Issues

The Ab repertoire is diversified through the acquisition of N-glycosylation sites.

Frequencies of V region N-glycosylation sites are isotype and subclass dependent.

Elevated Fab glycosylation is an additional hallmark of T_H2-like IgG4/IgE responses.

IRF3 is phosphorylated by Abl kinase family.

c-Abl and Arg regulate innate immunity by promoting type I IFN production.

AIM2 inflammasome activation during Ft LVS infection is prompted by Abl kinase.

Shp1-deficient iNKT cells are biased toward the iNKT2/17 subsets.

Shp1 deficiency does not alter TCR or Slam signaling.

Shp1 dampens iNKT cell proliferation in response to cytokines.

NKAP Y352 is required for association with HDAC3.

The interaction between NKAP and HDAC3 is critical for its function in HSCs.

The interaction between NKAP and HDAC3 is unimportant in some cell types.

Sostdc1 influences tNK to mNK cell differentiation and the Ly49 receptor repertoire.

NK cells in Sostdc1^−/− mice display impaired ability to kill β₂m^−/− target cells.

Sostdc1 expression in stromal and hematopoietic cells regulates NK cells.

We engineered the Fc of human IgG to increase its affinity for TRIM21 by 100-fold.

The engineered Fc enhances cross-presentation in monocyte-derived dendritic cells.

Our finding may be applied to vaccine design to boost CD8 T cell–based immunity.

IFN-β promotes host resistance to M. tuberculosis via induction of NO production.

Capacity to inhibit IFN-β signaling correlates with mycobacterial virulence.

M. tuberculosis limits activation of receptor-associated tyrosine kinases TYK2 and JAK1.

Knockout of USP20 inhibits HSV-1– but not Sendai virus–triggered signaling.

USP20-deficient mice exhibit increased susceptibility to HSV-1 infection.

USP20 deconjugates K48-linked polyubiquitin chains from and thereby stabilizes MITA.

FTRCA1 is a crucian carp–specific member of finTRIM.

FTRCA1 downregulates fish IFN response through lysosomal degradation of TBK1.

The E3 ligase activity is likely required for FTRCA1 function on TBK1 degradation.

Loss of adipocyte and macrophage H2Ab1 leads to no change in metabolic phenotype.

Specific loss of macrophage H2Ab1 leads to improvements in glucose tolerance.

Adipocytes on HFD express LysM and are targeted by the LysMCre model.

Notch favors RUNX1 and MYB recruitment to activate enhancer-dependent transcription.

These results decipher the mechanism for Tcrd and Tcrg silencing during β-selection.