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Regulation of Murine Splenic B Cell CR3 Expression by Complement Component 3¹

Division of Cell Biology and Immunology, Department of Pathology, University of Utah School of Medicine, Salt Lake City, UT 84132

Complement component C3 has established roles in both innate and adaptive immune responses. C3 cleavage products function in B cell activation through the complement receptors CD21/35. Phenotypes of Ab production between CD21/35^–/– and C3^–/– mice are not always congruent, implicating additional roles for C3 in B cell responses. To further characterize complement and complement receptors, we have identified a role for C3 in the regulation of CR3 on splenic B cells. Splenic B2 cells are not defined as expressing CR3, yet the analysis of splenic B cells from C3^–/– animals demonstrate cell surface expression of CR3. B cells from both wild-type (WT) and C3^–/– animals express CR3/CD11b/Itgam (integrin M) gene transcripts although the level of such transcripts is 2- to 3-fold higher in B cells from the C3^–/– animal vs WT cells. C3^–/– and WT animals have similar B cell subpopulations with identical CR3 expression on B220^– cells from the spleen, marrow, and lymph nodes. The C3-deficient environment is responsible for altered CR3 expression as WT splenic B cells transferred into C3^–/– animals expressed cell surface CR3 within 48 h while transfer of C3^–/– splenic B cells into WT animals depressed surface expression of CR3. Furthermore, transfer of C3-producing splenic macrophages into C3^–/– mice depressed CR3 expression by resident B cells. These data suggest a role for C3 in influencing the level of expression of CR3 by modulating the transcript levels encoding the CD11b integrin protein.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by grants from the National Institute of Allergy and Infectious Diseases (AI-24158, to J.H.W. and AI-32223, to J.J.W.). The content is solely the responsibility of the authors and does not necessarily represent the official views of the Institute of Allergy and Infectious Diseases or the National Institutes of Health. A.C.J. was supported by the Training Program in Microbial Pathogenesis, 5T32-AI-055434.

² Address correspondence and reprint requests to Dr. John Weis, University of Utah School of Medicine, 15 North Medical Drive East, Salt Lake City, UT 84112. E-mail address: john.weis{at}path.utah.edu

³ Abbreviations used in this paper: C3, complement component 3; CR3, complement receptor 3; WT, wild type; FM, follicular mature; MZ, marginal zone; PerC, peritoneal cavity.