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PD-1 and its ligand in the role of chronic hepatitis B immunization
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PD-1 and its ligand in the role of chronic hepatitis B immunization
[Keywords:] Hepatitis B Immunization
HBV-specific T lymphocytes and HBV to escape immune dysfunction caused by HBV is the cause of chronic persistent infection, T lymphocyte functional status determines the virus is cleared, or persistent infection. Abnormal expression of T lymphocytes in certain immune molecules in patients with chronic hepatitis B (CHB) of the occurrence and development processes. PD-1 as the CD28 family of recently discovered new member of its unique biological functions of concern have been found in patients with chronic hepatitis B immune response play an important role, but the specific immune mechanism needs further study [1] .
1 PD-1 biological characteristics of
PD-1 was originally from the T-cell hybridoma 2B4.11 was cloned to be that associated with apoptosis has been named as programmed cell death molecule. Human PD-1 gene located in 2q37, encoding molecular weight of about 50 000 immunoglobulin superfamily type I transmembrane glycoprotein, the extracellular end of the IgV-like domain, this structure may be combined with the ligand may play an important effect. PD-1 molecule striking feature is its cytoplasmic tail contains two tyrosine residues, N terminal tyrosine residue involved in the immune receptor tyrosine-based inhibitory constitute a motif (ITIM), C terminal tyrosine residues constitute the base is involved in immune receptor tyrosine-based activation motif (ITAM), so PD-1 may be mediated by negative signals. However, the negative nature of the signal is not mediated by the N terminal ITIM but the C terminal ITAM through the recruitment of SHP-2 and the realization of [2]. The other CD28 family members are in the form homodimer, while the PD-1 in monomer form, because of the lack of conserved cysteine. PD-1 major inducible expression in activated T cells, B cells, monocytes and myeloid cells, but CD4-CD8-thymocytes and immature
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