Lactate Dehydrogenase-elevating Virus Induces Anti-Golgi Apparatus Antibodies

Weiland, Emilie; Weiland, Frank; Grossmann, Angelika

doi:10.1099/0022-1317-68-7-1983

Cited by 26 publications

(31 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These findings support our view that the immune complexes consist of autoantibodies formed in the course of the polyclonal activation of B cells and their cellular antigens. That various types of autoantibodies are produced during a persistent LDV infection has been demonstrated (Grossman et al, 1989;Weiland et al, 1987;Cafruny & Hovinen, 1988). Whether these immune complexes exert any pathogenic effect is not known.…”

Section: Discussionmentioning

confidence: 99%

Neonatal Infection of Mice With Lactate Dehydrogenase-elevating Virus Results in Suppression of Humoral Antiviral Immune Response but does not Alter the Course of Viraemia or the Polyclonal Activation of B Cells and Immune Complex Formation

Rowland

Even

Anderson

et al. 1994

Journal of General Virology

View full text Add to dashboard Cite

Neonatal infection of FVB mice with lactate dehydrogenase-elevating virus (LDV) prevented the normal formation of anti-LDV antibodies observed in mice infected at 5 days of age or older. Even 22 weeks post-infection, the concentration of circulating anti-LDV antibodies in neonatally infected mice was insignificant. However, the time course and level of persistent viraemia were the same in neonatally infected mice lacking anti-LDV antibodies as in mice infected at 5 or 15 days of age which developed normal antiviral immune responses. The results support the view that LDV replication in mice is unaffected by antiviral immune responses and instead is primarily dependent on the rate of regeneration of LDV-permissive macrophages. This view is further supported by the following findings. Treatment of mice with cyclophosphamide or dexamethasone, which are known to increase plasma LDV levels, increased the proportion of LDV-permissive macrophages in the peritoneum. Injection of mice with interleukin-3, which is known to stimulate macrophage development, increased plasma LDV levels in persistently infected mice 10-to 100-fold. During the first month of age when mice possess a higher proportion of LDV-permissive macrophages than older mice and peritoneal macrophages exhibit self-sustained growth, the persistent plasma LDV titres were also 10-to 100-fold higher than in older mice. The polyclonal activation of B cells induced by LDV that results in a permanent elevation of IgG2a or IgG2b in the circulation, and the formation of 180K to 300K immune complexes containing IgG2a or IgG2b were also the same in neonatally infected mice and mice infected 5 or 15 days after birth. Thus, the polyclonal activation of B cells occurs in the absence of an antiviral humoral immune response and the immune complexes do not contain anti-LDV antibodies. The immune complexes probably consist of autoantibodies formed in the course of the polyclonal activation of B cells and their cellular antigens.

show abstract

Section: Discussionmentioning

confidence: 99%

Neonatal Infection of Mice With Lactate Dehydrogenase-elevating Virus Results in Suppression of Humoral Antiviral Immune Response but does not Alter the Course of Viraemia or the Polyclonal Activation of B Cells and Immune Complex Formation

Rowland

Even

Anderson

et al. 1994

Journal of General Virology

View full text Add to dashboard Cite

show abstract

“…Support for this concept is found in studies demonstrating that other polyclonal activators stimulate autoantibodies (Hang et al, 1983; Garzelli et al, 1984), and that clones of autoantibodyproducing lymphocytes exist in normal animals (Dresser, 1978;Steele & Cunningham, 1978). Weiland et al (1987) have recently described anti-Golgi apparatus autoantibodies resulting from LDV infection. Therefore, our work confirms and extends the autoantibody-producing potential of LDV infection.…”

Section: (A)mentioning

confidence: 99%

Infection of Mice with Lactate Dehydrogenase-elevating Virus Leads to Stimulation of Autoantibodies

Cafruny

Hovinen

1988

Journal of General Virology

View full text Add to dashboard Cite

SUMMARYThe development of autoimmunity was investigated in BALB/c and C58 mice infected with lactate dehydrogenase-elevating virus (LDV). Autoantibodies reactive by ELISA with syngeneic central nervous system antigens appeared early during LDV infection of both strains of mice, and were maintained for many months. Western blot analysis indicated that the LDV-induced autoantibodies reacted with a variety of different brain antigens, and mouse strain differences in the pattern of autoreactivity were observed. LDV infection of C58 and BALB/c mice also stimulated antibodies reactive with syngeneic liver-, kidney-and spleen-derived antigens, and in Swiss outbred mice heart-reactive antibodies were observed following LDV infection. These results show that autoimmunity is a feature of the deregulation of the immune system which occurs during LDV infection.

show abstract

“…vidence has accumulated that viral infections can produce dysregulation of the immune system and immunopathology (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13). This includes polyclonal B cell activation (3,4,7,8,11), the appearance of autoantibodies (1,2,5,6,9,12,13), and kidney histopathology (14,15).…”

mentioning

confidence: 99%

“…This includes polyclonal B cell activation (3,4,7,8,11), the appearance of autoantibodies (1,2,5,6,9,12,13), and kidney histopathology (14,15). Most recently, it was reported that lymphocytic choriomeningitis virus (LCMV) 3 infection of mice induced polyclonal B cell activation that resulted in hypergammaglobulinemia and autoantibody production (13).…”

mentioning

confidence: 99%

“…Therefore, the possibility that increased B cell numbers observed during PRRSV infection (28) result from the expansion of a monoclonal B cell population cannot be excluded. In any case, the purported polyclonal activation of B cells in mice infected with LDV was associated with circulating immune complexes (IC) and autoantibodies (1,2,4,7,8,10). The IC, which ranged in size from 150 to 300 kDa, contained mainly IgG2a and IgG2b.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Lymphoid Hyperplasia Resulting in Immune Dysregulation Is Caused by Porcine Reproductive and Respiratory Syndrome Virus Infection in Neonatal Pigs

Lemke¹,

Haynes

Spaete

et al. 2004

The Journal of Immunology

View full text Add to dashboard Cite

Amid growing evidence that numerous viral infections can produce immunopathology, including nonspecific polyclonal lymphocyte activation, the need to test the direct impact of an infecting virus on the immune system of the host is crucial. This can best be tested in the isolator piglet model in which maternal and other extrinsic influences can be excluded. Therefore, neonatal isolator piglets were colonized with a benign Escherichia coli, or kept germfree, and then inoculated with wild-type porcine reproductive and respiratory syndrome virus (PRRSV) or sham medium. Two weeks after inoculation, serum IgM, IgG, and IgA levels were 30- to 50-, 20- to 80-, and 10- to 20-fold higher, respectively, in animals receiving virus vs sham controls, although <1% was virus specific. PRRSV-infected piglets also had bronchial tree-associated lymph nodes and submandibular lymph nodes that were 5–10 times larger than colonized, sham-inoculated animals. Size-exclusion fast performance liquid chromatography revealed that PRRSV-infected sera contained high-molecular-mass fractions that contained IgG, suggesting the presence of immune complexes. Lesions, inflammatory cell infiltration, glomerular deposits of IgG, IgM, and IgA, and Abs of all three isotypes to basement membrane and vascular endothelium were observed in the kidneys of PRRSV-infected piglets. Furthermore, autoantibodies specific for Golgi Ags and dsDNA could be detected 3–4 wk after viral inoculation. These data demonstrate that PRRSV induces B cell hyperplasia in isolator piglets that leads to immunologic injury and suggests that the isolator piglet model could serve as a useful model to determine the mechanisms of virus-induced immunopathology in this species.

show abstract

Lactate Dehydrogenase-elevating Virus Induces Anti-Golgi Apparatus Antibodies

Cited by 26 publications

References 27 publications

Neonatal Infection of Mice With Lactate Dehydrogenase-elevating Virus Results in Suppression of Humoral Antiviral Immune Response but does not Alter the Course of Viraemia or the Polyclonal Activation of B Cells and Immune Complex Formation

Neonatal Infection of Mice With Lactate Dehydrogenase-elevating Virus Results in Suppression of Humoral Antiviral Immune Response but does not Alter the Course of Viraemia or the Polyclonal Activation of B Cells and Immune Complex Formation

Infection of Mice with Lactate Dehydrogenase-elevating Virus Leads to Stimulation of Autoantibodies

Lymphoid Hyperplasia Resulting in Immune Dysregulation Is Caused by Porcine Reproductive and Respiratory Syndrome Virus Infection in Neonatal Pigs

Contact Info

Product

Resources

About