A novel method predicts cancer and immune cell types from bulk tumor gene expression data with the ability to consider uncharacterized and possibly highly variable cell types, which is validated in human genome.

Virus infection of the central nervous system disrupts the homeostasis of the immune-neural-synaptic axis via induction of pleiotropic genes with an unintended off-target negative impact on the neurotransmission.

The human cytomegalovirus US12 gene family work co-operatively to degrade large numbers of immune ligands and prevent recognition by natural killer cells.

An eco-evolutionary model shows that heterozygote advantage can maintain over 100 major histocompatibility complex alleles, providing a potent explanation for extraordinary immune gene diversity and challenges previous models that predicted limited allele coexistence.

Parasite variants associated with severe malaria do not have an intrinsic growth or survival advantage in vivo, which indicates that a change in host environment is required for their selection.

As a result of frequent gene duplication and haplotypic variation, a family of immune genes in the model vertebrate zebrafish has thousands of gene copies that are population- or individual-specific.

Pathogens, particularly viruses, target the same genes over deep evolutionary time, resulting in shared signatures of positive selection and transcriptional responses at the same genes.

Alternative first exon usage was the major event observed in macrophages during inflammation, which resulted in the elucidation of a novel isoform and regulatory mechanism of the protein-coding gene, Aim2.

Infected cells superinduce expression of mRNA in order to initiate an immune response to a bacterial pathogen that blocks host protein synthesis.

Genetic variations that underlie common autoimmune disease genes are predominantly regulatory and modify the expression of multiple genes within the HLA gene complex and throughout the immune system.