The monoclonal antibody 8A/E6 recognizes mouse complement receptor type-1 related gene Y (Crry/p65), a type I membrane protein (MW 56-60 kDa). Complement comprises a system of soluble serum proteins that, upon activation by antibody (classical pathway), sugars (lectin pathway), or bacterial and foreign surfaces (alternative pathway), directly causes cell damage. Complement is constantly activated at low levels in serum, requiring cells to protect themselves from damage. In human, cells are protected from complement-mediated damage by expression of membrane-bound complement regulatory proteins, which act at serveral points along the cascade. Human cells are protected by decay-accelerating factor (DAF, CD55), membrane cofactor protein (MCP, CD46) and membrane attack complex inhibitor protein 1 (MIN1, CD59). Rat and mouse express a unique membrane complement regulator of the activating pathways, called complement receptor type-1 related gene Y (Crry). Crry/p65 is expressed on a wide variety of cells. Crry/p65 contains tandem short consensus repeats (SCR) characteristic of C3/C4 binding proteins. Mouse Crry/p65 has been shown to regulate both classical and alternative complement pathway C3 deposition on cell membranes. Crry/p65 must, therefore, exert its effects prior to, or at the level of, the C3 convertases, in a fashion similar to that of the human membrane factors DAF and MCP. Crry/p65 is an evolutionarily unique, complement regulatory protein which has developed in mouse and rat. Besides the involvement in control of complement damage to cell membranes Crry has also a role in T cell activation. Crry basically enhances the signals triggered by TCR/CD3 activation.