Related Experiment Video
Updated: Oct 17, 2026

The CYP2D6 Animal Model: How to Induce Autoimmune Hepatitis in Mice
Published on: February 3, 2012
[A case with HTLV-I associated myelopathy (HAM) accompanied by primary biliary cirrhosis (PBC) and autoimmune
We reported a 60-year-old female patient with HTLV-I associated myelopathy (HAM) accompanied by primary biliary cirrhosis (PBC) and autoimmune hepatitis (AIH). The diagnosis of PBC and AIH was confirmed by liver biopsy. HAM is considered to be mediated by cellular immune mechanisms, while humoral immune mechanisms may play a predominant role in the development of PBC and AIH. Flowcytometric analysis of lymphocyte subset of peripheral blood was within normal limits. We then collected CD4 positive cells from the patient. These cells expressed T helper 2 (Th 2) cytokine mRNA such as IL-4 and IL-10, but did not express Th 1 cytokines, indicating the predominance of Th 2 in this patient. This case suggested the possibility that disease associated Th 2 might develop in the course of Th1-mediated disease like HAM.
We reported a 60-year-old female patient with HTLV-I associated myelopathy (HAM) accompanied by primary biliary cirrhosis (PBC) and autoimmune hepatitis (AIH). The diagnosis of PBC and AIH was confirmed by liver biopsy. HAM is considered to be mediated by cellular immune mechanisms, while humoral immune mechanisms may play a predominant role in the development of PBC and AIH. Flowcytometric analysis of lymphocyte subset of peripheral blood was within normal limits. We then collected CD4 positive cells from the patient. These cells expressed T helper 2 (Th 2) cytokine mRNA such as IL-4 and IL-10, but did not express Th 1 cytokines, indicating the predominance of Th 2 in this patient. This case suggested the possibility that disease associated Th 2 might develop in the course of Th1-mediated disease like HAM.
Related Concept Videos
Hepatitis
Viral Hepatitis I: Introduction
Graves' Disease I: Introduction
Hepatic Encephalopathy
Encephalitis ll: Pathophysiology
Cirrhosis II: Pathophysiology