ITGAL and autoimmune disease: An LABL peptide derived from the α-subunit of LFA-1 blocked ICAM-1/LFA-1 interaction through ICAM-1 binding.29,30 In addition to cell adhesion, ICAM-1/LFA-1 interactions have a role in differentiation and proliferation of immune cells because they act as a co-stimulatory signal during the activation of T cells.31–34 In autoimmune diseases, stimulation of proinflammatory T cells involves ICAM-1/LFA-1 interactions in propagating autoimmune response.