“…192, 193 Also, agonistic or antagonistic anti-CD40 antibodies failed in diverse clinical disorders as the treatment was not efficient, or side effects including thrombocytopenia, neutropenia, and pleural effusion led to the discontinuation of trials. 194–196 An alternative therapeutic strategy harnesses interactions of CD40L with Mac-1, also known as CD11b/CD18 integrin, which is abundantly expressed of neutrophils, NK cells, monocytes, and macrophages. 197 The intraperitoneal application of a small peptide prevented interaction of CD40L with Mac-1 and reduced atherosclerotic burden in Ldlr −/− mice, potentially by reducing leukocyte recruitment to the inflammatory site.…”