The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/1998/7/145/ $5.00
The Journal of Experimental Medicine, Volume 188, Number 1, July 1, 1998 145-155

Articles

Antiviral Protection and Germinal Center Formation, But Impaired B Cell Memory in the Absence of CD19

Thomas Fehr*, Robert C. Rickert{ddagger}, Bernhard Odermatt*, Jürgen Roes{ddagger}, Klaus Rajewsky{ddagger}, Hans Hengartner*, and Rolf M. Zinkernagel*

From the * Institute of Experimental Immunology, Department of Pathology, University Hospital, CH-8091 Zürich, Switzerland; and the {ddagger} Institute for Genetics, University of Cologne, D-50931 Cologne, Germany

Coligation of CD19, a molecule expressed during all stages of B cell development except plasmacytes, lowers the threshold for B cell activation with anti-IgM by a factor of 100. The cytoplasmic tail of CD19 contains nine tyrosine residues as possible phosphorylation sites and is postulated to function as the signal transducing element for complement receptor (CR)2. Generation and analysis of CD19 gene–targeted mice revealed that T cell–dependent (TD) antibody responses to proteinaceous antigens were impaired, whereas those to T cell–independent (TI) type 2 antigens were normal or even augmented. These results are compatible with earlier complement depletion studies and the postulated function of CD19. To analyze the role of CD19 in antiviral antibody responses, we immunized CD19–/– mice with viral antigens of TI-1, TI-2, and TD type. The effect of CD19 on TI responses was more dependent on antigen dose and replicative capacity than on antigen type. CR blocking experiments confirmed the role of CD19 as B cell signal transducer for complement. In contrast to immunization with protein antigens, infection of CD19–/– mice with replicating virus led to generation of specific germinal centers, which persisted for >100 d, whereas maintenance of memory antibody titers as well as circulating memory B cells was fully dependent on CD19. Thus, our study confirms a costimulatory role of CD19 on B cells under limiting antigen conditions and indicates an important role for B cell memory.

Key Words: CD19 • antiviral immunity • complement • germinal center • B cell memory

Address correspondence to Rolf M. Zinkernagel, Institute of Experimental Immunology, Department of Pathology, University Hospital, Schmelzbergstrasse 12, CH-9091 Zürich, Switzerland. Phone: 41-1-255-29-89; Fax: 41-1-255-4420; E-mail: thfehr{at}bluewin.ch

T. Fehr's present address is Department of Internal Medicine, Stadtspital Triemli, Birmensdorferstrasse 497, 8063 Zürich, Switzerland. R.C. Rickert's present address is Department of Biology, Bonner Hall Rm. 3106, University of California, San Diego, 9500 Gilman Dr., La Jolla, CA 92093-0322.

Abbreviations used: AFC, antibody-forming cell; Bac VSV-G, baculovirus-derived VSV-G; BSS, balanced salt solution; CVF, cobra venom factor; FDC, follicular dendritic cell; GC, germinal center; LCMV, lymphocytic choriomeningitis virus; LCMV-NP, LCMV nucleoprotein; PNA, peanut agglutinin; RT, room temperature; sIg, surface Ig; TD, T cell–dependent; TI, T cell–independent; vacc VSV-G, recombinant vaccinia virus expressing VSV-G; VSV, vesicular stomatitis virus; VSV-G, VSV glycoprotein; VSV-IND, VSV Indiana serotype.


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