Anastassakos C, Alexander G J, Wolstencroft R A, Dumonde D C, Eddleston A L, Williams R
Liver Unit, King's College School of Medicine and Dentistry, London.
Clin Exp Immunol. 1987 Apr;68(1):15-22.
To test the hypothesis that reduced lymphocyte transformation in response to PHA in chronic hepatitis B virus infection might be due to deficient lymphokine production, lymphocyte transformation was measured in the presence or absence of exogenous interleukin 1, interleukin 2 or both, or, as a source of mixed lymphokines, supernatants from mixed lymphocyte reactions. The response to PHA was significantly impaired in patients compared to controls, but was not corrected by interleukin 1, interleukin 2 or supernatant from mixed lymphocyte reactions over a wide range of concentrations. Variation of the proportion of monocytes in culture or the addition of indomethacin had no effect on lymphocyte transformation. Thus, reduced lymphocyte proliferation in response to PHA in patients with chronic hepatitis B virus infection cannot be attributed to deficient lymphokine production or to active suppression by monocytes or prostaglandins and a direct role for the hepatitis B virus or a viral product is under investigation.
为检验慢性乙型肝炎病毒感染时淋巴细胞对PHA反应性降低可能是由于淋巴因子产生不足这一假说,在有或无外源性白细胞介素1、白细胞介素2或两者同时存在的情况下,或者作为混合淋巴因子来源,使用混合淋巴细胞反应的上清液来检测淋巴细胞转化。与对照组相比,患者对PHA的反应明显受损,但在广泛的浓度范围内,白细胞介素1、白细胞介素2或混合淋巴细胞反应的上清液均不能纠正这种受损情况。培养中单核细胞比例的变化或加入消炎痛对淋巴细胞转化均无影响。因此,慢性乙型肝炎病毒感染患者淋巴细胞对PHA反应性降低不能归因于淋巴因子产生不足,也不能归因于单核细胞或前列腺素的主动抑制作用,目前正在研究乙型肝炎病毒或病毒产物的直接作用。