[1] LFA-1 plays a key role in emigration, which is the process by which leukocytes leave the bloodstream to enter the tissues.
[2] LFA-1/ICAM-1 interactions have recently been shown to stimulate signaling pathways that influence T cell differentiation.
[5] In an inactive state, LFA-1 rests in a bent conformation and has a low affinity for ICAM binding.
[2] The conformational change stimulates a recruitment of proteins to form an activation complex.
[2] The antigen that bound to the monoclonal antibodies was identified as an important molecule in cellular recognition processes.
[2] LAD1, a subtype of LAD, is caused by a lack of integrins that contain the beta subunit, including LFA-1.
[3] LAD1 is characterized by recurring bacterial infection, delayed (>30 days) separation of umbilical cord, ineffective wound healing and pus formation, and granulocytosis.