Cytotoxic Lymphocytes in the Lungs of Mice Infected with Respiratory Syncytial Virus

Taylor, Geraldine; Stott, E. J.; Hayle, Allan J.

doi:10.1099/0022-1317-66-12-2533

Cited by 69 publications

(49 citation statements)

References 24 publications

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“…Thus, the virus specificity of these primary cells appears comparable with that of secondary CTLs activated from the spleens of experimentally infected mice in convalescence (Bangham & Askonas, 1986). The correlation between the rise of pulmonary CTL activity and the decline of virus shedding made in our study confirms observations made previously (Taylor et al, 1985). …”

Section: Discussionsupporting

confidence: 81%

“…Such research has led to the emergence of two species of rodents, namely cotton rats and more recently laboratory mice, as the primary small laboratory animal models of RS virus infection (Dreizen et al, 1971 ;Prince et al, 1978;Taylor et al, 1984b). In this report the grade of infection produced in the lungs of the Newcastle colony of BALB/c mice proved to be significantly lower than that described in previous studies (Taylor et al, 1984b(Taylor et al, , 1985Graham et al, 1988). This is highlighted by both the lower yield and the duration of virus shedding, as well as by the sparse distribution of viral antigen and mild histopathological lesions which were apparent within the lungs of our animals.…”

Section: Discussioncontrasting

confidence: 49%

“…The use of suitable animal models, however, provides an alternative means of analysing these immune responses. Cellular responses to RS virus infection in the lungs of both cotton rats and inbred laboratory mice have been described (Kumagi et al, 1985;Sun et al, 1983a, b;Taylor et al, 1985). A correlation has been found between the decline of virus shedding within the lungs of infected cotton rats and the activation of a pulmonary population of natural killer (NK) cells.…”

confidence: 92%

“…Immunocompromised as well as immunodeficient BALB/c mice have each been shown to be unable to resolve experimental RS virus infection (Taylor et al, 1985;Cannon et al, 1987). Adoptive transfer of secondary virus-specific CTLs to these animals has also been shown to clear the virus rapidly from the lungs of these otherwise persistently infected animals (Cannon et al, 1987).…”

Section: Discussionmentioning

confidence: 99%

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Analysis of the local and systemic immune responses induced in BALB/c mice by experimental respiratory syncytial virus infection

Anderson

Norden²,

Saunders³

et al. 1990

Journal of General Virology

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Section: Discussionsupporting

confidence: 81%

Section: Discussioncontrasting

confidence: 49%

confidence: 92%

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Analysis of the local and systemic immune responses induced in BALB/c mice by experimental respiratory syncytial virus infection

Anderson

Norden²,

Saunders³

et al. 1990

Journal of General Virology

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“…CTL and NK cell activities have been found in the cerebrospinal fluid during vaccinia virus-induced meningitis (13), and CTL are present in meningeal exudates during LCMV-induced meningitis (14). CTL have also been isolated from the lung during infection with influenza (15) and respiratory syncytial (16) viruses, but to our knowledge, virus-specific CTL have not been demonstrated in the virus-infected liver.…”

mentioning

confidence: 99%

Accumulation of natural killer and cytotoxic T large granular lymphocytes in the liver during virus infection.

McIntyre¹,

Welsh²

1986

The Journal of Experimental Medicine

102

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The immunologic mechanisms involved in virus-induced hepatitis were examined by measuring the cytotoxic capabilities and the morphologic and antigenic phenotypes of leukocytes isolated from livers of virus-infected mice. Large granular lymphocytes (LGL) of both natural killer (NK) cell and cytotoxic T lymphocyte (CTL) phenotypes were found to accumulate in livers of mice infected with either the nonhepatotropic Armstrong strain of lymphocytic choriomeningitis virus (LCMV-ARM) or the hepatotropic WE strain (LCMV-WE). Between days 1 and 5 postinfection (p.i.), both viruses induced a three- to fourfold increase in NK cell lytic activity in the livers of C3H/St mice and a three- to fourfold increase in the number of LGL in the organ. These LGL were characterized as NK cells on the basis of cell surface antigens, kinetics of appearance, target cell range, and morphology. By day 7 p.i., virus-specific, H-2-restricted, Thy-1+, Lyt-2+, CTL activity was present in the liver, and its appearance correlated with a second wave of LGL accumulation. CTL activity, total leukocyte number, and CTL/LGL number were at least fivefold higher in the livers of mice infected with LCMV-WE than with LCMV-ARM. The dramatic LCMV-WE-induced day 7 increases in total leukocytes and LGL were absent in athymic nude (nu/nu) mice, suggesting that the increases were T cell-dependent. LCMV-ARM infection of C57BL/6 mice induced significant spleen CTL activity but little liver CTL activity, whereas LCMV-WE infection resulted in significant liver CTL activity but minimal spleen CTL activity. Mice infected with the cytopathic hepatotropic viruses, mouse hepatitis virus (MHV) and murine cytomegalovirus (MCMV), experienced much greater increases in liver NK/LGL by day 3 p.i. than did mice infected with LCMV or injected with the interferon-inducer poly(I-C). MHV-infected mice homozygous for the beige (bg/bg) mutation also exhibited significant increases in liver NK/LGL cell number and activity, although the activity was less than heterozygote controls, and the morphology of the LGL granules was aberrant. These data show that the LGL accumulate in virus-infected organs, in this case, the liver. An early NK/LGL influx is most pronounced during infection with cytopathic hepatotropic viruses. This initial influx of NK/LGL is followed later by an influx of CTL also possessing LGL morphology. The CTL/LGL response in the liver is significantly greater during hepatotropic virus infections, even when a strong CTL response in the spleen is lacking.

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Pulmonary epithelial T cells induced by viral infection express T cell receptors α/β

Openshaw

1991

Eur J Immunol

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Cells were recovered from the lungs of mice by bronchoalveolar lavage before and after infection with respiratory syncytial (RS) virus. Uninfected mice yielded mostly macrophages, but after RS virus infection lymphocytes also appeared. Recovered cells were stained for CD4, CD8' and either CD3, T cell receptor (TcR) alpha/beta or TcR gamma/delta and analyzed by 3-color flow cytometry. Both the CD4+CD8- and CD4-CD8+ subpopulations stained uniformly for CD3 and TcR alpha/beta, while none stained for TcR gamma/delta. Of the CD4-CD8- cells, about 5% stained for CD3 and TcR alpha/beta during the first week after infection, although this figure increased during the second week. A small and variable fraction of this subset stained for TcR gamma/delta. These results oppose the view that lymphocytes expressing TcR gamma/delta predominate in initial epithelial immune responses to viral infections.

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Cytotoxic Lymphocytes in the Lungs of Mice Infected with Respiratory Syncytial Virus

Cited by 69 publications

References 24 publications

Analysis of the local and systemic immune responses induced in BALB/c mice by experimental respiratory syncytial virus infection

Analysis of the local and systemic immune responses induced in BALB/c mice by experimental respiratory syncytial virus infection

Accumulation of natural killer and cytotoxic T large granular lymphocytes in the liver during virus infection.

Pulmonary epithelial T cells induced by viral infection express T cell receptors α/β

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