In vivo polyclonal B-lymphocyte activation elicited by murine viruses

Coutelier, Jean‐Paul; Coulie, Pierre G.; Wauters, Pierre; Heremans, Hubertine; Logt, J T van der

doi:10.1128/jvi.64.11.5383-5388.1990

Cited by 78 publications

(55 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…MHV is known to be lymphotropic and to induce diverse alterations of immune responses that depend on the mouse genetic background [5,20,21]. Thus, a model of MHV-induced anti-FAH autoAb was based on antigen mimicry -FAH N-terminal sequence is about 50% homologous with a MHV proteintogether with the alarm signals released by the MHV-injured liver.…”

Section: Discussionmentioning

confidence: 99%

“…Mice were inoculated intraperitoneally with 10 4 TCID 50 of MHV-A59 grown in NCTC 1469 cells [5]. Thirty days after the infection, the mice were injected intraperitoneally with 100 µl of mineral oil containing 0.16 µl of CCl 4 (dilution: 1:625).…”

Section: Viral Infection and Carbon Tetrachloride (Ccl4) Treatmentmentioning

confidence: 99%

“…Viruses have been long associated with autoimmune diseases [1][2][3][4]. It was proposed that these infectious agents trigger an autoimmune response by diverse mechanisms, including polyclonal B-lymphocyte activation, release of sequestered autoantigens (autoAg), antigenic mimicry, modification of self-antigen, epitope spreading of the anti-viral immune response, enhancement of major histocompatibility complex molecule expression, bystander activation or viral persistence [2,[4][5][6].…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

The autoimmune response induced by mouse hepatitis virus A59 is expanded by a hepatotoxic agent

Aparicio

Vega

Loureiro

et al. 2009

International Immunopharmacology

View full text Add to dashboard Cite

Mouse hepatitis virus strain A59 (MHV-A59) triggers various pathologies in several mouse strains, including hypergammaglobulinaemia, hepatitis and thymus involution. We reported previously the presence of autoantibodies (autoAb) to liver and kidney fumarylacetoacetate hydrolase (FAH) in sera from mice infected with MHV-A59. Long-term MHV-infected mice represented a good model of non-pathogenic autoimmune response since the animals were apparently healthy in spite of the presence of autoAb. The aim of this work was to see whether a severe liver injury, which releases endogenous adjuvants, i.e. danger signals, could elicit a broader spectrum of autoAb and perhaps signs of autoimmune hepatitis. Carbon tetrachloride (CCl(4)) was injected into mice 30 days after MHV infection, and serum was assayed for autoAb and total IgG 20 days later. The association of MHV infection with the toxic effects of CCl(4) resulted in hypergammaglobulinaemia and the production of autoAb to various liver and kidney proteins. Histological examination of liver samples showed tissue damages but without significant differences between the animals submitted to MHV+CCl(4) and controls, which were either infected by MHV without CCl(4), or poisoned by CCl(4) in the absence of MHV infection. Those results show that liver injury after viral infection may lead to the spreading of the immune response and to an increase of serum IgG, suggesting that the procedure used herein could simulate the onset of autoimmune hepatitis.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Viral Infection and Carbon Tetrachloride (Ccl4) Treatmentmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

The autoimmune response induced by mouse hepatitis virus A59 is expanded by a hepatotoxic agent

Aparicio

Vega

Loureiro

et al. 2009

International Immunopharmacology

View full text Add to dashboard Cite

show abstract

“…Thus, it was suggested that structural features of autoantigens, their locations, and catabolism during cell death and their translocation to cells that can present antigens to the immune system could contribute to selection of the autoimmune repertoire [16,17]. MHV is known to be lymphotropic and to induce diverse alterations of immune responses that depend on the mouse genetic background [1e4, 18,19], but why liver FAH was chosen as autoantigen among the large variety of liver proteins? As said by P. H Plotz [17]: ''The repertoire of target autoantigens is a wunderkammer e a collection of curiosities e of molecules with no obvious linking principle''.…”

Section: Discussionmentioning

confidence: 99%

The peptide specificities of the autoantibodies elicited by mouse hepatitis virus A59

Vega

Loureiro

Mathieu

et al. 2006

Journal of Autoimmunity

View full text Add to dashboard Cite

Synthetic decapeptides (N=206) covering the entire sequence of mouse liver fumarylacetoacetate hydrolase (FAH) were used to analyze the specificities of the autoantibodies (autoAb) elicited towards this enzyme in mice infected with mouse hepatitis virus (MHV). These autoAb bound mainly to N- and C-terminal FAH peptides, the most reactive sequences being 1-50 and 390-420, respectively. Surprisingly, although FAH sequence 1-50 shares a high degree of homology with various MHV proteins, the C-terminal portion does not. Moreover, whereas the autoAb reacted with homologous peptides surrounding residues 70, 160 and 360, non-similar sequences around residues 130, 210, 240, 250, and 300 were also recognized, indicating that autoAb were not restricted to epitopes with sequence homologies. There was also a lack of correlation between the amount of anti-MHV or anti-FAH antibodies produced and the reactivity towards the peptides. Moreover, the spectrum of peptides recognized by the autoAb of a given mouse did not change significantly with time, which suggests that the MHV-elicited autoimmune response does not induce an epitope recognition spreading. Finally, anti-FAH Ab produced after immunization with rat liver FAH recognized essentially the same mouse FAH regions than autoAb from MHV-infected mice. Results indicated that the induction of the autoAb is not only related to molecular or structural mimicry, but rather supports the Danger model, in which any aggression, in this case the MHV infection, is susceptible to trigger the production of autoAb.

show abstract

“…Viruses have been implicated in the generation of autoimmune disorders over the last 20 years [1e3]. It has been proposed that these infectious agents trigger an autoimmune humoral response by diverse mechanisms, including polyclonal B-lymphocyte activation, release of sequestered autoantigens (autoAg), antigenic mimicry, modification of self-antigen, epitope spreading of the anti-viral immune response or enhancement of major histocompatibility complex molecule expression [2,4,5].…”

Section: Introductionmentioning

confidence: 99%

Sequence similarity and structural homologies are involved in the autoimmune response elicited by mouse hepatitis virus A59

Mathieu

Gómez

Coutelier

et al. 2004

Journal of Autoimmunity

View full text Add to dashboard Cite

The features of autoantibodies (autoAb) to liver fumarylacetoacetate hydrolase (FAH) elicited in mice infected with mouse hepatitis virus (MHV) were studied by ELISA and western-blot competition assays. All sera tested contained Ab to cryptic FAH epitopes according with results from western-blot tests, whereas ELISA data indicated that some of these same sera did recognize native epitopes of the autoantigen (autoAg). Such differences were detected in individual sera from various mouse strains, and were ascribed to the fact that proteins insolubilized on solid supports expose a variety of conformational and cryptic antigenic determinants. On the other hand, whereas results from both experimental protocols showed that anti-MHV Ab did not cross-react with the soluble autoAg, the opposite situation did not show analogous results. Thus, binding of autoAb to insolubilized FAH could be inhibited by MHV depending on the mouse serum or the experimental protocol used. Additionally, a set of synthetic homologous peptides from mouse FAH and various viral proteins was employed to analyze the Ab repertoire of MHV-infected mice. Results indicated that two homologous peptides were recognized by most Ab: the N-terminal sequences (1-10) from FAH and the nucleocapside, both sharing 50% of identity, and sequence 2317-2326 of the RNA polymerase, a peptide showing 30% of identity with FAH 11-20. Results indicated that MHV-infection triggers at least three distinct Ab populations: anti-MHV, anti-FAH and cross-reacting Ab. This cross-reaction implies either sequential or conformational epitopes from both the viral proteins and the autoAg and may differ between individuals.

show abstract

In vivo polyclonal B-lymphocyte activation elicited by murine viruses

Cited by 78 publications

References 33 publications

The autoimmune response induced by mouse hepatitis virus A59 is expanded by a hepatotoxic agent

The autoimmune response induced by mouse hepatitis virus A59 is expanded by a hepatotoxic agent

The peptide specificities of the autoantibodies elicited by mouse hepatitis virus A59

Sequence similarity and structural homologies are involved in the autoimmune response elicited by mouse hepatitis virus A59

Contact Info

Product

Resources

About