Anti-Human ILT1, Isotype Control, Fc Muted (Clone 135.5 (LALAPG))
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LILRA2 (ILT1) is an activating cell surface glycoprotein1 that is a member of the leukocyte immunoglobulin-like receptor (LILRA) family and forms part of the innate immune response against microbial infection2, 3.
LILRA proteins are divided into two different classes, with ILT1 designated as a Class I protein that interacts with classical and non-classical human leukocyte antigen class I molecules2.
ILT1 is associated with autoimmune and autoinflammatory diseases, including rheumatoid arthritis, systemic lupus erythematosus, and microscopic polyangiitis, as well as Hansen’s disease (leprosy), where it is upregulated in the lesions.
FcεRIγ is required for efficient cell surface expression1.
Anti-human LILRA2 clone 135.5 is an Fc mutated (LALAPG) recombinant monoclonal antibody specific for human ILT1, a receptor not encoded in mice4.
It has been used as a control for anti-TREM2 clone 178 in murine studies of TREM2 expression and function in tumor growth.
The LALAPG mutation prevents recognition by Fc receptors and complement, thereby minimizing antibody-dependent cellular cytotoxicity and antibody-dependent phagocytosis. The original IgG2a 135 monoclonal antibody was generated by immunizing Wister rats with ILT1/FLAG-transfected rat basophilic leukemia cells1.
The LALAPG mutated version was generated by mutating the Fc domain4.
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