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Integrin‐dependent role of human T cell matrix metalloproteinase activity in chemotaxis through a model basement membrane
Author(s) -
Xia Menghang,
Sreedharan Sunil P.,
Dazin Paul,
Damsky Caroline H.,
Goetzl Edward J.
Publication year - 1996
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/(sici)1097-4644(19960601)61:3<452::aid-jcb12>3.0.co;2-l
Subject(s) - matrigel , fibronectin , chemotaxis , integrin , basement membrane , laminin , microbiology and biotechnology , type iv collagen , matrix metalloproteinase , extracellular matrix , t cell , biology , chemistry , cell , immunology , receptor , biochemistry , immune system
Human T lymphoblastoma cells of the CD4 + 8 + Tsup‐1 line, that express alpha4 and alpha5 but not alpha6 integrins of the beta1 family, and CD4 + human blood T cells bind vasoactive intestinal peptide (VIP) with high affinity, leading to increased adherence, secretion of matrix metalloproteinases (MMPs), and chemotaxis. VIP‐enhanced adherence of T cells to fibronectin was inhibited significantly by neutralizing monoclonal antibodies to beta1 > alpha4 >> alpha5, but not to alpha6. Antibodies to beta1 and alpha4 suppressed to a similarly significant extent VIP stimulation of both MMP‐dependent T cell chemotaxis through fibronectin‐enriched Matrigel and T cell degradation of 3 H‐type IV collagen in the Matrigel, without affecting VIP‐evoked secretion of MMP by suspensions of T cells. The lesser inhibition of VIP‐enhanced adherence of T cells to fibronectin by anti‐alpha5 antibody, than antibodies to beta1 or alpha4 chains, was associated with lesser or no suppression of MMP‐dependent T cell chemotaxis through Matrigel and T cell degradation of type IV collagen in the Matrigel in response to VIP. Specific beta1 integrins thus mediate interactions of stimulated T cells with basement membranes, including adherence, localized digestion by MMPs, and chemotactic passage, that promote entry of T cells into extravascular tissues. © 1996 Wiley‐Liss, Inc.