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- Call for Papers and Participation, Deadline: October 11, 2010
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- Deadline for Submissions: October 31, 2010
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Scientific Update
- Black patients, women miss out on strongest medications for...
- Article highlighting research of Carmen Green
- A Meta-Study of Black Male Mental Health and Well-Being
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Scientific News
Th17 and regulatory T cells: implications for AIDS pathogenesis
Kanwar, B., Favre, D., and McCune, J. M.
2010-02-04 15:04:47
Th17 and regulatory T cells: implications for AIDS pathogenesis
Kanwar, B., Favre, D., and McCune, J. M.
Current Opinion in HIV and AIDS:
March 2010 - Volume 5 - Issue 2 - p 151–157
doi: 10.1097/COH.0b013e328335c0c1
journals.lww.com/co-hivandaids/pages/articleviewer.aspx
Purpose of review: The present review discusses recent reports showing that reciprocal changes in T helper interleukin-17-secreting CD4+ Th17 cells and CD4+CD25highFoxP3+ regulatory T cells (Tregs) may play a role in the progressive disease caused by the HIV and by simian immunodeficiency virus.
Recent findings: Studies in nonhuman primate models of lentiviral infection and in HIV-infected human individuals have shown that pathogenic infection is associated with loss of Th17 cells and an increase in the frequency of Tregs. Because interleukin-17 serves to maintain the integrity of the mucosal barrier, loss of Th17 cells may permit the increase in microbial translocation across the gastrointestinal mucosa that is observed in pathogenic lentiviral disease. It remains unclear, however, whether Th17 cells are preferentially infected or if, instead, their loss is induced by bystander effects of lentiviral infection, for example, the induction of indoleamine 2,3-dioxygenase.
Summary: Progressive lentiviral disease is associated with preferential depletion of Th17 cells and loss of Th17/Treg balance. Further analysis of such changes in the composition of subset CD4+ T helper and Tregs may shed new light on the immunopathology of HIV disease and suggest new strategies for therapeutic and preventive interventions.
Kanwar, B., Favre, D., and McCune, J. M.
Current Opinion in HIV and AIDS:
March 2010 - Volume 5 - Issue 2 - p 151–157
doi: 10.1097/COH.0b013e328335c0c1
journals.lww.com/co-hivandaids/pages/articleviewer.aspx
Purpose of review: The present review discusses recent reports showing that reciprocal changes in T helper interleukin-17-secreting CD4+ Th17 cells and CD4+CD25highFoxP3+ regulatory T cells (Tregs) may play a role in the progressive disease caused by the HIV and by simian immunodeficiency virus.
Recent findings: Studies in nonhuman primate models of lentiviral infection and in HIV-infected human individuals have shown that pathogenic infection is associated with loss of Th17 cells and an increase in the frequency of Tregs. Because interleukin-17 serves to maintain the integrity of the mucosal barrier, loss of Th17 cells may permit the increase in microbial translocation across the gastrointestinal mucosa that is observed in pathogenic lentiviral disease. It remains unclear, however, whether Th17 cells are preferentially infected or if, instead, their loss is induced by bystander effects of lentiviral infection, for example, the induction of indoleamine 2,3-dioxygenase.
Summary: Progressive lentiviral disease is associated with preferential depletion of Th17 cells and loss of Th17/Treg balance. Further analysis of such changes in the composition of subset CD4+ T helper and Tregs may shed new light on the immunopathology of HIV disease and suggest new strategies for therapeutic and preventive interventions.