| First Author | van den Berg CW | Year | 1992 |
| Journal | Proc Natl Acad Sci U S A | Volume | 89 |
| Issue | 22 | Pages | 10711-5 |
| PubMed ID | 1438267 | Mgi Jnum | J:3299 |
| Mgi Id | MGI:51812 | Doi | 10.1073/pnas.89.22.10711 |
| Citation | van den Berg CW, et al. (1992) Slp is an essential component of an EDTA-resistant activation pathway of mouse complement. Proc Natl Acad Sci U S A 89(22):10711-5 |
| abstractText | Slp (sex-limited protein) is a mouse serum protein encoded by a major histocompatibility complex class III gene. It is considered to be a product of a duplicated complement component C4 gene, but without functional activity. Originally it has been found expressed only in adult males with the S region of the H-2d or H-2s haplotype. In this report we present evidence that Slp is involved in a form of mouse complement activation that occurs after fractionation of serum by polyethylene glycol precipitation. This activation pathway is EDTA-resistant (i.e., independent of classical and alternative pathway activation), is regulated by C1 inhibitor, and leads to the generation of hemolytically active membrane attack complexes. A positive correlation between this EDTA-resistant mouse complement activity and reported Slp levels was found. Direct evidence for a functional role of Slp came from substitution experiments in which purified Slp induced hemolytic activity in polyethylene glycol-fractionated, Slp-deficient mouse serum. Selective depletion of other complement components suggested a role for C1s-, C2, and C5, but not C3, in the Slp-dependent complement activation. A model for this type of mouse complement activation is presented. |
