Literature DB >> 3107842

Angiotensin II is chemotactic for a T-cell subset which can express migration inhibition factor activity in murine schistosomiasis mansoni.

J V Weinstock, A M Blum, J T Kassab.   

Abstract

In murine schistosomiasis mansoni, ova induce a delayed-type hypersensitivity, granulomatous response in which angiotensins are produced. Angiotensin II (AII) elicits a chemotaxis for splenic mononuclear cells derived from these infected animals. The effect of AII upon the migration of a T-lymphocyte subset was defined functionally to further delineate this observation. A chemotaxis chamber was developed that permitted collection of large numbers of viable cells which migrate in response to AII. In a direct migration inhibition factor (MIF) assay, MIF activity was demonstrated with 100-fold fewer chemotactically attracted cells as opposed to whole splenic leukocytes. The MIF activity was eliminated by treatment of the cells with anti-Lyt 1.1 or-Thy 1.2 serum and complement. This observation was particularly interesting since migrated and whole spleen cell populations comprised equal numbers of T cells. Incubation of spleen cells with AII prior to assay did not alter MIF activity. These findings suggest that AII is chemotactic for at least one important T-cell subset relevant to the granulomatous response.

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Year:  1987        PMID: 3107842     DOI: 10.1016/0008-8749(87)90278-4

Source DB:  PubMed          Journal:  Cell Immunol        ISSN: 0008-8749            Impact factor:   4.868


  3 in total

1.  Angiotensin II increases host resistance to peritonitis.

Authors:  K Rodgers; S Xiong; T Espinoza; N Roda; S Maldonado; G S diZerega
Journal:  Clin Diagn Lab Immunol       Date:  2000-07

2.  Angiotensin I-converting enzyme in human circulating mononuclear cells: genetic polymorphism of expression in T-lymphocytes.

Authors:  O Costerousse; J Allegrini; M Lopez; F Alhenc-Gelas
Journal:  Biochem J       Date:  1993-02-15       Impact factor: 3.857

3.  Deletion polymorphism in the angiotensin I converting enzyme (ACE) gene as a genetic risk factor for sarcoidosis.

Authors:  K Furuya; E Yamaguchi; A Itoh; N Hizawa; N Ohnuma; J Kojima; N Kodama; Y Kawakami
Journal:  Thorax       Date:  1996-08       Impact factor: 9.139

  3 in total

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