers of at least two Abs. An autoAb burden was detected in individuals with hepatitis A, hepatitis B, toxoplasma or Q-fever infections. In nonautoimmune individuals with various (bacterial, viral, parasitic, and rickettsial) infections, elevated titers of Abs to annexin-V, prothrombin, laminin, ASCA, ANA, and phospholipids were most frequently detected.

Regulatory T Cells Resist Virus Infection-Induced Apoptosis

“…However, most of the time viruses do not induce autoimmunity. It is not uncommon to see some self-reactive antibodies generated during infection (43)(44)(45), but most of the time the host survives a viral infection without serious autoimmune manifestations. It was, therefore, of interest to determine whether Foxp3 ϩ CD4 ϩ natural Treg cells, present at the beginning of viral infections, were resistant or sensitive to the T cell apoptosis that occurs early during infection.…”

Etiology of hemolysis in two patients with hepatitis A infection: glucose-6-phosphate dehydrogenase deficiency or autoimmune hemolytic anemia

“…For this reason, we could not totally relate our patients' acute hemolysis to postinfectious autoimmune hemolytic anemia. Berlin and associates [4] reported that in nonautoimmune individuals with various infections, elevated titers of autoantibodies could be detected by molecular mimicry of microbial peptides similar to self-tissues. The transient nature of the autoantibodies in our patients could be explained by this.…”

“…Although the results of direct Coombs' tests were negative, both patients reported here had the presence of autoimmune antibodies such as ANA, SMA, and antidsDNA. In genetically predisposed individuals, infections could act as environmental triggers inducing or promoting autoimmune disease [4]. It has been suggested that acute hepatitis A virus infection induces autoimmune hemolytic anemia [15].…”

Immunostimulation in the era of the metagenome

“…25 A 2007 study examined blood sera from 88 patients with acute infections (41 bacterial, 23 viral, 17 parasitic and 7 rikettsial). 26 Elevated titers of autoantibodies including annexin V, prothrombin, anti-Saccharomyces cerevisiae antibody, antinuclear antibody (ANA) or antiphospholipid antibodies were detected in about 50% of the subjects, with 34 individuals harboring elevated titers of at least two autoantibodies.…”