الفهرس | Only 14 pages are availabe for public view |
Abstract Systemic immune suppression is often seen in cancer patients and is thought to contribute to patient morbidity via tumor-mediated immune evasion. Indeed, patients with compromised immune systems are at increased risk of developing non-Hodgkin lymphoma (NHL). Non-Hodgkin’s lymphomas represent malignant proliferations of the immune system cells which start and affect predominantly the lymphoid organs, but may have as onset or may involve during their evolution any organ or tissue where these cells are. Myeloid -derived suppressor cells (MDSCs) are a heterogeneous population of immature myeloid cells at different stages of maturation that play a role in cancer tolerance and function as an immune-suppressive cell subpopulation. They utilize different mechanisms to block both innate and adaptive arms of anti-tumour immunity, mostly through inhibition of T cell activation and expansion. Two major classes have been recognized Granulocytic MDSCs (GMDSCs) and monocytic MDSCs (M-MDSCs).M-MDSCs express CD14with minimal or no HLDR expression. The aim of this study is to detect CD14+HLA-DRlow/-immunosuppressive monocytes in NHL patients as major contributor to systemic immunosuppression which could have an effect on disease aggressiveness and treatment strategy. This study was carried out on 42 NHL patients, 14 males and 28 females, with age range of 33 to 71 years old attending the Oncology department, Minoufiya University hospitals. Of the 42 NHL cases 16 were relapsed or refractory and 26 were newly diagnosed cases. Tweenty age and gender matched individuals were selected as a control . We analysed CD14+ HLA DRlow/- monocytes by flowcytometry and arginase 1 enzyme analysis by ELISA. On statistical analysis of the collected data there was increased ratio of CD14+ HLA DRlow/- monocytes in patients with higher stage disease ,more aggressive pathology and also with refractory and relapsed disease with the agreement of arginase-1 results with CD14+ HLA DRlow/- monocytes. |