Virus-Induced Immunopathology

Rouse, Barry T.

doi:10.1016/s0065-3527(08)60739-3

Cited by 34 publications

(15 citation statements)

References 103 publications

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“…In some instances, tissue damage is the direct consequence of virus replication, whereas in others, lesions are the sequel to immune responses against viral components (1,2). In such instances, either CD4 ϩ or CD8 ϩ T cells usually act as the principal mediators of the immunopathology.…”

Section: Nflammatory Lesions Caused By Viruses Involve Many Eventsmentioning

confidence: 99%

“…A less frequent, and still poorly understood, outcome of virus infection is the induction of an autoinflammatory reaction (1). Explanations for the mechanism of viral-induced breakdown in self-tolerance include unveiling of "hidden self," molecular mimicry between viral and host components, determinant spreading, and bystander damage associated with recruited cells and aberrant cytokine production (1)(2)(3). One viral-induced immunopathology that could involve an autoinflammatory reaction is herpetic stromal keratitis (HSK) 3 (4,5).…”

Section: Nflammatory Lesions Caused By Viruses Involve Many Eventsmentioning

confidence: 99%

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Bystander Activation Involving T Lymphocytes in Herpetic Stromal Keratitis

Deshpande

Zheng

Banerjee

et al. 2001

The Journal of Immunology

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Herpes simplex virus infection of mouse corneas can lead to the development of an immunopathological lesion, termed herpetic stromal keratitis (HSK). Such lesions also occur in TCR-transgenic mice backcrossed to SCID (TgSCID) that are unable to mount detectable HSV-specific immune responses. The present study demonstrates that lesion expression in such mice depends on continuous viral replication, whereas in immunocompetent mice, lesions occurred even if virus replication was terminated at 4 days after infection. The continuous replication in TgSCID mice was considered necessary to produce an activating stimulus to CD4+ T cells that invade the cornea. Lesions in TgSCID were resistant to control by cyclosporin A, but were inhibited by treatment with rapamycin. This result was interpreted to indicate that T cell activation involved a non-TCR-mediated cytokine-driven bystander mechanism. Bystander activation was also shown to play a role in HSK lesions in immunocompetent mice. Accordingly, in immunocompetent DO11.10 mice, lesions were dominated by KJ1.26+ OVA-specific CD4+ T cells that were unreactive with HSV. In addition, KJ1.26+ HSV nonimmune cells parked in ocularly infected BALB/c mice were demonstrable in HSK lesions. These results provide insight for the choice of new strategies to manage HSK, an important cause of human blindness.

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Section: Nflammatory Lesions Caused By Viruses Involve Many Eventsmentioning

confidence: 99%

Section: Nflammatory Lesions Caused By Viruses Involve Many Eventsmentioning

confidence: 99%

Bystander Activation Involving T Lymphocytes in Herpetic Stromal Keratitis

Deshpande

Zheng

Banerjee

et al. 2001

The Journal of Immunology

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“…Infection with this virus has been associated with abortion, neonatal diseases, classical rhinotracheitis, chronic conjunctivitis and keratitis, recurrent rhinitis, chronic sinusitis, and central nervous system disease (19,24). One dreaded complication associated with reactivation of FeHV-1 is herpetic stromal keratitis (HSK) (19,24), which is supposed to rely on an immunopathological basis (1,21,24,28,33,36). However, a chronic course of primary infection may also lead to HSK.…”

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confidence: 99%

Quantification of Feline Herpesvirus 1 DNA in Ocular Fluid Samples of Clinically Diseased Cats by Real-Time TaqMan PCR

et al. 2002

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“…It is conceivable that exposure to various agents (such as bacteria and viruses) is one of the instrumental causes in modulating the incidence, severity, or even the type of autoimmune process acquired by an individual (45)(46)(47)(48)(49)(50)(51). Likewise, this type of adventitious microbial stimulation occurring throughout the life of an individual could play an important role in establishing expanded repertoires of pathogenic/regulatory memory T cells (52)(53)(54).…”

Section: Discussionmentioning

confidence: 99%

Environmental Modulation of Autoimmune Arthritis Involves the Spontaneous Microbial Induction of T Cell Responses to Regulatory Determinants Within Heat Shock Protein 65

Moudgil

Kim

Yun³

et al. 2001

The Journal of Immunology

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Both genetic and environmental factors are believed to be involved in the induction of autoimmune diseases. Adjuvant arthritis (AA) is inducible in susceptible rat strains by injection of Mycobacterium tuberculosis, and arthritic rats raise T cell responses to the 65-kDa mycobacterial heat-shock protein (Bhsp65). We observed that Fischer 344 (F344) rats raised in a barrier facility (BF-F344) are susceptible to AA, whereas F344 rats maintained in a conventional facility (CV-F344) show significantly reduced incidence and severity of AA, despite responding well to the arthritogenic determinant within Bhsp65. The acquisition of protection from AA can be circumvented if rats are maintained on neomycin/acidified water. Strikingly, naive unimmunized CV-F344 rats but not BF-F344 rats raised T cell responses to Bhsp65 C-terminal determinants (BCTD) (we have previously shown that BCTD are involved in regulation of acute AA in the Lewis rat); however, T cells of naive CV-F344 and BF-F344 gave a comparable level of proliferative response to a mitogen, but no response at all to an irrelevant Ag. Furthermore, adoptive transfer into naive BF-F344 rats of splenic cells of naive CV-F344 rats (restimulated with BCTD in vitro) before induction of AA resulted in a considerably reduced severity of AA. These results suggest that spontaneous (inadvertent) priming of BCTD-reactive T cells, owing to determinant mimicry between Bhsp65 and its homologues in microbial agents in the conventional environment, is involved in modulating the severity of AA in CV-F344 rats. These results have important implications in broadening understanding of the host-microbe interaction in human autoimmune diseases.

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Virus-Induced Immunopathology

Cited by 34 publications

References 103 publications

Bystander Activation Involving T Lymphocytes in Herpetic Stromal Keratitis

Bystander Activation Involving T Lymphocytes in Herpetic Stromal Keratitis

Quantification of Feline Herpesvirus 1 DNA in Ocular Fluid Samples of Clinically Diseased Cats by Real-Time TaqMan PCR

Environmental Modulation of Autoimmune Arthritis Involves the Spontaneous Microbial Induction of T Cell Responses to Regulatory Determinants Within Heat Shock Protein 65

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