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HCV‐specific CD27 − CD28 − memory T cells are depleted in hepatitis C virus and Schistosoma mansoni co‐infection
Author(s) -
Elrefaei Mohamed,
Elsheikh Nabila,
Kamal Karim,
Cao Huyen
Publication year - 2003
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/j.1365-2567.2003.01769.x
Subject(s) - schistosoma mansoni , hepatitis c virus , immunology , biology , cd8 , virology , population , t cell , cytotoxic t cell , cd28 , antigen , virus , immune system , medicine , schistosomiasis , biochemistry , environmental health , helminths , in vitro
Summary Factors that influence the generation and maintenance of memory CD8 + T cells are not fully understood. The homeostasis of memory T cells is highly dynamic and tightly regulated by various stimuli, including cytokines and antigen–major histocompatibility complex ligands. We characterized the hepatitis C virus (HCV)‐specific CD8 + T‐cell responses in a cohort of HCV‐infected individuals with or without Schistosoma mansoni co‐infection from Egypt. We observed a significantly decreased CD27 − CD28 − (late differentiated) memory T‐cell population in the HCV co‐infected individuals compared to those with HCV infection alone. In contrast, there was no significant difference in the CD27 + CD28 + (early differentiated) memory T cells between the two groups. Analysis of human cytomegalovirus‐specific CD8 + T‐cell responses in the same individuals failed to reveal a similar pattern of altered memory T‐cell differentiation. Thus, S. mansoni co‐infection targets a specific subset of memory CD8 + T cells in HCV infection.