Raqib R, Reinholt F P, Bardhan P K, Kärnell A, Lindberg A A
Department of Clinical Bacteriology, Huddinge Hospital, Karolinska Institute, Stockholm, Sweden.
APMIS. 1994 May;102(5):371-80. doi: 10.1111/j.1699-0463.1994.tb04886.x.
Expression of HLA-DR antigens and infiltration of T-lymphocyte subsets (CD4, CD8), cell activation marker (CD25), B cells (CD20), macrophages (CD68 and Ber-Mac 3) and natural killer cells (CD56) in the rectal mucosa of patients with bacillary dysentery and in healthy controls were studied in an effort to interpret the immunopathological changes taking place in the rectal mucosa during the acute phase of shigellosis. The epithelium of the rectal mucosa from 21 of 32 patients was HLA-DR+. Conventional histology showed acute inflammation in 16 of these patients, chronic inflammation in 3, and in 2 histology was normal. In 7 of 20 controls the epithelium was HLA-DR+; 4 of these 7 were found to suffer from chronic inflammation, whilst in 3 the mucosa was normal. The number of HLA-DR+ intraepithelial lymphocytes in biopsies from patients with Shigella infection was significantly higher (p = 0.005) than in controls. The infiltration of CD8+ cells in the surface epithelium and in the lamina propria, and of CD4+ cells in the lamina propria alone, was significantly higher (p < 0.001) in patients than in controls. The results demonstrate that infiltration of T cells with suppressor/cytotoxic or helper/inducer phenotype in the epithelium and in the lamina propria in Shigella-infected patients may be related to the induction of HLA-DR expression in non-lymphoid cells during acute Shigella infection.
为了解释志贺菌病急性期直肠黏膜发生的免疫病理变化，对细菌性痢疾患者和健康对照者直肠黏膜中HLA - DR抗原的表达以及T淋巴细胞亚群（CD4、CD8）、细胞活化标志物（CD25）、B细胞（CD20）、巨噬细胞（CD68和Ber - Mac 3）和自然杀伤细胞（CD56）的浸润情况进行了研究。32例患者中有21例直肠黏膜上皮HLA - DR阳性。常规组织学检查显示，其中16例为急性炎症，3例为慢性炎症，2例组织学正常。20例对照中有7例上皮HLA - DR阳性；这7例中有4例患有慢性炎症，3例黏膜正常。志贺菌感染患者活检中HLA - DR阳性上皮内淋巴细胞数量显著高于对照组（p = 0.005）。患者表面上皮和固有层中CD8 +细胞的浸润以及仅固有层中CD4 +细胞的浸润均显著高于对照组（p < 0.001）。结果表明，志贺菌感染患者上皮和固有层中具有抑制/细胞毒性或辅助/诱导表型的T细胞浸润可能与急性志贺菌感染期间非淋巴细胞中HLA - DR表达的诱导有关。
