Soluble BAFF Levels Inversely Correlate with Peripheral B Cell Numbers and the Expression of BAFF Receptors

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KREUZALER Matthias RAUCH Melanie SALZER Ulrich BIRMELIN Jennifer RIZZI Marta GRIMBACHER Bodo PLEBANI Alessandro LOUGARIS Vassilios QUINTI Isabella THON Vojtěch LITZMAN Jiří SCHLESIER Michael WARNATZ Klaus THIEL Jens ROLINK Antonius G. EIBEL Hermann

Rok publikování 2012
Druh Článek v odborném periodiku
Časopis / Zdroj The Journal of Immunology
Fakulta / Pracoviště MU

Lékařská fakulta

Obor Epidemiologie, infekční nemoci a klinická imunologie
Klíčová slova chronic lymphocytic leukemia; Creactive protein; common variable immunodeficiency; primary antibody deficiency; systemic lupus erythematosus
Popis The TNF family member protein BAFF/BLyS is essential for B cell survival and plays an important role in regulating class switch recombination as well as in the selection of autoreactive B cells. In humans, increased concentrations of soluble BAFF are found in different pathological conditions, which may be as diverse as autoimmune diseases, B cell malignancies, and primary Ab deficiencies (PAD). Because the mechanisms that regulate BAFF levels are not well understood, we newly developed a set of mAbs against human BAFF to study the parameters that determine the concentrations of soluble BAFF in circulation. Patients with PAD, including severe functional B cell defects such as BTK, BAFF-R, or TACI deficiency, were found to have higher BAFF levels than asplenic individuals, patients after anti-CD20 B cell depletion, chronic lymphocytic leukemia patients, or healthy donors. In a comparable manner, mice constitutively expressing human BAFF were found to have higher concentrations of BAFF in the absence than in the presence of B cells. Therefore, our data strongly suggest that BAFF steady-state concentrations mainly depend on the number of B cells as well as on the expression of BAFF-binding receptors. Because most patients with PAD have high levels of circulating BAFF, the increase in BAFF concentrations cannot compensate defects in B cell development and function.
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