Background-Despite improvement in short-term patient survival after heart transplantation (HTx), long-term survival rates have not improved much, mainly because of cardiac allograft vasculopathy (CAV). Cytokines and chemokines are considered to play an important role in CAV development. Interleukin-4 and interleukin-10 were expressed at the same level in both HTx groups and references. In HTxϩCAV, all CϩCR, but especially the T-helper 1 (TH1) CϩCR, were more abundant than in the HTxϪCAV and references. However, TH2 CCR4 expression did not differ significantly between both HTx groups. Conclusions-In coronary arteries with CAV, most T cells are CD4 ϩ and express human leukocyte antigen DR. These activated TH cells are mainly memory TH1 cells on the basis of their CϩCR profile and cytokine expression.
Methods and Results-We
BackgroundBcl-2/adenovirus E1B 19 kDa-interacting protein 3 (BNIP3) is a pro-apoptotic member of the Bcl-2 family induced under hypoxia. Low or absent expression has recently been described in human tumors, including gastrointestinal tumors, resulting in poor prognosis. Little is known about BNIP3 expression in invasive breast cancer. The aim of the present study was to investigate the expression of BNIP3 in invasive breast cancer at the mRNA and protein level in correlation with the hypoxic response and clinicopathological features.MethodsIn 40 cases of invasive breast cancer, BNIP3 mRNA in situ hybridization was performed on frozen sections with a digoxigenin labeled anti-BNIP3 probe. Paraffin embedded sections of the same specimens were used to determine protein expression of BNIP3, Hypoxia Inducible Factor 1 alpha (HIF-1α) and its downstream targets Glucose Transporter 1 (Glut-1) and Carbonic Anhydrase (CAIX) by immunohistochemistry.ResultsBNIP3 mRNA was expressed in 16/40 (40%) of the cases and correlated with BNIP3 protein expression (p = 0.0218). Neither BNIP3 protein nor mRNA expression correlated with expression of HIF-1α expression or its downstream targets. Tumors which showed loss of expression of BNIP3 had significantly more often lymph node metastases (82% vs 39%, p = 0.010) and showed a higher mitotic activity index (p = 0.027). BNIP3 protein expression was often nuclear in normal breast, but cytoplasmic in tumor cells.ConclusionBNIP3 expression is lost in a significant portion of invasive breast cancers, which is correlated with poor prognostic features such as positive lymph node status and high proliferation, but not with the hypoxic response.
The tissue distribution of human IgG Fc receptors (FcyRs) classified in three clusters of differentiation (CD16, using 5 antibodies, CD32, using 2 antibodies; and CD64, using 3 antibodies) was evaluated by immunohistochemistry on lymphoid (lymph node, spleen, thymus, tonsil) and non-lymphoid (heart, jejunum, kidney. liver, lung, muscle, stomach, and skin) tissues. Macrophage-like cells, including Kupffer cells, expressed all three classes of FcyR. Part of the cells coexpressed HLA-DR. lnterdigitating dendritic cells that were present in high density in interfollicular areas of a lymph node showing dermatopathic lymphadenopathy were immunoreactive for CD32, but not for CDI 6 or CD64 antibodies. In lymphoid tissue, mantle zones of secondary follicles were labelled by CD32 and some CD16 antibodies. The immunolabelling of mantle zones was not present after washing the sections at low pH, which suggests that the molecules detected were passively absorbed on the cell surface (i.e. soluble FcyR). The immunolabelling of tonsil sections by various CDI 6 antibodies showed three patterns. The first (anti-Leu-I 1 b) revealed labelling of solitary macrophage-like cells. The second (BW20912 and 3G8) revealed, in addition, labelling of germinal centres. The third (CLBgranI and CLBgranI I ) revealed labelling of solitary cells and follicle mantles. This labelling on tissue sections was also seen in the analysis of follicular dendritic cells isolated from tonsil. The cells were faintly immunoreactive for 3G8, as well as for CD16 mAb CLBgranI, and both CD32 mAbs. In all tissues investigated there was immunoreactivity for FcyRs in varying intensity on endothelial cells of blood vessels.
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