Abstract
CD4 T cells are well known for their supportive role in CD8 T cell and B cell responses during viral infection. However, during murine cytomegalovirus (MCMV) infection in the salivary glands (SGs), CD4 T cells exhibit direct antiviral effector functions to control the infection. In this mucosal organ, opposed to other infected tissues, MCMV establishes a sustained lytic replication that lasts for several weeks. While the protective function of CD4 T cells is exerted through the production of the pro-inflammatory cytokines interferon gamma (IFNγ) and tumor necrosis factor alpha (TNF), the reasons for their markedly delayed control of lytic MCMV infection remain elusive. Here, we review the current knowledge on the dynamics and mechanisms of the CD4 T cell-mediated control of MCMV-infected SGs, including their localization in the SG in relation to MCMV infected cells and other immune cells, their mode of action, and their regulation.
Highlights
We summarize the current understanding of the immune control mediated by CD4 T cells in MCMV-infected salivary glands (SGs)
This review summarizes the current understanding of the CD4 T cell-mediated immune control in MCMV-infected SGs
Investigations on Th1-related chemokine receptors revealed an organ-dependent function of CXCR3 and chemokine receptor type 5 (CCR5) for the organ infiltration of T cells, with no apparent role for infiltration of the SGs [24,37]
Summary
A persistent phase may result from the acute infection due to diverse immune evasion mechanisms, in particular in the salivary glands (SGs) These are a preferred mucosal site of persistent CMV replication, playing a central role in horizontal transmission. Cytotoxic CD8 T cells can control lytic infection in most organs, and despite a significant higher ratio in the SGs during MCMV infection, early studies defined this mucosal organ as an exception, where only virus-specific CD4 T cells are able to achieve control of lytic replication [15,20,21,22]. IFNγ producing CD4 T cells—reflecting higher ratio in the SGs during MCMV infection, early studies defined this mucosal organ as an exception, where only virus-specific CD4 T cells are able to achieve control of lytic replication [15,20,21,22]. We describe the control exerted by CD4 T cells during latency to prevent reactivation and re-infection
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