Abstract：
AIMS:We investigated the pathophysiological changes in mice lacking α2-antiplasmin (α2-AP) and plasminogen activator inhibitor type-1 (PAI-1) genes, and elucidated the involvement of these inhibitors for fibrinolysis in immune response. MAIN METHODS:The pathophysiological changes induced by a lack of both α2-AP and PAI-1 were investigated using double knockout (KO) mice. The lung, liver, kidney and spleen tissues from α2-AP/PAI-1-double KO mice were compared with those from wild-type (WT) mice. Furthermore, the bone marrow cells from α2-AP/PAI-1-double KO mice were transplanted into 10-Gy X ray irradiated WT mice, and then the effects of the transplantation were studied. KEY FINDINGS:Plasma IgE levels in the α2-AP/PAI-1-double KO mice increased with age and exceeded 1000 ng/mL after 6 months of age. The plasma cells that produced IgE were detected in perivascular assembled lymphocytes. In the α2-AP/PAI-1-double KO mice, perivascular lymphocyte infiltration was observed in the lung, liver, and kidneys and peribronchial lymphocyte infiltration was present in the lung. When the bone marrow cells from α2-AP/PAI-1-double KO mice were transplanted into 10-Gy X ray irradiated WT mice, the phenotypes of the recipients were similar to those of α2-AP/PAI-1-double KO mice. SIGNIFICANCE:The simultaneous expression of both the α2-AP and PAI-1 genes contributes to the maintenance of immunological functions that are related to IgE. Moreover, it is suggested that both α2-AP and PAI-1 are involved in the recruitment of lymphocytes in the peripheral tissues.
journal_name
Life Scijournal_title
Life sciencesauthors
Okada K,Ueshima S,Kawao N,Yano M,Tamura Y,Tanaka M,Sakamoto A,Hatano M,Arima M,Miyata S,Nagai N,Tokuhisa T,Matsuo Odoi
10.1016/j.lfs.2013.05.023subject
Has Abstractpub_date
2013-07-30 00:00:00pages
89-95issue
2-3eissn
0024-3205issn
1879-0631pii
S0024-3205(13)00312-3journal_volume
93pub_type
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