Akut interstisyel nefritis’in immunopatogenezi
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Date
2001-03-09
Authors
Durgut, Ramazan
Çelik, Sefa
Journal Title
Journal ISSN
Volume Title
Publisher
Uludağ Üniversitesi
Abstract
Akut interstisyel nefritis (AIN), difteri ve streptokok enfeksiyonları ile ilişkili olan ve primer mononükleer hücre infiltrasyonu, bakteri içermeyen eksudatın varlığı ve epitel dejenerasyonu ile karakterize edilen bir hastalıktır. Hastalığın etiyolojik faktörleri; enfeksiyonlar, ilaçlar, immun hastalıklar ve idiopatik olmak üzere 4 grup altında incelenir. Lokal immun yanıtta artış enfeksiyon başladıktan sonra görülür. Böbrek tubulus epitel hücreleri antijen sunan hücreler olarak görev yapar. Böbrek interstisyumu, yabancı antijenlere karşı immun yanıtın başlatılmasından sorumlu antijen sunan hücreler ile T lenfositlerden oluşan 2 tip hücre içerir. Makrofajlar ve T lenfositleri akut interstisyel nefritis olgularında böbrek epitellerinde yaygın olarak görülen hücrelerdir. Hastalığın immunopatogenezinde Gell ve Coombs aşırı duyarlılık reaksiyonu etkili olmakta ve antikora bağlı ortaya çıkan aşırı duyarlılık reaksiyonu ise nadiren görülmektedir. Tip I aşırı duyarlılığı veya anaflaktik reaksiyonların şekillenmesi spesifik olarak B lenfositler tarafından üretilen antijenlerden kaynaklanır. Tip II aşırı duyarlılıkta doku antijenlerine karşı gelişen reaksiyon; komplement aktivasyonu ve kemotaktik faktörlerin salınmasına neden olur. Bu reaksiyonda nötrofiller ve eozinofiller yangısel bölgeye infiltre olurlar; immunoglobulin G, komplement (daha çok C5a) ve lökotrienler gibi bir çok faktör ortama salınırlar. Akut interstisyel nefritiste gözlenen semptomlar; proksimal ve distal tubul epitellerinin fonksiyon bozukluğuna bağlı aşırı duyarlılığın ve nadiren de anafilaktik reaksiyonların sonucu olarak ortaya çıkmaktadır. İmmun sistemin, akut interstisyel nefritisin patogenezinde önemli rol oynadığı düşünülmektedir. Bu nedenle bu derlemede AIN’in immunopatogenezi mevcut literatür ışığı altında tartışılmıştır.
Acute interstitial nephritis (AIN) is associated with diphteria and streptococcal infections and are characterized by primary mononuclear cell-infiltration, existince of exudate without bacteria and epitelial degeneration. The etiological factors of the disease are classified into 4 groups: infections, pharmacological agents, immune diseases and idiopathic factors. The increase in local immune responses is seen after begining of infection. Kidney tubulus epithelial cells functions as antigen presenting cells. Kidney interstitium include two kinds of cells, antigen presenting cells and T lymphocytes, which are responsible for the initition of immune response against foreign antigens. Macrophage and T lymphocytes are commonly found cell types in acute interstitial nephritis. Gell and Coombs hypersensitivity reactions are play vital roles in immunopathogenesis of the disease and anticore coupled hypersensitivity reaction is seen rarely. Type I hypersensitivity or anaphlactic reactions originate specifically from antigens produced by B lymphocytes. In type II hypersensitivity reactions developed against tissue antigens result in complement activation and release of chemotactic factors. In such kind of reactions neutrophils and eosinophil infiltrates in inflamated cites; immunoglobuline G comploment (mainly C5a) and leucotriens are released in to the medium. The symptoms in the AIN are resulted from the hypersensitivity due to disorders of the proximal and distal tubul epithels and occasionally anaphlactic reactions. The immune system is thought to play important roles in the pathogenesis of AIN. Therefore, in this article, in the lights of the present publications the pathogenesis of AIN is discussed
Acute interstitial nephritis (AIN) is associated with diphteria and streptococcal infections and are characterized by primary mononuclear cell-infiltration, existince of exudate without bacteria and epitelial degeneration. The etiological factors of the disease are classified into 4 groups: infections, pharmacological agents, immune diseases and idiopathic factors. The increase in local immune responses is seen after begining of infection. Kidney tubulus epithelial cells functions as antigen presenting cells. Kidney interstitium include two kinds of cells, antigen presenting cells and T lymphocytes, which are responsible for the initition of immune response against foreign antigens. Macrophage and T lymphocytes are commonly found cell types in acute interstitial nephritis. Gell and Coombs hypersensitivity reactions are play vital roles in immunopathogenesis of the disease and anticore coupled hypersensitivity reaction is seen rarely. Type I hypersensitivity or anaphlactic reactions originate specifically from antigens produced by B lymphocytes. In type II hypersensitivity reactions developed against tissue antigens result in complement activation and release of chemotactic factors. In such kind of reactions neutrophils and eosinophil infiltrates in inflamated cites; immunoglobuline G comploment (mainly C5a) and leucotriens are released in to the medium. The symptoms in the AIN are resulted from the hypersensitivity due to disorders of the proximal and distal tubul epithels and occasionally anaphlactic reactions. The immune system is thought to play important roles in the pathogenesis of AIN. Therefore, in this article, in the lights of the present publications the pathogenesis of AIN is discussed
Description
Keywords
Akut intersitisyel nefritis, Acute interstitial nephritis, Immunopatogenez, Böbrek, Immunopathogenesis, Kidney
Citation
Durgut, R. ve Çelik, S. (2001). "Akut interstisyel nefritis’in immunopatogenezi". Uludağ Üniversitesi Veteriner Fakültesi Dergisi, 20(3), 147-150.