Skip to Main Content


Skip Nav Destination



Pandolfi et al. provide an in-depth discussion on the synergism between all-trans-retinoic acid and arsenic trioxide treatment and their mechanisms of action on acute promyelocytic leukemia.

Brief Definitive Report

T cells are crucial effectors of glioma rejection induced by local IL-12 application and CTLA-4 blockade.

A subset of broadly neutralizing anti-HIV antibodies inhibits cell to cell transmission of the virus.

Ikaros is essential for pre-BCR down-regulation, Igκ germline transcription, Ig light chain recombination, and pre-B cell differentiation, in part by antagonizing IL-7–dependent gene regulation.

Cis-element requirement for the emergence of HSCs in the AGM and for hemogenic endothelium to generate HSC-containing c-Kit+ cell clusters.

GATA2 function is essential for the generation of HSCs during the stage of endothelial-to-hematopoietic cell transition and thereafter for HSC survival


Chemotherapy stimulates cancer-associated fibroblasts to secrete interleukin-17A to provide maintenance cues to support the growth of colorectal cancer-initiating cells.

Imatinib reduces tumor cell KIT signaling and causes tumor cell apoptosis, which drives TAMs to shift from M1- to M2-like in mouse and human GIST.

The transcription factor IRF4 limits the retention of B cells in the marginal zone by inhibiting NOTCH2 signaling.

High expression level of human TLR8 in mice results in spontaneous, multiorgan inflammation attributable in part to increased DC activation.

Antigen presentation, but not antibody secretion, by B cells drives CNS autoimmunity induced by immunization with human MOG.

Type 2 innate lymphoid cells promote skin inflammation in mice and men, in part by producing IL-5 and IL-13 in response to IL-33

IL-9 acts as an autocrine amplifier of type 2 innate lymphoid cell function to promote tissue repair in the recovery phase of helminth-induced lung infection.

Langerhans cell homeostasis and differentiation depends on PU.1, the latter via regulation of TGF-β–dependent binding of PU.1 to the regulatory elements of RUNX3.

Inflammatory cytokines drive NK cell expansion in the absence of the transcription factor Nfil3, and Nfil3 is dispensable for the maintenance and function of mature NK cells.

Close Modal

or Create an Account

Close Modal
Close Modal