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Published on: July 6, 2013
Influence of cytomegalovirus infection on immune cell phenotypes in patients with common variable immunodeficiency
Sayed Mahdi Marashi1, Mohammed Raeiszadeh, Victoria Enright
1Medical Research Council Centre for Medical Molecular Virology, Division of Infection and Immunity, Royal Free Campus, University College London Medical School, London, United Kingdom.
Insights
Cytomegalovirus (CMV) infection drives T-cell abnormalities in common variable immunodeficiency (CVID), linking CMV to inflammatory complications and explaining treatment efficacy.
Area of Science:
- Immunology
- Virology
- T-cell biology
Background:
- Common variable immunodeficiency (CVID) patients can experience severe inflammatory issues.
- Cytomegalovirus (CMV) infection is linked to these inflammatory complications and abnormal T-cell responses.
Purpose of the Study:
- To investigate the T-cell response to CMV in CVID patients.
- To assess CMV's impact on immune effector cells in CVID.
Main Methods:
- Utilized antibody staining, peptide stimulation, and proliferation assays.
- Profiled CMV-specific T-cell function and immune cell populations.
Main Results:
- CMV infection causes the characteristic CD4/CD8 ratio inversion in CVID.
- Expanded late effector CD8(+) T-cells, driven by CMV, correlate with inflammation.
- CMV-specific CD8(+) cells release factors (IFN-γ, TNF-α) that promote proliferation, explaining inflammatory mechanisms.
Conclusions:
- Reinforces the link between CMV and CVID-associated inflammation.
- Explains T-cell abnormalities and provides a mechanism for anti-inflammatory and antiviral therapies in CVID.
Background:
A subset of patients with common variable immunodeficiency (CVID) have debilitating inflammatory complications strongly associated with cytomegalovirus (CMV) infection and a hyperproliferative CMV-specific T-cell response.
Objectives:
We studied the T-cell response to CMV and the global effect of this virus on immune effector cell populations in patients with CVID.
Methods:
Antibody staining, peptide stimulation, and proliferation assays were used to profile CMV-specific T-cell function.
Results:
CMV infection drives the CD4/CD8 ratio inversion that is characteristic of CVID. The late effector CD8(+) T-cell subset is expanded in CMV-infected patients with CVID. This expansion is largely attributable to CMV-specific cells and correlates with inflammatory disease; within the CMV-specific population, the frequency of late effector cells correlates inversely with the frequency of cells expressing programmed death 1. Supernatants from proliferating CMV-specific CD8(+) cells from patients with inflammatory disease can confer proliferative potential on cells from patients with noninflammatory CVID and healthy subjects. Blocking experiments showed that this proliferation is mediated in part by IFN-γ and TNF-α.
Conclusions:
These data strengthen the association of CMV with inflammatory pathology in patients with CVID, explain some of the well-known T-cell abnormalities associated with this condition, and provide a plausible mechanism for the documented therapeutic activity of anti-TNF-α and antiviral chemotherapy in managing CVID-associated inflammatory disease.
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