Pathogens must evolve rapidly in response to host or environmental challenges.Clonal and invasive species adapt quickly despite a lack of genetic diversity.Evasion of host immunity can result from silencing of relevant effectors.Epigenetic reprogramming of gene expression can aid in pathogen adaptation.
A feature of pathogenic and invasive organisms is their adaptability when confronted with host and environmental challenges. Recent studies have demonstrated that plant pathogens rely on epigenetic processes for this purpose. Epiallelic variation of effector genes that results in evasion of host immunity is one emerging phenomenon. Another is the epigenetically induced reprogramming and diversification of transcriptional patterns by de-repression of transposable elements. These observations indicate that epigenetic control of gene expression provides a versatile means of generating phenotypic diversity that is adaptable and heritable across generations.
As cells age, they eventually stop multiplying, a state known as “senescence”. Accumulation of senescent cells is thought to contribute to the symptoms of aging. A study examining T cells, a type of immune cell, found that lung cancer patients had more senescent T cells, much like healthy patients during aging. T cells from both aged individuals and lung cancer patients had increased levels of senescence-promoting proteins, and lower levels of proteins that promote continued cell multiplication. This “artificial aging” of immune cells may weaken the immune system’s ability to attack the cancer. The study’s authors suggest that treatments to ward off senescence in immune cells may in the future help avoid the weakening of the immune system seen in cancer and other aging-related diseases.
Immune cells are like the Hatfields and McCoys of our bodies--once wronged, they never, ever forget. This is how we gain immunity, and it’s why vaccines work: Immune cells develop a memory of an invading pathogen, and they build an alert system to find and fight it should it ever return. But a new study by Stanford researchers adds a new wrinkle to this long-held immune theory. It turns out immune cells can develop this memory-like state even for pathogens they’ve never met. This may come from exposure to harmless microbes -- or the memories may actually be borrowed from other, more experienced cells.