Anelli T

Benson MJ

Bossen C

Castigli E

Cortini M

Elsawa SF

Gorelik L

Jones DD

Kanswal S

Katsenelson N

Liu Z

Mackay F

Racine R

Ramanujam M

Schiemann B

Schmittgen TD

Scholz JL

Shaffer AL

Shimizu Y

Shulga-Morskaya S

von Bülow GU

Wolf AI

Xia XZ

Xu S

Yu G

ABSTRACT
          
            B cell activating factor of the tumor necrosis factor family (BAFF) is an essential survival factor for B cells and has been shown to regulate T cell-independent (TI) IgM production. During
            Ehrlichia muris
            infection, TI IgM secretion in the spleen was BAFF dependent, and antibody-mediated BAFF neutralization led to an impairment of IgM-mediated host defense. The failure of TI plasmablasts to secrete IgM was not a consequence of alterations in their generation, survival, or early differentiation, since all occurred normally in infected mice following BAFF neutralization. Gene expression characteristic of plasma cell differentiation was also unaffected by BAFF neutralization
            in vivo
            , and except for CD138, plasmablast cell surface marker expression was unaffected. IgM was produced, since it was detected intracellularly, and impaired secretion was not due to a failure to express the IgM secretory exon. Addition of BAFF to plasmablasts
            in vitro
            rescued IgM secretion, suggesting that BAFF signaling can directly regulate secretory processes. Our findings indicate that BAFF signaling can modulate TI host defense by acting at a late stage in B cell differentiation, via its regulation of terminal plasmablast differentiation and/or IgM secretion.
          </jats:p

Derek D. Jones

Maura Jones

Gregory A. DeIulio

Rachael Racine

Katherine C. MacNamara

Gary M. Winslow

Crossref

Infection and Immunity

B Cell Activating Factor Inhibition Impairs Bacterial Immunity by Reducing T Cell-Independent IgM Secretion

B Cell Activating Factor Inhibition Impairs Bacterial Immunity by Reducing T Cell-Independent IgM Secretion

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