Experimental hypersensitivity pneumonitis in the rat: histopathology and T-cell subset compartmentalization.
The pathogenesis of hypersensitivity pneumonitis (HP) appears to depend largely on T-cell specificity and interactions with monocytes/macrophages. We studied T-cell subset populations, defined by surface membrane markers with putative functional correlates, present in lung parenchyma and bronchoalveolar spaces of sensitized LEW rats following acute and chronic inhalational challenges with antigen. Our initial hypothesis was that the CD4+ RT6- ( TDH) subset, the effector cell of delayed hypersensitivity, would dominate in HP lesions and that CD8+ RT6+ (TS) or CD8+ CD45R+ (TS) subsets, constituting putative suppressor T-cell populations, would dominate in lungs of animals with resolving lesions. We found, however, a heterogeneous population involving all eight of the T-cell subsets that were evaluated. Percentages of the RT6+ phenotype diminished as T cells moved from peripheral blood to lung. Dominant numbers of T cells in acute HP included CD8+ RT6- (TCYT) and CD8+ CD45R- (TCYT) subsets, with putative cytotoxic T-cell activity, in addition to CD4+ RT6- ( TDH) cells. We did not demonstrate increases in T suppressor cells as the disease waned.[1]References
- Experimental hypersensitivity pneumonitis in the rat: histopathology and T-cell subset compartmentalization. Richerson, H.B., Coon, J.D., Lubaroff, D. Am. J. Respir. Cell Mol. Biol. (1991) [Pubmed]
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