Contribution of T Lymphocytes to the Development of Bleomycin‐Induced Pulmonary Fibrosis^a

H2-EaDeficiency Is a Risk Factor for Bleomycin-Induced Lung Fibrosis in Mice

“…It is known that pulmonary fibrosis is caused by abnormal immune responses to insults (4,12), and it is well established that T cells play an important role in pulmonary fibrosis in mouse models (13)(14)(15). Thus, it is possible that H2-Ea and other class II MHC molecules are involved in lung injuries by activating CD4 ϩ T cells.…”

Respiratory Reovirus 1/L Induction of Intraluminal Fibrosis, a Model of Bronchiolitis Obliterans Organizing Pneumonia, Is Dependent on T Lymphocytes

“…Intratracheal administration of bleomycin in rodents, a model for idiopathic pulmonary fibrosis (IPF), results in interstitial fibrosis accompanied by a significant infiltration of both T and B lymphocytes. 17,18 In this model, some reports have demonstrated that the inhibition or depletion of lymphocytes by anti-lymphocyte antibody, mAb to T-cell subsets, or treatment with steroids inhibited the development of bleomycin-induced fibrosis, 34 -36 while other studies found no effect of T-cell depletion on fibrotic lesions induced by bleomycin instillation. [37][38][39] Similarly, in nude mice lacking T cells or SCID mice deficient in both T and B cells, conflicting evidence for a role of T cells in the fibrotic process has been reported.…”

“…2,5,7,10 -12 Several studies have shown that the infiltration of T lymphocytes may be important in the development of other forms of pulmonary fibrosis, although the data from both animal models and patients has been equivocal. [13][14][15][16][17][18] Although these existing models of experimental pulmonary fibrosis have been useful for histopathological and functional investigations of other types of fibrotic events in the lung, the process of fibrotic lesion development in these models may be distinct from BOOP lesion development. Thus, differences in the phenotype of the inflammatory cell infiltrate, expression of soluble mediators, and response to various treatments may be different and, therefore, may fail to accurately reflect the intraluminal and fibroblastic nature of the bronchoalveolar obliteration observed in BOOP lesions.…”

Accessory cells with immunophenotypic and functional features of monocyte-derived dendritic cells are recruited to the lung during pulmonary inflammation

“…T cell numbers are increased in the lungs and regional lymph nodes after the administration of BLM, and APC activities may be required for this expansion. A specific role for T lymphocytes in the pathogenesis of BLM-induced lung injury has been suggested by the finding of diminished fibroinflammatory changes in mice or rats whose T lymphocytes were congenitally absent [37], depleted by antibodies [27,[38][39][40], or inhibited with cyclosporin A [41,42]. Although the majority of investigations support a requirement for T lymphocytes in the pathogenesis of BLM pulmonary injury, others indicate no reduction in BLMinduced fibrosis in nude mice [43], SCID mice [42], or T lymphocyte-depleted mice [18].…”