ABSTRACT
This study highlights the prognostic impact of FOXP3 and CD68 expression in DLBCL, NOS and in its GCB and non-GCB subtypes. This may help the development of individualized therapy, prognostic prediction and therapy stratification.
Subject(s)
Germinal Center , Lymphoma, Large B-Cell, Diffuse , Humans , Germinal Center/metabolism , Germinal Center/pathology , Prognosis , Lymphoma, Large B-Cell, Diffuse/diagnosis , Lymphoma, Large B-Cell, Diffuse/pathology , Forkhead Transcription Factors/metabolismABSTRACT
INTRODUCTION: The role of intrinsic pathway of apoptosis in pathogenesis of lupus nephritis (LN) is still not clear. We investigated the relation between the expression of two major proteins of the intrinsic pathway of apoptosis; bcl2 as an antiapoptotic protein and bax as a proapoptotic one; in renal tissue of LN. METHODS: The study included fifty paraffin embedded renal tissue obtained from renal biopsy specimens of LN patients (8 cases class II, 10 cases class III, 21 cases class IV and 11 cases class V) and five paraffin embedded apparently normal renal tissue obtained from nephrectomy specimens due to renal neoplasms as a control group. Immunohistochemical staining for bcl2 and bax antibodies was done. Ki67 immunohistochemical staining was done for class III and IV to assess the degree of proliferation. The number of intraglomerular bcl2, bax and ki67 positive cells per glomerular cross section was evaluated for each case. The results were analysed in different LN classes and correlated to different glomerular lesions. RESULTS: The expression of bax and bcl2 proteins was higher in LN glomeruli compared to normal. The expression of bcl2 was significantly higher in class IV and was correlated to the degree of endocapillary hypercellularity. The bax to bcl2 ratio was significantly correlated to the percentage and degree of glomerular sclerosis. CONCLUSION: The intrinsic pathway of apoptosis interfere in the pathogenesis of lupus glomerulonephritis. The balance between bax and bcl2 proteins might have a role in regulating the progression of glomeruli from proliferative to sclerotic state.
