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ICAMs: mAbs

Since adhesion molecules are of pivotal importance in cell trafficking and thus inflammation, they could constitute good therapeutic targets in RA. In fact, a murine mAb to intercellular adhesion molecule (ICAM)-l proved to lead to clinical improvement, (140) but repeated administration may have less effects, and the side-effect profile was also of major concern (141). Thus, anti-ICAM-1 may not be the strategy of choice. In this context it should be mentioned that TNFa blockade leads not only to clinical benefit but also to reduction of adhesion molecule expression. [Pg.386]

Human respiratory tract DCs express la in conjunction with CDla or CDlc (e.g. Soler etal., 1989), T-200 (Sertl etal., 1987 Casolaro etal., 1988), RFDl (Munro etal., 1987 Nicod etal., 1990), and in addition are stained by a variety of mAbs against sur ce molecules associated with trafficking and cell-cell interaction. The latter include both 01 and 02 integrins, and the adhesins leucocyte function-associated antigen-3 (LFA-3) and ICAM-1 (Nicod and El Habre, 1992). [Pg.2]


See other pages where ICAMs: mAbs is mentioned: [Pg.1]    [Pg.87]    [Pg.690]    [Pg.260]    [Pg.247]    [Pg.920]    [Pg.437]    [Pg.435]    [Pg.451]    [Pg.454]    [Pg.247]    [Pg.435]    [Pg.451]    [Pg.454]   
See also in sourсe #XX -- [ Pg.454 ]

See also in sourсe #XX -- [ Pg.454 ]




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