Deficiency of the Autologous Mixed Lymphocyte Reaction in Patients with Primary Biliary Cirrhosis

Overview

Journal J Clin Invest

Specialty General Medicine

Date 1980 Dec 1

PMID 6449520

Citations 23

Authors

S P James

C O Elson

J G WAGGONER

E A Jones

W Strober

Affiliations

Soon will be listed here.

Abstract

In this study we show that patients with primary biliary cirrhosis (PCB) have a marked deficiency in the ability to generate an autologous mixed lymphocyte reaction (AMLR) but have a normal ability to generate an allogeneic mixed lymphocyte reaction (MLR). This deficiency is not due to differences in the time-course of the proliferative response or to an altered response to variable numbers of stimulator cells. The deficiency was consistently found irrespective of the methods used to isolate autologous stimulator cells. Both responder cells and stimulator cells obtained from patients with PBC were similar to normal cells in their ability to generate an MLR in allogeneic normal human serum. In addition, serum from patients with PBC inhibited the ability of normal lymphocytes to generate both the AMLR and MLR to a similar degree, suggesting that the defect of the AMLR in PBC is not due to a serum factor. It has been shown that the responder cell population in the AMLR contains a subpopulation of cells that mediate suppression. Therefore, it is possible that the deficiency of the AMLR may be related to previously described abnormalities of suppressor function in patients with PBC.

Citing Articles

Primary biliary cirrhosis. Is (and how much of) the pathology preventible?.

Bar-Dayan Y, Gershwin M, Levi Y, Amital H, Shoenfeld Y Immunol Res. 1998; 18(2):117-23.

PMID: 9844830 DOI: 10.1007/BF02788754.

Increased nitric oxide (NO) production by antigen-presenting dendritic cells is responsible for low allogeneic mixed leucocyte reaction (MLR) in primary biliary cirrhosis (PBC).

Yamamoto K, Akbar S, Masumoto T, Onji M Clin Exp Immunol. 1998; 114(1):94-101.

PMID: 9764609 PMC: 1905073. DOI: 10.1046/j.1365-2249.1998.00696.x.

T cell responses to tuberculin purified protein derivative in primary biliary cirrhosis: evidence for defective T cell function.

Jones D, Palmer J, Leon M, Yeaman S, Bassendine M, Diamond A Gut. 1997; 40(2):277-83.

PMID: 9071945 PMC: 1027062. DOI: 10.1136/gut.40.2.277.

Effects of chenodeoxycholic and ursodeoxycholic acids on interferon-gamma production by peripheral blood mononuclear cells from patients with primary biliary cirrhosis.

Saeki R, Ogino H, Kaneko S, Unoura M, Kobayashi K J Gastroenterol. 1995; 30(6):739-44.

PMID: 8963391 DOI: 10.1007/BF02349640.

Interleukin 6 production by peripheral blood mononuclear cells in patients with chronic hepatitis B virus infection and primary biliary cirrhosis.

Kakumu S, Shinagawa T, Ishikawa T, Yoshioka K, Wakita T, IDA N Gastroenterol Jpn. 1993; 28(1):18-24.

PMID: 8440420 DOI: 10.1007/BF02774999.

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