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2014 ; 27
(10
): 484-96
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gab.com Text
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English Wikipedia
Intraepithelial T-cell cytotoxicity, induced bronchus-associated lymphoid tissue,
and proliferation of pneumocytes in experimental mouse models of influenza
#MMPMID25479178
Sell S
; Guest I
; McKinstry KK
; Strutt TM
; Kohlmeier JE
; Brincks E
; Tighe M
; Blackman MA
; Woodland DL
; Dutton RW
; Swain SL
Viral Immunol
2014[Dec]; 27
(10
): 484-96
PMID25479178
show ga
Immunopathologic examination of the lungs of mice with experimental influenza
virus infection reveals three prominent findings. (i) There is rapidly developing
perivascular (arterial) and peribronchial infiltration with T-cells and invasion
of T-cells into the bronchiolar epithelium, separation of epithelial cells from
each other and from the basement membrane, leading to defoliation of the
bronchial epithelium. This reaction is analogous to a viral exanthema of the
skin, such as measles and smallpox. This previously described but unappreciated
reaction most likely is an effective way to eliminate virus-infected cells, but
may contribute to acute toxicity and mortality. (ii) After this, there is
formation of dense collections of lymphocytes adjacent to bronchi consisting
mainly of B-cells, with a scattering of T-cells and macrophages. This is known as
induced bronchial-associated lymphoid tissue (iBALT) and correlates with
increased interleukin (IL)-17 in the lung. iBALT provides sites for a local
immune reaction in the lung to both the original infection and related viral
infections (heterologous immunity). (iii) Within the first 2-3 weeks, there is
proliferation of type II pneumocytes and/or terminal bronchial epithelial cells
extending from the terminal bronchioles into the adjacent alveoli, eventually
leading to large zones of the lung filled with tumor-like epithelial cells with
squamous metaplasia. The proliferation correlates with IL-17 and IL-22
expression, and the extent of this reaction appears to be determined by the
availability of T-regulatory cells.