Browse our latest Immunology and Inflammation articles

Lymphocytes and monocytes maintain their cell surface HLA-B via different mechanisms, which in turn differently influence cell-surface expression, half-life and peptide receptivity of HLA-B allotypes.

By attenuating the translation of key mRNA targets, ZFP36 RNA binding proteins restrain the expansion and effector activity of T cells.

Long-term exposure to recipient's alloantigens promotes major metabolic defects in T cells that are independent of PD-1-mediated regulation.

Red blood cells infected by the malaria parasite Plasmodium falciparum are destroyed by human natural killer cells in the presence of antibodies from people who have acquired clinical immunity to malaria.

In vivo study of arbovirus infections reveals the dominant role of pDC IRF7-signaling in directing both type I and II IFN responses, and leading to viral control.

Macrophages respond to elevated levels of CSF-1 in tumor micro-environments by expressing a ligand for the NKG2D immunoreceptor.

HLA-B*35:01 molecules that are peptide-deficient are thermostable, bind CD8 with higher affinity than their peptide-filled versions, accumulate at immunological synapses and enhance antigen-specific CD8+ T cell immune responses.

A new form of chemokine signaling bias that depends on cell state is identified.

In zebrafish larvae, it is the cell type that determines how the cell responds to a chemokine signal.

mTORC1 and mTORC2 play a central role in the development of natural killer (NK) cells.