Infliximab Does Not Lead to Reduction in the Interferon-gamma and Lymphoproliferative Responses of Patients with Moderate to Severe Psoriasis

Abstract

Treatment of patients with immune-mediated inflammatory diseases with anti-tumour necrosis factor (anti-TNF) agents increases the risk of tuberculosis reactivation, suggesting that it may affect their cellular immune responses. We evaluated cellular immune responses of 12 severe psoriasis patients before and during infliximab treatment. Peripheral blood mononuclear cells were stimulated with phytohaemagglutinin, the superantigen enterotoxin B (SEB), a cytomegalovirus lysate (CMV), and Mycobacterium tuberculosis (Mtb) antigens. The lymphocyte proliferative and IFN-γ responses were evaluated. Treatment with infliximab did not lead to reduction in the IFN-γ and lymphoproliferative responses: it rather increased the overnight release of IFN-γ in phytohaemagglutinin and SEB stimulated cultures. This effect was most noted at the peak of the anti-TNF clinical effect and less prominent at its nadir. Immunoreactivity to CMV was also either unaffected or slightly increased by the anti-TNF. Of note, the IFN-γ and proliferative responses to Mtb by the two tuberculin skin test-reactors were also increased at the peak of infliximab, declining at its nadir. The deleterious consequences of TNF blockade in severe psoriasis patients undergoing infliximab treatment are apparently attenuated by the abbreviation of the immunosuppressive effect of TNF overexpression.

CD4+T-Cell Dysfunction in Severe COVID-19 Disease Is Tumor Necrosis Factor-α/Tumor Necrosis Factor Receptor 1–Dependent

“…Indeed, Cope and colleagues demonstrated that chronic TNF-α exposure inhibited T-cell proliferation and cytokine production through TNFRI (p55-receptor) and that in vitro proliferative and type-1 cytokine responses could be rescued using anti-TNF–α therapy, consistent with our observations ( 36 ). Interestingly, several reports have shown increased IFNγ T-cell responses in patients on infliximab therapy, consistent with our findings on Day 6 in vitro ( 37 – 40 ). In contrast to our findings, other studies have found a T-cell inhibitory role of T-cell–receptor-dependent activation through TNFRII and chronic TNF-α exposure ( 41 ).…”

Does biological therapy affect interferon-γ release assay response? A long-term follow-up of patients with psoriasis using QuantiFERON-TB

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Incidence of human cytomegalovirus infection and T-cell response in patients with psoriasis before and during antitumour necrosis factor-α therapy

“…In previous studies, anti‐TNF‐α treatment did not reduce interferon‐γ production or proliferation by HCMV‐specific T cells in patients with moderate‐to‐severe psoriasis or rheumatoid arthritis . Furthermore, we observed that anti‐TNF‐α drugs did not alter the polyfunctionality (ability of T‐cell subsets to produce more than one cytokine) of HCMV‐specific T cells (data not shown).…”