This time, we would like to introduce a paper

published by a research group led

by Professor Motoko Yanagiｔa, Department of Nephrology,

Graduate School of Medicine, Kyoto University.

 

I am a collaborating doctor for CKD (chronic kidney disease) in Kumamoto City.

I was interested in this study

because I treat many patients with CKD every Saturday

as an outpatient at a dialysis hospital in the city.

Another reason is that I myself have involved in CD30 research.

It has been reported that kidney disease in the elderly is more difficult to cure

than in younger people.

 

Previous research has shown that

ectopic lymphoid tissue called “tertiary lymphoid tissue” is induced

in the kidneys of aged individuals during the chronic phase after injury,

and the possibility that

this tissue prolongs inflammation and may interfere with normal tissue repair.

In this study, two types of lymphocytes that increase with age,

senescence-associated T (SAT) cells,

and age-associated B cells (ABCs),

were newly identified in the mouse kidney.

They discovered that

it interacts within tertiary lymphoid tissue and

promotes the formation of tertiary lymphoid tissue.

 

They identified the CD153-CD30 pathway as an interacting molecule,

and clarified that blocking this pathway

inhibits the induction of tertiary lymphoid tissues and

promotes renal tissue repair,

thereby improving the prognosis of renal injury.

Moreover, these cells and molecules have also been identified

in similar human pathological conditions.

Therefore, therapeutics targeting immune cells and interacting molecules discovered in this study

may promote recovery from kidney disease in the elderly and delay the introduction of dialysis.