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CD2 — ICAM1

Text-mined interactions from Literome

Magnani et al., Eur J Immunol 2011 (beta-Thalassemia) : Here, we defined that Tr1 cells specifically lyse myeloid APC through a granzyme B (GZB)- and perforin ( PRF ) -dependent mechanism that requires HLA class I recognition, CD54/lymphocyte function associated antigen ( LFA ) -1 adhesion, and activation via killer cell Ig-like receptors ( KIRs ) and CD2
Altomonte et al., Cancer Res 1993 (Melanoma) : CD11a and CD2 were not detected on melanoma cells while CD54 and CD58 were coexpressed on the majority of the melanoma cell populations investigated
Tsuji et al., Arerugi 1993 (Mucocutaneous Lymph Node Syndrome) : To clarify the activation of peripheral blood T-cells in Kawasaki Disease ( KD ) patients, we investigated whether the expression of lymphocyte function associated antigen-1 ( LFA-1 ) and/or intercellular adhesion molecule-1 ( ICAM-1 ) on peripheral blood T-cells and serum levels of soluble CD2 ( sCD2 ) increase during the acute stage
Lin et al., Cell Immunol 1996 : Analysis of expression of other adhesion molecules demonstrated that CD11a, CD18, CD44, CD45, CD48, CD54 , and CD62L were significantly increased by either anti-CD2 or anti-CD3 mAbs while the combination was not synergistic
Lin et al., Pathobiology 1995 : Expression of other integrin, selectin, or immunoglobulin superfamily molecules ( CD11a, CD18, CD44, CD45, CD48, CD54 and CD62L ) were all significantly increased by anti-CD2 or anti-CD3 mAbs
Petruzzelli et al., J Immunol 1998 : Our results demonstrate that activation of LFA-1 binding to ICAM-1 by CBR LFA-1/2 , in contrast to inside-out signaling mechanisms, does not require protein kinase C activation or protein phosphatase 2A activity nor is it affected by agents that interfere with reorganization of the cytoskeleton