Cellular response to respiratory viruses with particular reference to children with disorders of cell-mediated immunity

Fishaut, Mark; Tubergen, David G.; McIntosh, Kenneth

doi:10.1016/s0022-3476(80)80799-2

Cited by 229 publications

(109 citation statements)

References 63 publications

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“…RSV-infected children with prolonged viral shedding, severe disease, and giant cell pneumonia have not had isolated cell-mediated deficiencies, but have had severe combined immunodeficiency syndrome with deficits in both T cell and B cell functions (16,17). RSV-specific lymphocyte proliferation has been detected in normal children after RSV infection (18,19), but there is no clear correlation with age or severity ofdisease ( 18) and neither the phenotype nor the function of the proliferating cells was defined.…”

Section: Discussionmentioning

confidence: 99%

Role of T lymphocyte subsets in the pathogenesis of primary infection and rechallenge with respiratory syncytial virus in mice.

Graham¹,

Bunton²,

Wright³

et al. 1991

J. Clin. Invest.

468

441

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The role of CD4+ and CD8+ T lymphocytes in terminating respiratory syncytial virus (RSV) replication, causing disease, and protecting from reinfection was investigated using a BALB/c mouse model in which CD4+ or CD8+ lymphocytes or both were depleted by injections of Mab directed against the respective mouse lymphocyte determinants. Kinetics of RSV replication, illness, and pathology were assessed after primary infection and rechallenge. Both CD4+ and CD8+ lymphocyte subsets were involved in terminating RSV replication after primary infection. When both T lymphocyte subsets were depleted RSV replication was markedly prolonged, yet no illness was evident, suggesting that host immune response rather than viral cytocidal effect was the primary determinant of disease in mice. Both CD4+ and CD8+ lymphocytes contributed to illness, although CD8+ lymphocytes appeared to play the dominant role in this particular system. Analysis of histological responses suggested that CD4+ lymphocytes were required for the appearance of peribronchovascular lymphocytic aggregates seen in normal mice after rechallenge, and that the presence of alveolar lymphocytes was correlated with illness. It is postulated that antibody is an illness-sparing mechanism for protecting mice from RSV infection, and that T lymphocytes are an important determinant of illness. Further delineation of RSVinduced immunopathogenesis in primary infection and reinfection will provide important information for the development of vaccine strategies. (J. Clin. Invest. 1991. 88:1026-1033

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Section: Discussionmentioning

confidence: 99%

Role of T lymphocyte subsets in the pathogenesis of primary infection and rechallenge with respiratory syncytial virus in mice.

Graham¹,

Bunton²,

Wright³

et al. 1991

J. Clin. Invest.

468

441

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“…28 Hall et al 29 demonstrated that long-term steroid use in children resulted in prolonged shedding of respiratory syncytial virus, which was proposed to be due to uninhibited replication from an impaired cell-mediated immune response. It is likely that the pronounced changes noted in CD4 ϩ cells and in the CD4/CD8 ratio in premature infants treated with dexamethasone may explain the mechanism of action of steroids by decreasing the inflammatory mediators and also may account for the increased predilection of these infants to viral infections, particularly respiratory syncytial virus.…”

Section: Discussionmentioning

confidence: 99%

Effect of Dexamethasone on Lymphocyte Subpopulations in Premature Infants with Bronchopulmonary Dysplasia

et al. 1999

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OBJECTIVE:This study was designed to determine the effect of dexamethasone treatment on peripheral blood lymphocyte counts and subpopulations in premature infants with bronchopulmonary dysplasia (BPD). STUDY DESIGN:Peripheral blood lymphocyte subpopulations in 12 premature infants with BPD were analyzed before treatment with a 6-week course of dexamethasone (day 0), on days 3 and 10 of treatment, and 2 weeks after discontinuing dexamethasone therapy (day 56). Lymphocyte immunophenotypes were determined using direct two-color immunofluorescent staining followed by flow cytometry. RESULTS:The percentage of lymphocytes was significantly lower on days 3 (17.55 Ϯ 2.55) and 10 (20 Ϯ 11.8) of dexamethasone therapy compared with before (30.36 Ϯ 6.41) or after treatment. The percentage of T cells was significantly lower on days 3 and 10 of dexamethasone therapy (mean Ϯ SEM; 58.09 Ϯ 1.93 and 60.09 Ϯ 2.47, respectively) compared with before (67.09 Ϯ 4.24) or after treatment. The absolute number of T cells was significantly lower on day 10 of therapy. The percentage of CD4 ϩ cells was significantly lower on days 3 (38.91 Ϯ 2.49) and 10 (40.45 Ϯ 2.24) of therapy, and this decrease persisted after dexamethasone was stopped (36.73 Ϯ 3.41). The absolute number of CD4 cells was significantly lower on day 10 (1328 Ϯ 216) of therapy and reached a nadir on day 56 (1143 Ϯ 106). Similarly, the CD4/CD8 ratio was also significantly lower on days 3 and 10 of treatment (1.56 Ϯ 0.18 and 1.64 Ϯ 0.14, respectively) and reached a nadir on day 56 (1.04 Ϯ 0.13). CONCLUSION:Dexamethasone significantly reduced the percentage and absolute number of lymphocytes, T cells, and CD4 cells, as well as the CD4/CD8 ratio. A reduction in CD4 cells and in the CD4/CD8 ratio persisted 2 weeks after dexamethasone therapy was stopped. In contrast, the absolute number of B cells increased transiently, and CD8 cells were unaffected by dexamethasone. This alteration in lymphocyte subpopulations may help account for the clinically beneficial anti-inflammatory effect of dexamethasone in the treatment of BPD complicated by respiratory failure. The dexamethasone-induced decrease in CD4 cells may also increase the susceptibility of these infants to infection.Bronchopulmonary dysplasia (BPD) is a chronic lung disease associated with mechanical ventilation in premature infants and a common cause of morbidity in the neonatal intensive care unit. The incidence of BPD is Յ40% among infants with respiratory distress syndrome who require mechanical ventilation. 1 Treatment with intravenous dexamethasone has been shown to shorten the duration of mechanical ventilation in premature infants, 2 and to improve pulmonary function. 3 However, dexamethasone therapy has many potential side effects in premature infants, including hyperglycemia, 4 hypertension, 5 cardiomyopathy, 6 adrenal suppression, 7-9 and gastrointestinal bleeding. 10 Dexamethasone has been shown to cause neutrophilia and eosinopenia 11,12 in addition to inhibition of colony formation of the hematopoietic progenito...

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“…Also, reinfection by the same strain can occur in the face of neutralizing antibody (Coates et al, 1963;Beem, 1967;Henderson et al, 1979). A successful vaccine may, therefore, need to elicit a cellular immune response to RSV in addition to antibody; there is evidence in man (Fishaut et al, 1979), cotton rats (Sun et al, 1983) and mice (M. J. Cannon & E. J. Stott, unpublished observations) that cell-mediated immunity plays a part in combating RSV infection. We have recently t Present address: Nuffield Department of Clinical Medicine, Job.n Radcliffe Hospital, Oxford OX3 9DU, U.K. 0000-6943 O 1986 SGM described the generation in mice of RSV-specific, major histocompatibility complex-(MHC)-restricted cytotoxic T cells (Tc) (Bangham et al, 1985).…”

Section: Introductionmentioning

confidence: 99%

Murine Cytotoxic T Cells Specific to Respiratory Syncytial Virus Recognize Different Antigenic Subtypes of the Virus

Bangham¹,

Askonas²

1986

Journal of General Virology

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SUMMARYThe aim of this study was to establish whether cytotoxic T cells (Tc), raised against respiratory syncytial virus (RSV) in the mouse, are specific to the strain of immunizing virus, or cross-reactive between virus strains. Several recent studies using monoclonal antibodies have begun to define the antigenic variation among strains of RSV. It is likely that a successful RSV vaccine will need to contain antigenic determinants from more than one subtype, but since only the highest levels of neutralizing antibody are able to give complete protection against RSV infection, a vaccine may also need to elicit a cellular immune response. We have recently described H-2-restricted, RSVspecific Tc following RSV infection in the mouse; we present here evidence that polyclonal RSV-specific Tc in the mouse recognize syngeneic target cells infected with every human strain of RSV tested, whatever the subtype. The only RSV strain that appeared not to be recognized was bovine RSV, which seems unable to infect mouse cells; however, bovine cells, infected with bovine RSV and fixed with glutaraldehyde, primed mice for Tc which recognized human strains of RSV.

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Cellular response to respiratory viruses with particular reference to children with disorders of cell-mediated immunity

Cited by 229 publications

References 63 publications

Role of T lymphocyte subsets in the pathogenesis of primary infection and rechallenge with respiratory syncytial virus in mice.

Role of T lymphocyte subsets in the pathogenesis of primary infection and rechallenge with respiratory syncytial virus in mice.

Effect of Dexamethasone on Lymphocyte Subpopulations in Premature Infants with Bronchopulmonary Dysplasia

Murine Cytotoxic T Cells Specific to Respiratory Syncytial Virus Recognize Different Antigenic Subtypes of the Virus

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