Cytotoxic T lymphocyte response to murine cytomegalovirus infection

Quinnan, Gerald V.; Manischewitz, Jody; Ennis, Francis A.

doi:10.1038/273541a0

Cited by 86 publications

(67 citation statements)

References 24 publications

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“…The cytotoxic responses were, in other respects, similar to those described previously in Balb/c mice Quinnan et al, 1978;Quinnan et al, 1980). Two components of the virus-specific cytotoxic response could be distinguished after i.p.…”

Section: Nk Cell and Ctl Responses To Intraperitoneal Infectionsupporting

confidence: 65%

“…The cytotoxic T cell responses developed later, between days 6 and 21. We have previously demonstrated that the CTL response of C3H/HeN mice is H-2-restricted (Quinnan et al, 1978). Experiments were also performed which confirmed that these CTL were non-adherent and were killed by treatment with anti-theta serum and complement.…”

Section: Nk Cell and Ctl Responses To Intraperitoneal Infectionmentioning

confidence: 55%

“…The only documented exception is the interferon response which begins on day 1, as demonstrated in the present study. The other specific responses which have been measured include CTL, from days 6 to 21 (Quinnan et al, 1978;Quinnan et aL, 1980), serum antibody which mediates antivirus antibody-dependent cell-mediated cytotoxicity (ADCC) beginning about day 10 (Manischewitz & Quinnan, 1980), serum neutralizing antibo.dy which develops about day 21 Wise et al, 1979) and a virus-specific lymphocyte proliferation response which develops about day 7 (Howard et al, 1977). It is not possible to exclude the possibility that local antibody production at the site of infected tissue begins at an earlier time, but this phenomenon has not been documented during this infection.…”

Section: Discussionmentioning

confidence: 99%

“…In a preliminary report, a similar response was noted during murine influenza virus infection (Daisy et al, 1980). In each case the response begins within 3 days of onset of infection and then wanes as an H-2-restricted cytotoxic T cell response begins, about 6 days after initiation of infection (Quinnan et al, 1978;Quinnan et al, 1980;Ennis et al, 1978;Zinkernagel & Doherty, 1974). In these infections the NK cell response is, thus, one of the earliest components of the immune response.…”

Section: Introductionmentioning

confidence: 99%

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Involvement of Natural Killer Cells in the Pathogenesis of Murine Cytomegalovirus Interstitial Pneumonitis and the Immune Response to Infection

Quinnan

Manischewitz

Kirmani

1982

Journal of General Virology

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SUMMARYThe significance of the natural killer (NK) cell response to murine cytomegalovirus (MCMV) infection was evaluated in C3H/HeN mice. This strain was selected for study after preliminary demonstration that the NK cell response, occurring between 3 and 6 days post-infection was relatively high in comparison to other mouse strains studied. A dose-response effect of hydrocortisone treatment on suppression of this response was found. A dose of hydrocortisone, given subcutaneously on two successive days, which was found to markedly inhibit the NK cell response, had no effect on development of serum interferon or antibody levels, or spleen cytotoxic T cell activity under the conditions studied. Suppression of the NK cell response by this treatment, however, was accompanied by enhanced spleen and pulmonary virus replication in vivo and increased susceptibility of mice to lethal infection. MCMV interstitial pneumonitis was characterized histologically and lung lymphocytes studied at 4 days post-infection were found to have increased NK cell activity. Treatment of mice with hydrocortisone was found to inhibit development of gross and histological evidence of pneumonitis. These findings indicate that NK cells are involved in the pathogenesis of MCMV interstitial pneumonitis and may function early in infection to restrict the extent of virus replication.

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Section: Nk Cell and Ctl Responses To Intraperitoneal Infectionsupporting

confidence: 65%

Section: Nk Cell and Ctl Responses To Intraperitoneal Infectionmentioning

confidence: 55%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Involvement of Natural Killer Cells in the Pathogenesis of Murine Cytomegalovirus Interstitial Pneumonitis and the Immune Response to Infection

Quinnan

Manischewitz

Kirmani

1982

Journal of General Virology

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“…A microcytotoxicity assay involving an 18-h incubation of lymphocytes with target cells similar to that which we have previously described was used throughout (1). The RBL5 cell line has been previously shown to be susceptible to lysis by NK cells and, when sensitized by allotypic antisera, to lysis by K cells (7).…”

Section: Nk-cell and Adcc Assaysmentioning

confidence: 99%

The role of natural killer cells and antibody-dependent cell-mediated cytotoxicity during murine cytomegalovirus infection.

Quinnan¹,

Manischewitz²

1979

The Journal of Experimental Medicine

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Definition of the functions by which the cellular immune system contributes to control of cytomegalovirus (CMV) infection should permit determination of the specific defects which result in the increased susceptibility to infection of immunosuppressed individuals. Using a murine model, we studied the cytotoxic lymphocyte response to murine CMV infection. This response was found to be biphasic. The initial phase extended from the 3rd to the 6th d after infection, was not genetically restricted, and correlated to a rise in numbers of natural killer (NK) and antibody-dependent killer (K) cells in spleens. The NK- and K-cell responses were preceded, by 24 h, by a rise in serum interferon levels, and occurred before the time when antibody could be measured in serum by neutralization. NK and K cells appear to develop the capacity for specific recognition of CMV-infected cells and the potential to contribute to control of the acute phase of CMV infection.

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Murine cytomegalovirus induces a Sj�gren's syndrome-like disease in C57Bl/6-lpr/lpr mice

Fleck

Kern

Zhou

et al. 1998

Arthritis & Rheumatism

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Objective. To analyze Fas and tumor necrosis factor receptor I (TNFRI) apoptosis pathways in sali-vary gland inflammatory disease induced by murine cytomegaloviru s (MCMV) infection. Methods. Four different strains of mice (C57B1/6 [B6]-+/ + , Fas-deficient B6-lprllpr, TNFRI-deficient B6-tnfrl"", and B6-tnfrlo"-lpr/lpr mice) were infected intra-peritoneally with the Smith strain of MCMV (1 X lo5 plaque-forming units). Viral load was determined by a plaque assay, inflammation and apoptosis by immuno-histochemistry and staining with terminal dUTP nick-end labeling, and autoantibodies by enzyme-linked im-munosorbent assay. Results. Infectious MCMV was not detectable by day 100. Although all MCMV-infected mice developed acute sialadenitis by day 28, a chronic (>lo0 days), severe salivary gland inflammation and anti-Ro and anti-La antibodies developed only in the B6-Zprllpr mice. Apoptotic cells were detected during the acute, but not the chronic, phase of inflammation. Conclusion. Both Fas-and TNFRI-mediated ap-optosis contribute to the clearance of MCMV-infected cells in the salivary glands. However, because Fas-. ~ ~~

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Cytotoxic T lymphocyte response to murine cytomegalovirus infection

Cited by 86 publications

References 24 publications

Involvement of Natural Killer Cells in the Pathogenesis of Murine Cytomegalovirus Interstitial Pneumonitis and the Immune Response to Infection

Involvement of Natural Killer Cells in the Pathogenesis of Murine Cytomegalovirus Interstitial Pneumonitis and the Immune Response to Infection

The role of natural killer cells and antibody-dependent cell-mediated cytotoxicity during murine cytomegalovirus infection.

Murine cytomegalovirus induces a Sj�gren's syndrome-like disease in C57Bl/6-lpr/lpr mice

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