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Cited by 409

The DOI matches its Crossref record; 72 of the 72 references it cites were found in a registry or an index.

B cell–intrinsic signaling through IL-21 receptor and STAT3 is required for establishing long-lived antibody responses in humans

Open access
Avery, Danielle T., Deenick, Elissa K., Ma, Cindy S., Suryani, Santi, Simpson, Nicholas, Chew, Gary Y., Chan, Tyani D., Palendira, Umamainthan, Bustamante, Jacinta, Boisson-Dupuis, Stéphanie, Choo, Sharon, Bleasel, Karl E., Peake, Jane, King, Cecile, French, Martyn A., Engelhard, Dan, Al-Hajjar, Sami, Al-Muhsen, Saleh, Magdorf, Klaus, Roesler, Joachim, Arkwright, Peter D., Hissaria, Pravin, Riminton, D. Sean, Wong, Melanie, Brink, Robert, Fulcher, David A., Casanova, Jean-Laurent, Cook, Matthew C., Tangye, Stuart G.·2010·Journal of Experimental Medicine

Abstract

Engagement of cytokine receptors by specific ligands activate Janus kinase–signal transducer and activator of transcription (STAT) signaling pathways. The exact roles of STATs in human lymphocyte behavior remain incompletely defined. Interleukin (IL)-21 activates STAT1 and STAT3 and has emerged as a potent regulator of B cell differentiation. We have studied patients with inactivating mutations in STAT1 or STAT3 to dissect their contribution to B cell function in vivo and in response to IL-21 in vitro. STAT3 mutations dramatically reduced the number of functional, antigen (Ag)-specific memory B cells and abolished the ability of IL-21 to induce naive B cells to differentiate into plasma cells (PCs). This resulted from impaired activation of the molecular machinery required for PC generation. In contrast, STAT1 deficiency had no effect on memory B cell formation in vivo or IL-21–induced immunoglobulin secretion in vitro. Thus, STAT3 plays a critical role in generating effector B cells from naive precursors in humans. STAT3-activating cytokines such as IL-21 thus underpin Ag-specific humoral immune responses and provide a mechanism for the functional antibody deficit in STAT3-deficient patients.

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Crossref · 10.1084/jem.20091706

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Metadata

Authors
Avery, D. T., Deenick, E. K., Ma, C. S., Suryani, S., Simpson, N., Chew, G. Y., Chan, T. D., Palendira, U., Bustamante, J., Boisson-Dupuis, S., Choo, S., Bleasel, K. E., Peake, J., King, C., French, M. A., Engelhard, D., Al-Hajjar, S., Al-Muhsen, S., Magdorf, K., Roesler, J., Arkwright, P. D., Hissaria, P., Riminton, D. S., Wong, M., Brink, R., Fulcher, D. A., Casanova, J.-L., Cook, M. C., & Tangye, S. G.
Venue
Journal of Experimental Medicine
Published
2010-01-04
Volume
207
Issue
1
Pages
155-171
ISSN
  • 0022-1007 (ISSN-L)
  • 1540-9538
OpenAlex
W2163229826
Cited by
409
References
72
FWCI
15.67
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: B cell–intrinsic signaling through IL-21 receptor and STAT3 is required for establishing long-lived antibody responses in humans. https://app.cochat.ai/papers/10.1084/jem.20091706
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Avery, D. T., Deenick, E. K., Ma, C. S., Suryani, S., Simpson, N., Chew, G. Y., Chan, T. D., Palendira, U., Bustamante, J., Boisson-Dupuis, S., Choo, S., Bleasel, K. E., Peake, J., King, C., French, M. A., Engelhard, D., Al-Hajjar, S., Al-Muhsen, S., Magdorf, K., . . . Tangye, S. G. (2010). B cell–intrinsic signaling through IL-21 receptor and STAT3 is required for establishing long-lived antibody responses in humans. Journal of Experimental Medicine. https://doi.org/10.1084/jem.20091706

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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