IRAK-4- and MyD88-dependent pathways are essential for the removal of developing autoreactive B cells in humans.

@article{Isnardi2008IRAK4AM,
  title={IRAK-4- and MyD88-dependent pathways are essential for the removal of developing autoreactive B cells in humans.},
  author={Isabelle Isnardi and Yen-shing Ng and Iva Srdanovic and Roja Motaghedi and Sergei Rudchenko and Horst von Bernuth and S Zhang and Anne Puel and Emmanuelle Jouanguy and Capucine Picard and Ben-zion Garty and Yildiz Camcioglu and Rainer Doffinger and Dinakantha Kumararatne and Graham E Davies and John I. Gallin and Soichi Haraguchi and Noorbibi K. Day and J. Hugo P{\'e}rez Casanova and Eric Meffre},
  journal={Immunity},
  year={2008},
  volume={29 5},
  pages={746-57}
}
Most autoreactive B cells are normally counterselected during early B cell development. To determine whether Toll-like receptors (TLRs) regulate the removal of autoreactive B lymphocytes, we tested the reactivity of recombinant antibodies from single B cells isolated from patients deficient for interleukin-1 receptor-associated kinase 4 (IRAK-4), myeloid differentiation factor 88 (MyD88), and UNC-93B. Indeed, all TLRs except TLR3 require IRAK-4 and MyD88 to signal, and UNC-93B-deficient cells… CONTINUE READING

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