Chitose Ishihara

TL;DR: Deletion of the gene encoding the Bcl-10 adaptor–binding partner CARD9 resulted in impaired myeloid cell activation of NF-κB signaling by several ITAM-associated receptors, and CARD9 was required for Toll-like receptor–induced activation of dendritic cells through the activation of mitogen-activated protein kinases.

TL;DR: It is demonstrated that the dynein motor complex colocalized and coimmunoprecipitated with the TCR complex and that TCR-MCs moved along microtubules (MTs) toward the center of the immune synapse in a dyne in-dependent manner to form cSMAC.

TL;DR: It is demonstrated that CRTAM identifies CD4 T cells with cytotoxic function, and new insights into CD4+CTL development are presented.

TL;DR: The CRTAM-mediated late interaction with DCs induced retention of activated CD8+ T cells in an Ag-independent fashion, and this possibly resulted in effective CTL development in the draining lymph node.

TL;DR: It is shown that the deficiency of CARMA1 or Bcl10, but not CARD9, resulted in severe impairment of cytokine/chemokine production mediated by activating NK cell receptors due to a selective defect in NF-κB activation, whereas cytotoxicity mediated by the same receptors did not require CarMA1-Bcl10-mediated signaling.