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

Openshaw, Peter

doi:10.1002/eji.1830210338

Cited by 23 publications

(17 citation statements)

References 26 publications

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“…Using a novel antibody (DX5) that identifies BALB\c NK cells, we have shown that NK cells accumulate in the lung during the first 4 CFJI days of infection, at the time that specific T cells are beginning to appear. We are now able to confirm our speculation (Openshaw, 1991) that pulmonary CD4 − \CD8 − cells that appear early during RSV infection are NK cells. Using intracellular cytokine staining, we also now show that these cells do not make IL-4 but do produce large amounts of IFN-γ.…”

Section: Discussionsupporting

confidence: 78%

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Intracellular IFN-gamma expression in natural killer cells precedes lung CD8+ T cell recruitment during respiratory syncytial virus infection.

Hussell

Openshaw

1998

Journal of General Virology

155

110

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Section: Discussionsupporting

confidence: 78%

“…Previous studies have shown that the uninfected mouse BAL cells are almost entirely alveolar macrophages with very few lymphocytes (Openshaw, 1991). By day 4 of infection, a large local accumulation of DX5 + \CD3 − cells was observed (approximately 1n7i10& cells per mouse).…”

Section: Nk Cell Recovery and Cytokine Expression During Primary Rsv mentioning

confidence: 84%

Intracellular IFN-gamma expression in natural killer cells precedes lung CD8+ T cell recruitment during respiratory syncytial virus infection.

Hussell

Openshaw

1998

Journal of General Virology

155

110

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“…Further definition of this cell population may be important for understanding RSV pathogenesis. Possible explanations for this population include doublenegative T-regulatory cells (DN Tregs) 25 that have not been studied in RSV infection; NK T cells that have been noted in the murine model of RSV; 26 or gd T cells that have not been identified in lungs of RSV-infected mice 27 or BRSV-infected cattle. 28 CD3 þ CD8 þ cells were also present, particularly in the interstitial alveolar infiltrates and associated with areas of virus-infected cells.…”

Section: Discussionmentioning

confidence: 99%

The histopathology of fatal untreated human respiratory syncytial virus infection

et al. 2007

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The pathology of respiratory syncytial virus (RSV) infection was evaluated 1 day after an outpatient diagnosis of RSV in a child who died in a motor vehicle accident. We then identified 11 children with bronchiolitis from the Vanderbilt University autopsy log between 1925 and 1959 who met criteria for possible RSV infection in the preintensivist era. Their tissue was re-embedded and evaluated by routine hematoxylin and eosin and PAS staining and immunostaining with RSV-specific antibodies. Tissue from three cases was immunostain-positive for RSV antigen and was examined in detail. Small bronchiole epithelium was circumferentially infected, but basal cells were spared. Both type 1 and 2 alveolar pneumocytes were also infected. Although, not possible for archival cases, tissue from the index case was evaluated by immunostaining with antibodies to define the cellular components of the inflammatory response. Inflammatory infiltrates were centered on bronchial and pulmonary arterioles and consisted of primarily CD69 þ monocytes, CD3 þ double-negative T cells, CD8 þ T cells, and neutrophils. The neutrophil distribution was predominantly between arterioles and airways, while the mononuclear cell distribution was in both airways and lung parenchyma. Most inflammatory cells were concentrated submuscular to the airway, but many cells traversed the smooth muscle into the airway epithelium and lumen. Airway obstruction was a prominent feature in all cases attributed to epithelial and inflammatory cell debris mixed with fibrin, mucus, and edema, and compounded by compression from hyperplastic lymphoid follicles. These findings inform our understanding of RSV pathogenesis and may facilitate the development of new approaches for prevention and treatment.

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“…The cytotoxic response is maximal 7-9 days after infection [18], mainly carried by CD8+ cells [4,9] and of major importance for both viral clearance and pathogenesis of disease [8,9]. Recently, flow cytometry studies defined in more detail the phenotypic characteristics ofthe T cells activated and attracted to the lungs after primary infection with RSV [5,6,19].…”

Section: Discussionmentioning

confidence: 99%

T cell redistribution kinetics after secondary infection of BALB/c mice with respiratory syncytial virus

Kimpen

Ogra

1993

Clinical and Experimental Immunology

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SUMMARYBALB/c mice were infected intranasally with live respiratory syncytial virus (RSV) and reinfected 4 weeks later. At regular intervals thereafter groups of animals were killed and T cell subsets were determined in blood, spleen and bronchoalveolar lavage (BAL) with flow cytometry employing T cell subset-specific MoAbs. Total lymphocyte counts in the peripheral blood decreased 1-3 days after infection, returning to preinfection levels on day 8 (/" = 00111). Simultaneously, a marked increase of lymphocytes was noted in the BAL, reaching a maximum at day 8 (/'<0 0001). Both CD4+ and CD8 + T cells decreased in the blood on day 1 -3 (P < 0 0097 and P = 0 003 respectively), and increased in the BAL progressively towards a maximum at day 8 (/'<0 0001). In BAL, CD4+ cells increased 35-fold and CD8+ cells 27-fold during the first week after reinfection. On the other hand, in the spleen a significant decline of CD4+ and CD8+ cells was noted 1 day post-infection (P = 0 0002). It is concluded that a strong T cell redistribution response among systemic and mucosal tissues occurs after reinfection with RSV. The kinetics of this response differ both quantitatively and qualitatively from the T cell response after primary infection. The magnitude of cell traffic is more pronounced in blood, spleen and BAL than after primary infection. CD4+ T cells are more intensively distributed to the lungs than after primary infection.

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

Cited by 23 publications

References 26 publications

Intracellular IFN-gamma expression in natural killer cells precedes lung CD8+ T cell recruitment during respiratory syncytial virus infection.

Intracellular IFN-gamma expression in natural killer cells precedes lung CD8+ T cell recruitment during respiratory syncytial virus infection.

The histopathology of fatal untreated human respiratory syncytial virus infection

T cell redistribution kinetics after secondary infection of BALB/c mice with respiratory syncytial virus

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