interferon (Oiaif / OIF)

Negative Interferon-gamma Release Assays and Purified Protein Derivative Does Not Exclude Tuberculosis in Inborn Errors of Immunity.

Hotaman Büşra B, Cagdas Deniz D

Serum Interferon-γ Is Associated With Refractory Mycoplasma pneumoniae Pneumonia in Children.

Han Hye Young HY, Oh Jeong-Min JM, Rhim Jung-Woo JW, Chang Mea-Young MY et al.

Mycoplasma pneumoniae (MP) infection is associated with refractory severe clinical course, and steroid therapy has been suggested as an effective treatment for refractory MP pneumonia. A total of 53 patients with MP pneumonia and 9 patients with viral pneumonia patients were enrolled. Point mutations at residues 2063, 2064, and 2067 in domain V of 23S rRNA gene were analyzed, and serum levels of interferon (IFN)-γ, interleukin (IL)-6, TNF-α, IL-10, and IL-1β were measured before and after steroid treatment. There was no significant difference in serum cytokine concentrations between the MP pneumonia group and the viral pneumonia group. The A2063G point mutation was identified in 72% (18/25) of tested MP pneumonia patients. IFN-γ and IL-6 levels showed significant positive correlations with the duration of hospitalization, fever after admission and duration of steroid treatment. The macrolide-resistant MP (MRMP) group tended to have higher IFN-γ levels than the macrolide-sensitive MP group (P = 0.055). Notably, all patients (n = 9) with the highest IFN-γ levels (ranked in descending order) belonged to the MRMP group. Steroid treatment significantly reduced IFN-γ and IL-6 levels, suggesting effective modulation of excessive immune responses. LDH and AST levels were also correlated with IFN-γ and IL-6. Therefore, IFN-γ may serve as a valuable biomarker for predicting a refractory clinical course of MP pneumonia. In addition, LDH and AST levels, which showed the closest correlation to IFN-γ and IL-6, may also be proposed as indicators of disease severity.

Nucleos(t)ide withdrawal vs Nucleos(t)ide withdrawal with adjuvant pegylated-interferon in HBeAg-negative hepatitis B virus infection (NUC-B Trial).

Thursz Mark M, Lemoine Maud M, Brown Ashley A, Carey Ivana I et al.

Finite therapy resulting in sustained hepatitis B surface antigen (HBsAg) loss for patients with chronic HBV infection (CHB) is an important therapeutic goal. In patients with HBeAg-negative infection, nucleos(t)ide analogue (NA) withdrawal may achieve HBsAg loss in 5-20% of patients after 3 years. Pegylated interferon (PEG-IFNa) is a recognised treatment for CHB. NUC-B was a randomised, multi-centre trial in NA-treated non-cirrhotic HBeAg negative patients with CHB. Patients were allocated to either NA withdrawal alone (control) or NA withdrawal followed by a 16 week course of PEG-IFNa 180ug weekly commencing 4 weeks after NA cessation (PEG-IFNa). The primary endpoint was HBsAg loss at 3 years. The target recruitment of 240 patients was not achieved. 156 patients, 82 to control arm , 74 to PEG-IFNa arm , were recruited between 2017 and 2021; median age 45 years, 24% female, HBV Genotypes -A 16%, B 6%, C 4%, D 24%, E 22%, other 1%, unknown 26%. At 3 years 3% of patients in the contol arm and 14% of patients in the PEG-IFNa arm lost HBsAg (odds ratio 5.39; 95% confidence interval, (1.11, 26.19); p=0.037). In the control arm 34.9% of patients returned to NA therapy compared to 28.4% in the PEG_IFNa- arm. Exaggerated flares occurred in 27.9% of patients in the control arm compared with 13.4% in the PEG-IFNa arm. The use of adjuvant PEG-IFNa therapy after withdrawal of NA therapy increases the rate of HBsAg loss whilst simultaneously reducing the number of exaggerated flares.

Therapy-Associated Vitiligo: Hypopigmentation Secondary to Programmed Cell Death Protein 1 Inhibitors, Interferon Alfa-2b, Cytotoxic T-Lymphocyte-Associated Protein 4 Inhibitors, and B-Raf/Mitogen-Activated Protein Kinase Kinase Inhibitors.

Verma Kritin K KK, Reddy Sreeya S, Beckham Caleb C, Nguyen Kevin T KT et al.

Background Malignant melanoma (MM) arises from melanocytes, and vitiligo is an autoimmune condition targeting these cells. Although an association between MM and vitiligo has been proposed, underlying mechanisms remain unclear. Because several melanoma treatments modulate immune responses, this study evaluated the relationship between MM and vitiligo across commonly used systemic therapies. Methods In September 2025, using the TriNetX network, patients with MM receiving programmed cell death protein 1 (PD-1) inhibitors, interferon alpha-2b (IFN-α2b), B-Raf serine/threonine kinases (BRAF)/ mitogen-activated protein kinase kinases (MEK) inhibitors, or cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) inhibitors were identified and 1:1 propensity score-matched to patients without MM receiving the same therapy. Demographics and vitiligo incidence were analyzed using risk ratios (RRs) and 95% confidence intervals (CIs) via Wald's method. Counts <10 were suppressed per platform guidelines. Results Baseline demographics were well balanced between MM and matched non-MM patients. MM was significantly associated with higher vitiligo risk among those treated with PD-1 inhibitors (RR: 24.84; 95% CI: 16.92-36.45), IFN-α2b (RR: 3.10; 95% CI: 1.53-6.30), and CTLA-4 inhibitors (RR: 32.04; 95% CI: 18.05-56.88). In the BRAF/MEK cohort, vitiligo occurred only in patients with MM, preventing RR calculation. Conclusions Across multiple therapeutic classes, MM consistently conferred a greater risk of developing vitiligo compared with matched non-MM patients. The strong associations observed with immune-modulating agents support vitiligo as a potential marker of antitumor immune activation rather than a coincidental adverse event. Even rare cases in BRAF/MEK-treated patients suggest that targeted therapy may also influence melanocyte-directed immunity. Further prospective studies are needed to characterize the clinical and immunologic significance of treatment-associated vitiligo.