Innate versus adaptive immunity in kidney immunopathology

被引:6
|
作者
Anders, Hans-Joachim [1 ]
机构
[1] Klinikum Univ Munchen, Div Renal, Med Klin & Poliklin 4, D-80336 Munich, Germany
来源
BMC NEPHROLOGY | 2013年 / 14卷
关键词
Glomerulonephritis; Acute kidney injury; Chronic kidney injury; Chemokines; Macrophages; B cells; T cells; RENAL INFLAMMATION; INJURY; DISEASE; CELLS; TOLL; PROGRESSION; RECEPTORS; TRANSPLANTATION; PATHOGENESIS; RESOLUTION;
D O I
10.1186/1471-2369-14-138
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
Most kidney disorders involve some degree of inflammation, i.e. induction of pro-inflammatory mediators and leukocyte recruitment. But what are the factors that determine inflammation as a trigger or a consequence of kidney injury? Which types of renal inflammation can be targeted by the novel more selective immunosuppressive and anti-inflammatory agents? How to dissect the mechanisms behind innate and adaptive immune responses that are orchestrated inside or outside the kidney but both cause renal immunopathology i.e. renal inflammation? How to dissect leukocytic cell infiltrates into pro-inflammatory leukocytes from anti-inflammatory and pro-regenerative leukocytes? How to dissect leukocytes that support epithelial repair from those that promote renal fibrosis. The term 'renal inflammation' has moved far beyond the descriptive category of 'mixed leukocytic cell infiltrates' as commonly described in kidney biopsies. It is time to face the complexity of renal inflammation to finally benefit from the new age of novel immunomodulatory medicines.
引用
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页数:3
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